StemCell Therapy

While the rate of death from cancer has been declining since the 1990s, an estimated 9.6 million people died from cancer in 2018, making it the second-leading cause of death worldwide [1]. According to the NCI Cancer Trends Progress Report, in the United States, the incidence and death rates of some cancer types have also been increasing. Together, these facts indicate that despite tremendous recent progress, the research community unfortunately still has a long list of tasks to complete to end global suffering from cancer.

The clinical management of cancer has long been rooted in morphological and histopathological analyses for diagnosis, and the triad of surgery, chemotherapy, and radiation for treatment. However, we are quickly moving towards a pervasive reliance on high resolution, high throughput, molecular marker-based diagnostic as well as precision-targeted therapeutic modalities. The progressive development of the paradigm that defined molecular drivers of cancer has exposed therapeutic vulnerabilities; for example, the BCR-ABL1 gene fusion in chronic myeloid leukemia, KIT mutations in gastrointestinal stromal tumors, ERBB2 amplification in a subset of breast cancers, or EGFR mutations and ALK/ ROS/ RET gene fusions in lung cancers to name a few. Fueled by advances in high-throughput sequencing, it is increasingly practical (and arguably affordable) to systematically pursue Targeted Anticancer Therapies and Precision Medicine in Cancer.

PLOS ONE, together with PLOS Computational Biology, launched a Call for Papers earlier this year to increase understanding of this clinically important area. The scope of this call encompassed four areas: identification and classification of driver genes and somatic alterations; target and drug discovery; mechanisms of drug resistance; and early detection and screening.

Today, we are very happy to announce the launch of the resulting Collection. Featuring an initial set of nearly two dozen papers, with more to be added as they are published, these articles represent diverse facets of ongoing efforts in this area, where general knowledge of cancers serves to inform individual patients care, and at the same time particulars from individual cancer cases contribute to improved resolution of our general knowledge pool.

Somatic aberrations that are critical to the development, growth and progression of cancer are defined as drivers that are typically accompanied by large numbers of incidental aberrations referred to as passengers, acquired in the tumors due to the general chromosomal instability characteristic of advanced cancers. Distinguishing driver aberrations from passengers in individual tumors represents an active area of research that involves development of smarter analytical algorithms, as well as definitive functional characterization of candidate aberrations.

Emilie A. Chapeau et al. developed a conditional inducible transgenic JAK2V617F mouse model that recapitulates aspects of human myeloproliferative neoplasms, including splenomegaly, erythroid expansion and hyperproliferation of bone marrow, with some intriguing differences seen between male and female mice. Importantly, the disease phenotype was reversible when transgene expression was switched off. This work underscores the key role for JAK2V617F in the initiation and maintenance of myeloproliferative neoplasms, and suggests that inhibitors specific to this JAK2 mutation might be efficacious in this disease [2].

Using targeted exon sequencing and array comparative genomic hybridization (CGH), Gayle Pageau Pouliot et al. identified monoallelic mutations in Fanconi-BRCA pathway genes in samples collected from children with T cell acute lymphoblastic leukemia (T-ALL). These mutations appeared to arise in early stages of tumorigenesis, suggesting a potential role for Fanconi-BRCA pathway insufficiency in the initiation of T-ALL. Although PARP inhibitors did not affect viability of isolated T-ALL cells with monoallelic Fanconi-BRCA mutations, these cells were hypersensitive to UV irradiation in vitro or ATR inhibition in vivo, suggesting that ATR inhibitors might have therapeutic value in T-ALL [3].

Three papers in this Collection examine links between genetic alterations and prognosis. Sumadi Lukman Anwar et al. report that LINE-1 hypomethylation in human hepatocellular carcinoma samples correlates with malignant transformation, decreased overall survival and increased tumor size [4]. Investigating HER2-positive breast cancer specimens, Arsalan Amirfallah et al. found that high levels of vacuole membrane protein 1 (VMP1) could potentially contribute to cancer progression and might be a marker of poor prognosis [5]. Finally, in their systematic review and meta-analysis, Chia Ching Lee et al. identified low discordance rates in EGFR mutations between primary lung tumors and distant metastases, although they note some differences depending on metastatic site. Notably, discordance rates appear to be higher in bone metastases compared to central nervous system or lung metastases [6]. These studies provide much-needed leads for the potential development of new diagnostic tests or targeted therapies.

Precision therapy of cancers is premised on the identification of tumor-specific driver aberrations that are necessary for tumor growth and survival. These aberrations represent potential therapeutic targets. While matching therapeutics have been developed for some of the tumor-specific targets, particularly many oncogenic kinases, a large number of defined driver aberrations remain in search of effective therapies. Drug discovery efforts to match defined targets represent a vigorous area of ongoing research with implications for survival and quality of lives of cancer patients worldwide. The development of drugs to treat cancers driven by transcription factors, chromatin modifiers, and epigenetic modulators has proved particularly challenging. On the other hand, recent development of novel immunotherapeutic approaches has spurred research to identify potential targets and matching drug discovery efforts.

This Collection highlights several interesting new strategies to identify potential lead compounds for cancer treatment. Thomas W. Miller et al. describe the development of a biochemical quantitative high-throughput screen for small molecules that disrupt the interaction between CD47 and SIRP. Preclinical studies have shown that disrupting this interaction may provide a new approach for cancer immunotherapy. Small molecular inhibitors that specifically target the interaction between CD47 and SIRP are potentially advantageous over biologics that target CD47, because they might have less on target toxicologic issues and greater tissue penetrance [7].

Work from Gabrielle Choonoo, Aurora S. Blucher et al. examines the feasibility of repurposing existing cancer drugs for new indications. The authors compiled information about somatic mutations and copy-number alterations in over 500 cases of head and neck squamous cell carcinoma (HNSCC) and mapped these data to potential drugs listed in the Cancer Targetome [8]. This approach uncovered pathways that are routinely dysregulated in HNSCC and for which potential anti-cancer therapies are already available, as well as those for which no therapies exist. The work opens new therapeutic avenues in the treatment of this disease and also illuminates which pathways could be prioritized for the development of therapies [9].

Another important approach in extending the clinical utility of existing anti-cancer drugs is to determine whether they are effective in other settings. Indeed, Kirti Kandhwal Chahal et al. have demonstrated that the multi-tyrosine kinase inhibitor nilotinib, which is approved for use in chronic myeloid leukemia, binds the Smoothened receptor and inhibits Hedgehog pathway signaling. Nilotinib decreased viability of hedgehog-dependent medulloblastoma cell lines in vitro and in patient-derived xenografts in vivo, suggesting that nilotinib might be an effective therapy in Hedgehog-dependent cancer [10]. (Check out the authors preprint of this article on bioRxiv.) Darcy Welch, Elliot Kahen et al. took a different approach to identify new tricks for old drugs. By testing two-drug combinations of five established (doxorubicin, cyclophosphamide, vincristine, etoposide, irinotecan) and two experimental chemotherapeutics (the lysine-specific demethylase 1 (LSD1) inhibitor SP2509 and the HDAC inhibitor romidepsin), they found that combining SP2509 with topoisomerase inhibitors or romidepsin synergistically decreased the viability of Ewing sarcoma cell lines in vitro [11].

Two papers in this collection describe potential new therapeutic approaches in cancer. Vagisha Ravi et al. developed a liposome-based delivery mechanism for a small interfering RNA targeting ferritin heavy chain 1 (FTH1) and showed that this increased radiosensitivity and decreased viability in a subpopulation of glioma initiating cells (GICs) [12]. Yongli Li et al. identified 2-pyridinealdehyde hydrazone dithiocarbamate S-propionate podophyllotoxin ester, a podophyllotoxin derivative that inhibits matrix metalloproteinases and Topoisomerase II. Treatment with this compound decreased the migration and invasion of human liver cancer cell lines in vitro, as well as growth of HepG2-derived tumors in mouse xenografts [13].

The success of precision cancer therapy targeting defined somatic aberrations is hampered by an almost inevitable, eventual treatment failure due to the emergence of drug resistance. Resistance often involves new mutations in the therapeutic target itself, or it may result due to activation of alternative pathways. Identification and therapeutic targeting of drug resistant clones represents an ongoing research problem with important practical implications for the clinical management of cancer.

Afatinib is a pan-human epidermal growth factor receptor (HER) inhibitor under investigation as a potential therapeutic option for people with gastric cancer; however, preclinical studies have found that some gastric cancer cell lines are resistant to afatinib treatment. Karolin Ebert et al. identify a potential mechanism behind this lack of response, demonstrating that siRNA-mediated knockdown of the receptor tyrosine kinase MET increases afatinib sensitivity of a gastric cancer cell line containing a MET amplification. As upregulation of MET has been linked to resistance to anti-HER therapies in other cancers, these findings support a role for MET in afatinib resistance in gastric cancer and suggest that combined afatinib and anti-MET therapy might be clinically beneficial for gastric cancer patients [14].

Identifying mechanisms to circumvent drug resistance is critically important to improve response and extend survival, but it is equally important to identify individuals who could be at risk of not responding to anti-cancer therapeutics. Lucas Maahs, Bertha E. Sanchez et al. report progress towards this end, showing that high expression of class III -tubulin in metastatic castration-resistant prostate cancer (CRPC) correlated with decreased overall survival and worse response rate (as measured by changes in prostate-specific antigen (PSA) levels) in CRPC patients who received docetaxel therapy. The development of a biomarker indicating potential treatment resistance to docetaxel could help develop treatment plans with the best chance of success [15].

The converse approach identifying biomarkers that correlate with drug sensitivity could help distinguish subsets of patients who would benefit most from a certain anti-cancer therapy. Kevin Shee et al. mined publicly available datasets to identify genes whose expression correlate with sensitivity and response to chemotherapeutics and found that expression of Schlafen Family Member 11 (SLFN11) correlates with better response to a variety of DNA-damaging chemotherapeutics in several types of solid tumors [16]. Separately, Jason C. Poole et al. validated the use of the Target Selector ctDNA assay, a technology developed by their group that allows the specific amplification of very low frequency mutant alleles in circulating tumor DNA (ctDNA). Testing for EGFR, BRAF and KRAS mutations yielded a very high, >99% analytical sensitivity and specificity with the capability of single mutant copy detection, indicating that accurate molecular disease management over time is possible with this minimally invasive method [17].

Work from Georgios Kaissis, Sebastian Ziegelmayer, Fabian Lohfe et al. uses a machine learning algorithm to differentiate subtypes of pancreatic ductal adenocarcinoma based on 1,606 different radiomic features. Intriguingly, the subtypes identified in their analysis correlated with response to chemotherapeutic regimens and overall survival [18]. An imaging approach taken by Seo Young Kang et al. demonstrates the potential power of fluorodeoxyglucose (FDG) PET/CT scans in determining the response of people with metastatic differentiated thyroid cancer to radioactive iodine treatment [19].

Since cancer growth and development accrues progressive accumulation of somatic aberrations, early detection holds the promise of more effective interventions. Similarly, screening of at risk demographics has been found effective in preventing or better managing cancer care, as exemplified by the significant reduction in cases of cervical cancer after the introduction of the Pap smear as well as human papillomavirus (HPV) testing.

Biomarker development is also critically important for the early detection of cancer and metastatic disease; moreover, biomarkers are being identified that can provide insight into patient prognosis. Several papers in this Collection report interesting findings in the area of biomarker development. A report from Lingyun Xu et al. describes a magneto-nanosensor-based multiplex assay that measures circulating levels of PSA and four proteins associated with prostate cancer. This approach segregates people with prostate cancer from those with benign prostate hyperplasia with high sensitivity and specificity [20].

Two articles provide new insight into markers of disease progression and survival. Vidya Balagopal et al. report the development of a 22-gene hybrid-capture next generation sequencing panel to identify measurable residual disease in patients with acute myeloid leukemia (AML). In their retrospective study, the panel was effective at detecting evidence for residual disease. Importantly, it correctly identified patients who had never relapsed in that no evidence of residual disease was detected in any of these respective samples. Once validated, this approach could potentially be useful in monitoring patients with AML to ensure that recurrence or relapse is identified as soon as possible [21]. Separately, Yoon-Sim Yap et al. use a label-free microfluidic platform to capture circulating tumor cells (CTCs) from people with breast cancer and show that absolute numbers of CTCs predict progression-free survival with higher levels of CTCs correlating with a worse prognosis [22].

Finally, Lucia Suzuki et al. report findings into a potential role for the intestinal stem cell marker olfactomedin 4 (OLFM4) as a biomarker for metastasis in esophageal adenocarcinoma. The authors found that OLFM4 expression was not significantly associated with disease-free or overall survival; however, low OLFM4 expression was detected in poorly differentiated early and advanced-stage esophageal adenocarcinoma and was an independent prognostic variable for lymph node metastasis [23].

This collection of studies encompassing the range of research topics under the banner of targeted anticancer therapies highlights the diversity, complexity and inter-disciplinary nature of research efforts actively contributing to our collective knowledge base with the hope to positively impact the lives of all cancer patients.

We would like to thank all Academic Editors and reviewers for their expert evaluation of the articles in this Collection as well as the authors for their contributions to this field. Special thanks to Senior Editor, Team Manager Emily Chenette for her invaluable help and guidance in publishing this Collection.

Andrew Cherniack

Andrew Cherniack is a group leader in the Cancer Program at the Broad Institute of MIT and Harvard and in the Department of Medical Oncology at the Dana Farber Cancer Institute. He led the Broad Institutes effort to analyze somatic DNA copy number alterations for The Cancer Genome Atlas (TCGA) and is now co-principal investigator of the Broad Institutes copy number Genome Data Analysis Center for the National Cancer Institutes Genomic Data Analysis Network (GDAN). He also leads the oncoming effort to identify new cancer therapeutic targets for the partnership with Bayer. Prior to joining the Broad Institute in 2010, Dr. Cherniack worked in both academia and industry, with a 9-year tenure at the Abbott Bioresearch Center following a similar time period in the Program in Molecular Medicine at UMass Medical School, where he was a postdoctoral researcher and a research assistant professor. Dr. Cherniack holds a Ph.D. in molecular genetics from Ohio State University and a B.A. in biology from the University of Pennsylvania.

Anette Duensing

Anette Duensing is an Assistant Professor of Pathology at the University of Pittsburgh School of Medicine and a Member of the Cancer Therapeutics Program at the University of Pittsburgh Medical Center (UPMC) Hillman Cancer Center. Dr. Duensings research focuses on bone and soft tissue sarcomas with the goal of identifying novel therapeutic approaches that target the underlying molecular biology of these malignancies. Her special interest and expertise are in gastrointestinal stromal tumors (GISTs), a sarcoma characterized by mutations in the KIT or PDGFRA receptor tyrosine kinases and the first solid tumor entity that was successfully treated with small molecule kinase inhibitors. Dr. Duensing holds an M.D. degree from the University of Hannover School of Medicine, Germany, and was a research scholar of the Dr. Mildred Scheel Stiftung fr Krebsforschung (German Cancer Aid/Deutsche Krebshilfe) at Brigham and Womens Hospital, Harvard Medical School. She is the recipient of an AACR Scholar-in-Training Award (AACR-AstraZeneca), a Young Investigator Award from The Liddy Shriver Sarcoma Initiative, a UPCI Junior Scholar Award, a Jeroen Pit Science Award, a Research Award from the GIST Group Switzerland and was named Hillman Fellow for Innovative Cancer Research. Dr. Duensing is co-founder and leader of the Pittsburgh Sarcoma Research Collaborative (PSaRC), a highly translational, interdisciplinary sarcoma research program. She is also affiliated with the Department of Urology at the University of Heidelberg, Germany. Dr. Duensing is an Academic Editor for PLOS ONE and author of nearly 70 original articles, reviews and book chapters.

Steven G. Gray

Steven Gray graduated from Trinity College Dublin in 1992. He joined the laboratory of Tomas J. Ekstrm at the Karolinska Institute (Sweden) in 1996 and received his PhD in 2000. He moved to the Van Andel Research Institute in Michigan, USA where he continued his studies on the therapeutic potential of histone deacetylase inhibitors in the treatment of cancer. He also spent time as a visiting fellow at Harvard Medical School, Boston working on epigenetic therapies for neurodegenerative disease. Returning to Europe, Dr. Gray spent some time at the German Cancer Research Centre (DKFZ Heidelberg), and subsequently moved to Copenhagen to work for Novo Nordisk as part of the research team of Prof Pierre De Meyts at the Hagedorn Research Institute working on epigenetic mechanisms underpinning diabetes pathogenesis. Dr. Gray is currently a senior clinical scientist at St Jamess Hospital at the Thoracic Oncology Research Group at St. Jamess Hospital. He holds adjunct positions at both Trinity College Dublin (senior clinical lecturer with the Dept. of Clinical Medicine), and at Technical University Dublin (adjunct senior lecturer, School of Biology DIT). Dr. Gray has published over 100 peer-reviewed articles, 15 book chapters and has edited 1 book. Research in Dr Grays laboratory focuses on Receptor Tyrosine Kinases as potential therapeutic targets for the treatment of mesothelioma; epigenetic mechanisms underpinning drug resistance in lung cancer; targeting epigenetic readers, writers and erasers for the treatment of mesothelioma and thoracic malignancy; circulating tumour cells; and non-coding RNA repertoires in mesothelioma and thoracic malignancy.

Sunil Krishnan

Sunil Krishnan is the Director of the Center for Radiation Oncology Research and the John E. and Dorothy J. Harris Professor of Gastrointestinal Cancer in the department of Radiation Oncology at MD Anderson Cancer Center. He received his medical degree from Christian Medical College, Vellore, India and completed a radiation oncology residency at Mayo Clinic, Rochester, Minnesota. In the clinic, he treats patients with hepatobiliary, pancreatic and rectal tumors with radiation therapy. His laboratory has developed new strategies and tools to define the roles and mechanisms of radiation sensitization with gold nanoparticles, chemotherapeutics, biologics and botanicals. Dr. Krishnan serves as the co-chair of the gastrointestinal scientific program committee of ASTRO, co-chair of the gastrointestinal translational research program of RTOG, consultant to the IAEA for rectal and liver cancers, chair of the NCI pancreatic cancer radiotherapy working group, and Fellow of the American College of Physicians. He has co-authored over 200 peer-reviewed scientific publications, co-authored 17 book chapters, and co-edited 3 books.

Chandan Kumar-Sinha

Chandan Kumar-Sinha is a Research Associate Scientist in the Department of Pathology at the University of Michigan. He obtained Masters in Biotechnology from Madurai Kamraj University, and PhD in Plant Molecular Biology from Indian Institute of Science. He completed a Postdoctoral Fellowship at the Department of Pathology, University of Michigan, where he worked on genomic profiling of cancers. Thereafter, he joined the Advanced Center for Treatment, Research and Education in Cancer in India as a faculty member. After establishing a cancer genomics group there, he moved back to the University of Michigan to pursue translational cancer research. Dr. Kumar-Sinhas current research involves integrative clinical sequencing using high-throughput genome and transcriptome analyses to inform precision oncology. He has authored over 50 peer-reviewed publications, two book chapters, and is named co-inventor on a patent on prostate cancer biomarkers.

Gayle E. Woloschak

Gayle Woloschak is Professor of Radiation Oncology, Radiology, and Cell and Molecular Biology in the Feinberg School of Medicine, Northwestern University. Dr. Woloschak received her Ph.D. in Medical Sciences from the University of Toledo (Medical College of Ohio). She did her postdoctoral training at the Mayo Clinic, and then moved to Argonne National Laboratory until 2001. Her scientific interests are predominantly in the areas of molecular biology, radiation biology, and nanotechnology studies, and she has authored over 200 papers. She is a member of the National Council on Radiation Protection, the International Commission on Radiation Protection and numerous other committees and also serves on the US delegation to the United National Scientific Committee on the Effects of Atomic Radiation.

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Introducing the Targeted Anticancer Therapies and Precision Medicine in Cancer Collection - PLoS Blogs

Innovation in the health care industry is seen by many as a way to address rising health care costs by improving technology, managing Big Data to develop best clinical practices, reducing pain and suffering or maybe even curing diseases.

Recent innovative developments in Michigan include a statewide telestroke program at the University of Michigan, a precision medicine program at Barbara Ann Karmanos Cancer Institute and a device that can identify pathogens developed by Seraph Biosciences Inc., a Detroit-based spinoff company of Wayne State University.

At Crain's 12th annual Health Care Leadership Summit, moderator David Ellis, a futurist and also head of the Detroit International Research and Education Foundation, led a three-member panel on a discussion about how innovation has changed medicine and patient care.

"I like to think that my colleagues here (on the panel) are representative of the people who are moving towards the speed of light, if not at the speed of light" to develop innovative clinical solutions, Ellis said. "Innovation is not just happening, but it is happening faster and faster."

Ellis asked the panel Mollie McDermott, M.D., a neurologist and stroke specialist with Michigan Medicine; Elisabeth Heath, M.D., a medical oncologist at Karmanos; and Greg Auner, a medical engineer at Wayne State University School of Medicine to describe the biggest innovation to happen in their field in the past five years and to project the next five years.

McDermott, who is the director of the telestroke program at Michigan Medicine, said the biggest innovation in her field is the widespread use of a special type of imaging called "perfusion imaging in acute stroke." This advancement can identify tissue that could be saved through the use of thrombolytic therapy, or "clot buster" drugs, in clogged arteries.

"When I started medical school, there were interventions available for stroke out to three hours from last known normal. And now that time has expanded to 24 hours with the idea that we're selecting patients who may benefit based on this specialized imaging. Stroke call has gotten very complicated," McDermott said. "It used to be, three hours and then you're done. Now we're getting called out to 24 hours. Decision-making is very complicated and there is a lack of vascular neurology expertise in our country."

McDermott said Michigan Medicine uses its telestroke program to pass along this vascular neurology expertise to small and rural hospitals where they don't have specialists trained in perfusion imaging.

Heath, who is Karmanos' associate center director of translational sciences, said the field of genomics and precision medicine more specifically precision oncology has grown tremendously over the past five years.

"Explosion would be a small word to characterize (the pace of change) because there's no meeting that you go to now in the world of oncology where that concept (using an individual's DNA to customize cancer treatment) is not discussed," she said.

Heath said Karmanos' partnership with McLaren Healthcare Corp., a 14-hospital system based in Grand Blanc, has been especially helpful in spreading knowledge of precision oncology throughout Michigan.

McDermott said the next five years for telemedicine will bring even more specialists closer to patients in helping to diagnose complex problems. "Patients (are) at home and trying to figure out, do I need to go to the emergency room? Do I need to go to urgent care? Do I need to set up an appointment with my primary care physician? Do I need to call 911? These kinds of decisions (influenced by telemedicine or virtual care) ... seems to be the next place we're headed."

Auner, one of the co-founders of Seraph, said individualized genetic analysis will transform cancer treatment. But the massive amount of data available will challenge researchers and clinicians going forward.

"Something that is quite interesting is deep learning (or) artificial intelligence that can gather through data from different sources, images, diagnostic signals ... and put that together and provide that as a tool," Auner said. "I see that probably is the biggest future breakthrough."

Heath said the next five years will challenge medical researchers because of all the clinical data on patients. "There's a fine line between a hoarder and a collector (of clinical data)," she said. "I would really like to be a collector, not a hoarder. And at this moment we're all hoarders of data and it's wonderful ... but really understanding what it means, especially if on a patient level, that's (another) discussion."

Ellis said one of the problems hospitals, doctors and health insurers have is trusting each other to share claims data and other medical records on patients to deliver appropriate care.

"One of the reasons for that of course, is purely technical. Not every system (electronic health record) is as good as the next and data breaches do occur," Ellis said. "That's got pretty severe implications."

But he said innovations occurring now to share "Big Data" using artificial intelligence and other systems could overcome trust and technical issues.

"I always see a solution. That's why I'm the perpetual optimist," Heath said. "As an oncologist, there's always a solution. I'm not saying it's right, but I think you have to have a plan" to share and use data.

McDermott said changing provider and hospital behavior is difficult. "We're taught basically from day one of medical school not to trust anybody. You have to verify for yourself, don't trust other people's exams," she said. "I don't trust research unless I have read the methods' section. So overcoming that is a cultural, not just a pragmatic phenomenon."

Auner said there is a "scary" aspect as clinical research becomes more individualized to patients "from the standpoint of what is known about a particular patient (and) knowing everything about you genetically."

For example, what if your genetic data and predisposition to disease or illness finds its way to your health insurance company? "(They) may then predict what's going to happen to you and how that may" affect your health and premium dollars charged to you or your employer.

"The knowledge of that can be unnerving," Auner said.

Heath said the big unanswered question out there is who owns the data. She wondered if patients own their data or does the health system, the university, the researcher?

"When you say it's in my medical record, that has a lot of implications when you're talking about genomic data," she said. "Is it just knowing that its the breast cancer gene itself? Is it knowing down to the nucleotide? Are you looking at things that exist only in the webspace because we can't house it in the computer? What is that sort of ownership from a patient level?"

Ellis said the reality is right now there are companies out there like Mark Zuckerberg's Facebook that contends if there is data out there "it's mine, I'll grab it. ... It's a free for all. It's the first come, first served."

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Health care innovation moving at 'speed of light' - Crain's Detroit Business

Clinical genetics experts see value in testing more women for BRCA mutations.

Two widely tested cancer-predisposition genes areBRCA1andBRCA2. Certain inherited mutations in these genes are known to greatly increase the risk of developing several types of cancer, includingbreast,ovarian,prostate, andpancreaticcancers. Genetic testing for BRCA mutations can identify people who may benefit from risk-reduction surgery, like a mastectomy; preventive medications; or targeted therapies.

But there is a huge catch: Commercial testing kits, like the one from 23andMe authorized by the US Food and Drug Administration, test for only the three most common BRCA mutations known to run in families of Ashkenazi Jewish ancestry. Someone could test negative for these specific mutations and still be at risk for cancer from other BRCA mutations that arent included in the test. This false sense of security might dissuade someone from finding out the full extent of their cancer risk.

This is just one of the many reasons why doctors typically recommend that genetic testing be done under the guidance of a clinical genetics expert who can test for more than the most common BRCA mutations and help explain the results. Even then, questions remain about who should have testing.

What the Experts SayCurrently, doctors refer someone for genetic testing if they meet various clinical criteria, like having a family history of cancer or being diagnosed with certain cancers at a young age. But there is evidence that by limiting testing to just these individuals, some people with a BRCA mutation will be missed.

We know from our data at Memorial Sloan Kettering that if you only test people with strong family histories, you miss half the cases, saysLarry Norton, Senior Vice President in the Office of the President and Medical Director of the Evelyn H. Lauder Breast Center at MSK.

Between those with a family history and the entire US population is a large unmapped territory. Just 0.3% of the population (one in 300 individuals) has a dangerous BRCA mutation. Its not clear how to step up testing in a logical and efficient manner to capture those who are at risk.

But testing guidelines are indeed becoming moreinclusive. In August, the US Preventive Services Task Force, an independent panel of health experts, issued updated BRCA testing recommendations. In addition to women with a known family history of breast or ovarian cancer, the updated recommendations include two additional groups: women who previously had breast or ovarian cancer and are now considered cancer free and women of an ancestry known to be at a higher risk, such as Ashkenazi Jewish women.One in 40 individuals of Ashkenazi Jewish ancestry (2.5%) have a harmful BRCA mutation. The updated recommendations were published August 20 in theJournal of the American Medical Association.

In anaccompanying editorial,Mark Robson, Chief of the Breast Medicine Service at MSK, and Susan Domcheck from the University of Pennsylvania, call the addition of women with prior breast and ovarian cancer an important step forward and applaud the decision to include ancestry as a reason for testing.

Identification of individuals at risk of carrying aBRCA1/2mutation can be lifesaving and should be a part of routine medical care, they write.

Low Uptake, Risks of OvertestingEven as testing guidelines are becoming broader, there is evidence that people who are good candidates for testing are not currently availing themselves of it. For example, approximately 15% of women with epithelial ovarian cancer have aBRCA1/2mutation. Given this high frequency, experts recommend testing for all people with ovarian cancer. But that doesnt happen: Less than 30% of such women are actually tested. The numbers are even lower for underrepresented minorities and those from a low socioeconomic background.

On the flip side, Dr. Robson and his co-author caution that there are dangers to overtesting, especially when the tests in question are large multigene panels that can include up to 80 genes.

While there may be value in expanding BRCAtesting, particularly in the Ashkenazi Jewish population, this does not automatically mean that this expansion should be conducted using multigene panel tests, they write.

MSK scientists, including a team led byKenneth Offit, Chief of the Clinical Genetics Service, are actively exploring the best and most strategically effective ways of testing. They are committed to making sure that the most beneficial testing is offered to the people who need it.

Information provided by MSK (Information) is not intended as a substitute for medical professional help or advice but is to be used only as an educational aid in understanding current medical knowledge. A physician should always be consulted for any health problem or medical condition. Use of the Information is further subject toMSKs Website Terms and Conditions.

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Who Should Be Tested for a BRCA Mutation? The Science Is Evolving - Curetoday.com

(MENAFN - The Peninsula) The legal and ethical implications of using stem cells and artificial intelligence (AI) in medicine were discussed at the latest instalment of Weill Cornell Medicine-Qatar's (WCM-Q) Intersection of Law & Medicine series.Expert speakers at the event discussed the impact of recent advances in stem cell science and AI on the practice of medicine in Qatar and explored how new legal frameworks could be developed to protect the rights and safety of patients in the MENA region. The day-long event was organized by WCM-Q in collaboration with Hamad Bin Khalifa University and the University of Malaya of Kuala Lumpur, Malaysia.Stem cells are an exciting area for medical researchers because they have the potential to repair damaged or diseased tissues in people with conditions such as Parkinson's disease, type 1 diabetes, stroke, cancer, and Alzheimer's disease, among many others. Stem cells can also be used by researchers to test new drugs for safety and effectiveness.WCM-Q's Dr. Amal Robay, WCM-Q assistant professor in genetic medicine and director of research compliance, said: 'Stem cells have the capacity for unlimited or prolonged self-renewal, and they can differentiate themselves into many different cell types to become tissue- or organ-specific cells with special functions. The central ethical dilemma of stem cell science arises from the fact that embryonic stem cells are derived from human embryos or by cloning, she explained.Visiting bioethics expert Dr. Jeremy Sugarman of Johns Hopkins University in Baltimore, US said that the public image of stem cell research had been damaged by a small number of high-profile cases in which scientists had behaved unethically. The field had also been hampered by different countries applying different laws to stem cell research, making international collaboration problematic, he said.Meanwhile, the use of AI in healthcare has the potential to leverage analysis of large amounts of data to improve patient outcomes, but poses ethical concerns regarding privacy, the diversity of data sources, biases and relying on non-human entities for potentially life-changing decisions.Dr. Barry Solaiman, assistant professor of law in the College of Law and Public Policy at HBKU said: 'It's very important that we bridge that gap between the professions of law and medicine, and that we understand the fundamental importance of ethicists to the advance of science. We need to consider how lawyers can help to develop laws to ensure that science advances and that it does so in ways that protect everyone involved.The event, which was co-directed by Dr. Solaiman and Dr. Thurayya Arayssi, professor of clinical medicine and senior associate dean for medical education and continuing professional development at WCM-Q, also featured other expert speakers.The event was accredited locally by the Qatar Council for Healthcare Practitioners-Accreditation Department (QCHP-AD) and internationally by the Accreditation Council for Continuing Medical Education (ACCME).

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Researchers from the University of California, Irvine developed a breakthrough cell therapy to improve memory and prevent seizures in mice following traumatic brain injury. The study, titled Transplanted interneurons improve memory precision after traumatic brain injury, was published today inNature Communications.

Traumatic brain injuries affect 2 million Americans each year and cause cell death and inflammation in the brain. People who experience a head injury often suffer from lifelong memory loss and can develop epilepsy.

In the study, the UCI team transplanted embryonic progenitor cells capable of generating inhibitory interneurons, a specific type of nerve cell that controls the activity of brain circuits, into the brains of mice with traumatic brain injury. They targeted the hippocampus, a brain region responsible for learning and memory.

The researchers discovered that the transplanted neurons migrated into the injury where they formed new connections with the injured brain cells and thrived long term. Within a month after treatment, the mice showed signs of memory improvement, such as being able to tell the difference between a box where they had an unpleasant experience from one where they did not. They were able to do this just as well as mice that never had a brain injury. The cell transplants also prevented the mice from developing epilepsy, which affected more than half of the mice who were not treated with new interneurons.

Inhibitory neurons are critically involved in many aspects of memory, and they are extremely vulnerable to dying after a brain injury, saidRobert Hunt, PhD, assistant professor of anatomy and neurobiology at UCI School of Medicine who led the study. While we cannot stop interneurons from dying, it was exciting to find that we can replace them and rebuild their circuits.

This is not the first time Hunt and his team has used interneuron transplantation therapy to restore memory in mice. In 2018, the UCI team used asimilar approach, delivered the same way but to newborn mice, to improve memory of mice with a genetic disorder.

Still, this was an exciting advance for the researchers. The idea to regrow neurons that die off after a brain injury is something that neuroscientists have been trying to do for a long time, Hunt said. But often, the transplanted cells dont survive, or they arent able to migrate or develop into functional neurons.

To further test their observations, Hunt and his team silenced the transplanted neurons with a drug, which caused the memory problems to return.

"It was exciting to see the animals memory problems come back after we silenced the transplanted cells, because it showed that the new neurons really were the reason for the memory improvement, said Bingyao Zhu, a junior specialist and first author of the study.

Currently, there are no treatments for people who experience a head injury. If the results in mice can be replicated in humans, it could have a tremendous impact for patients. The next step is to create interneurons from human stem cells.

So far, nobody has been able to convincingly create the same types of interneurons from human pluripotent stem cells, Hunt said. But I think were close to being able to do this.

Jisu Eom, an undergraduate researcher, also contributed to this study. Funding was provided by the National Institutes of Health.

Reference: Zhu, et al. (2019) Transplanted interneurons improve memory precision after traumatic brain injury. Nature Communications. DOI:https://doi.org/10.1038/s41467-019-13170-w

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Cell Therapy Aims To Improve Memory and Prevent Seizures Following Traumatic Brain Injury - Technology Networks

On this we can all agree: The lifespan of a dog is far too short. The Dog Aging Project hopes to change that.Researchers are hoping to study a group of 10,000 dogs over the course of 10 years to see whether they can improve the life expectancy of canines and their overall quality of life.Dogs' lives are six to 12 times shorter than that of humans, according to a study by the Frontiers in Veterinary Science.The researchers, which include teams from the University of Washington School of Medicine and the Texas A&M University College of Veterinary Medicine & Biomedical Sciences, are being funded by the National Institute of Aging, a division the National Institutes of Health.The researchers' expertise comes from a wide range of fields and institutions. All together, it will be the largest-ever study on aging in dogs. But their scope expands far beyond: The researchers hope that the information they learn could eventually be applied to humans as well."Dogs truly are science's best friends," the research team told CNN in a joint statement. "Though they age more rapidly than humans, they get the same diseases of aging, have a rich genetic makeup, and share our environment.""By studying aging in dogs," they said, "we can more quickly expand our knowledge of aging not just in dogs but also in humans." They added that the group is hopeful that their discoveries could lead to better "prediction, diagnosis, prognosis, treatment and prevention of disease."Now accepting applicantsApplications to the project are officially open.Owners can visit the Dog Aging Project's website to nominate their pooch. The submission process takes less than 10 minutes, and generally consists of questions about your canine to help the researchers learn whether he or she is the right fit.Have more questions? Here's a helpful FAQ.Dogs from all 50 states, and of all ages, sizes and breeds may apply. The researchers will even consider dogs with chronic illnesses, hoping to include as much genetic diversity as possible.That will help them identify biological and environmental factors critical to improving overall health and lifespan.And humans -- your participation is welcome too."Dogs and their owners are the heart of the Dog Aging Project," the researchers said. "People who nominate a dog will have the opportunity to partner with our research team as a citizen scientist."Owners will be asked to fill out surveys about their dog's health and life experience, and sample the dog's saliva, too.

On this we can all agree: The lifespan of a dog is far too short. The Dog Aging Project hopes to change that.

Researchers are hoping to study a group of 10,000 dogs over the course of 10 years to see whether they can improve the life expectancy of canines and their overall quality of life.

Dogs' lives are six to 12 times shorter than that of humans, according to a study by the Frontiers in Veterinary Science.

The researchers, which include teams from the University of Washington School of Medicine and the Texas A&M University College of Veterinary Medicine & Biomedical Sciences, are being funded by the National Institute of Aging, a division the National Institutes of Health.

The researchers' expertise comes from a wide range of fields and institutions. All together, it will be the largest-ever study on aging in dogs. But their scope expands far beyond: The researchers hope that the information they learn could eventually be applied to humans as well.

"Dogs truly are science's best friends," the research team told CNN in a joint statement. "Though they age more rapidly than humans, they get the same diseases of aging, have a rich genetic makeup, and share our environment."

"By studying aging in dogs," they said, "we can more quickly expand our knowledge of aging not just in dogs but also in humans." They added that the group is hopeful that their discoveries could lead to better "prediction, diagnosis, prognosis, treatment and prevention of disease."

Applications to the project are officially open.

Owners can visit the Dog Aging Project's website to nominate their pooch. The submission process takes less than 10 minutes, and generally consists of questions about your canine to help the researchers learn whether he or she is the right fit.

Have more questions? Here's a helpful FAQ.

Dogs from all 50 states, and of all ages, sizes and breeds may apply. The researchers will even consider dogs with chronic illnesses, hoping to include as much genetic diversity as possible.

That will help them identify biological and environmental factors critical to improving overall health and lifespan.

And humans -- your participation is welcome too.

"Dogs and their owners are the heart of the Dog Aging Project," the researchers said. "People who nominate a dog will have the opportunity to partner with our research team as a citizen scientist."

Owners will be asked to fill out surveys about their dog's health and life experience, and sample the dog's saliva, too.

Visit link:
Wanted: 10,000 dogs for the largest-ever study on aging in canines - WBAL Baltimore

Columnist Ben Maldonado traces the eugenicist history of Ray Lyman Wilbur. (Courtesy of Wikimedia Commons)

On Jan. 22, 1916, Ray Lyman Wilbur became the third president of Stanford University. In his inaugural speech, Wilbur promised that Stanford would aim for control of those unnecessary diseases that devour the very marrow of the [human] race and would lead in the fight against oppression, evil, ignorance, filth. These words would have perhaps been less ominous if Wilbur was not a eugenicist.

Between 1916 and 1929 and between 1933 and 1943, Ray Lyman Wilbur served as Stanfords president, leading the same university where he received his bachelors and masters degrees. A physician by training, Wilbur was influential in the development of Stanfords School of Medicine, first as dean then as university president. Wilburs key academic focus was public health: studying the health of America and methods of bettering it. This interest showed clearly in both his work at Stanford and in the Hoover Administration, where he served as Secretary of the Interior.

Wilburs interest in public health, however, also inspired his support of eugenics, the science of human improvement through selective breeding. As historian Martin S. Pernick has argued, public health and eugenics often historically went hand-in-hand what better way could there be of creating an ideal population than controlling who could reproduce and who could be born? Besides being a member of many health associations, Wilbur was also a prominent figure in eugenic organizations, such as the American Eugenics Society and the Eugenics Research Association, and often combined these two pursuits. As he put it in his 1937 article on the health of Black people, a pair of healthy grandfathers and of healthy grandmothers is the greatest personal asset a human being can have. In the name of public health, eugenic policies were therefore a necessity to Wilbur: We would not dream of treating a strain of race horses, he argued before Stanford alumni in 1935, the way we treat ourselves.

This emphasis on eugenics as a form of public health advocacy manifested in Wilburs work in the Hoover Administration as well. As historian Wendy Klein recounts, Wilbur served as conference chair at the 1930 White House Conference on Child Health and Protection, a massive convention attended by thousands of experts on child health, development and education. In his opening speech, Wilbur used eugenic language to emphasize the importance of fit future citizenry, encouraging the United States to become a fitter country in which to bring up children. Wilbur was not just supporting the health of children; he was supporting the goal of breeding eugenically fit children. As he put it in a 1913 speech, Wilbur believed that the products of the marriage of the weak and the unfit, of the criminal, of the syphilis and of the alcohol that fill many of our most splendid governmental buildings must largely disappear.

One of Wilburs greatest contributions to Stanford University as president was the development of the Stanford University School of Medicine, turning it into an organization at the forefront of medical education as well as eugenic education. Wilbur believed that all medical students should be taught the science of eugenics. He encouraged medical universities to study both the health and economic impact of the physically and mentally handicapped, promoting extensive research on eugenics. He presented before the Medical Society of the State of California in 1922, and argued that physicians must be educated to understand the importance of eugenically fit genetic material, for if it deteriorates a family or a race soon dies out. This genetic material must therefore be protected through eugenic means such as the sterilization or segregation of the unfit. With his development of the medical school, Wilbur aimed to emphasize the necessity of racial health in the name of eugenics.

Wilbur was also deeply concerned with race relations and the role of the United States in international affairs. In a 1926 speech, he expressed fear that white women were degenerating and becoming incapable of producing breast milk due to a reliance on dairy milk when nursing. For Wilbur, this was exceptionally frightening as the Chinese, who were immigrating to the American West (to the displeasure of many eugenicists) continued to use breast milk with their babies. Wilbur saw this as a eugenic threat to white dominance. If dairy production were to be halted, Chinese populations would overtake white populations a eugenicists nightmare.

Wilburs concerns with Chinese immigration led him to chair a 1923 survey looking into the potential dangers of Asian immigration into the American West. This Survey of Race Relations, as it was called, was led by many Stanford affiliates, and its findings were presented at a conference on Stanfords campus. Looking at both Chinese and Japanese immigration, this study chaired by Wilbur sought to objectively determine the value of allowing Asian immigrants to travel, stay, and reproduce in the United States. In the end, the survey concluded that Asian immigration was, for the time being, acceptable due to the cheap labor immigrants provided, but interracial marriages and reproduction were deeply discouraged. These attempts to objectively determine the value of immigrants to society was emblematic of a larger eugenic trend to quantify the value of human existence.

Wilburs belief in public health and the objective research of racial health inspired his promotion of eugenic thought. His legacy shows clearly the interconnections of medicine, public health and eugenic thought, and how many projects in the name of human health with noble intent were shaped by racist and ableist assumptions. Though he was less explicitly racist than some of his peers at Stanford, Wilbur still promoted the sterilization of unwanted people and still studied the potential dangers of non-white immigration. Today, Wilbur Hall bears his name, honoring his presidency and contributions to the University. I cannot help but wonder how many residents of that hall would be deemed unwelcome by its namesake.

Contact Ben Maldonado at bmaldona at stanford.edu.

We're a student-run organization committed to providing hands-on experience in journalism, digital media and business for the next generation of reporters.Your support makes a difference in helping give staff members from all backgrounds the opportunity to develop important professional skills and conduct meaningful reporting. All contributions are tax-deductible.

Link:
Eugenics on the Farm: Ray Lyman Wilbur - The Stanford Daily

Osteoarthritis is a degenerative joint disease that is the most common type of arthritis. Usually, it occurs among people of advanced age. But it can begin in middle age or even sooner, especially if theres been an injury to the joint.

While there are treatments available exercise, braces or canes, loss of excess weight, various pain relievers and anti-inflammatory medicines these are no cures, and none of the treatments are predictably effective. In fact, often they dont work at all, or help only a little. Injected steroids or synthetic lubricants can be tried as well. When all else fails, joint replacement surgery can be highly effective. In fact, about a million joint replacements (mostly knees and hips) are performed each year in the US.

So, its no surprise that people with osteoarthritis will try just about anything that seems reasonably safe if it might provide relief. My patients often ask about diet, including anti-inflammatory foods, antioxidants, low-gluten diets, and many others. Theres little evidence that most of these dietary approaches work. When there is evidence, it usually demonstrates no consistent or clear benefit.

Thats why a new study is noteworthy: it suggests that curcumin, a naturally occurring substance found in a common spice, might work for osteoarthritis.

In the study, researchers enrolled 139 people with symptoms of knee osteoarthritis. Their symptoms were at least moderately severe and required treatment with a nonsteroidal anti-inflammatory drug (NSAID). For one month, they were given the NSAID diclofenac (50 mg, twice daily) or curcumin (500 mg, three times daily).

Why curcumin? Its a naturally occurring substance, found in the spice turmeric, that has anti-inflammatory effects. Its use has been advocated for cardiovascular health, arthritis, and a host of other conditions. However, well-designed studies of its health benefits are limited.

Heres what this study found:

Not so fast. Its rare that a single study can change practice overnight, and this one is no exception. A number of factors give me pause:

Studies of this sort are vitally important in trying to understand whether dietary changes can be helpful for arthritis. While this new study provides support for curcumin as a treatment for osteoarthritis of the knee, Id like to see more and longer-term studies in osteoarthritis and other types of joint disease, as well as more extensive testing of its safety, before recommending it to my patients.

Read the rest here:
Curcumin for arthritis: Does it really work? - Harvard Health Blog - Harvard Health

Despite recent advances in the treatment of rheumatoid arthritis(RA) attributed to biologic medications, only a minority of patients achieve andmaintain disease remission without the need for continuous immunosuppressive therapy.1Complicating the treatment of RA further is the development of tolerance over timeor failure of patients to respond to currently available therapies.1Thus, the development of new treatment strategies for RA remains a priority.

Nanotherapies for RA have received increasing attention in the past decade because they offer several potential advantages compared with conventional systemic therapies.2 Nanocarriers are submicron transport particles designed to deliver the drug at the site of inflammation the synovium thereby maximizing its therapeutic effect and avoiding unwanted systemic adverse effects.1 This targeted drug delivery approach also has the potential to minimize the amount of drug required to control joint inflammation3 and increase local bioavailability by protecting it from degradation in the circulation.1

In essence, nanotechnology enables the redesign of alreadyeffective rheumatologic medications into nanoformulations that may confer greaterspecificity, longer therapeutic effect, and more amenable safety profile.4Nanoencapsulated nonsteroidal anti-inflammatory drugs (NSAIDs),5 liposomaland polymeric preparations of glucocorticoids,6 and nanosystems thatdirectly inhibit angiogenesis are just several examples of nanotherapies that havebeen tested in experimental models of inflammatory arthritis.7

Despite the promising findings observed in studies to date, further development and subsequent integration of nanotherapies in the management of RA remains hampered by the lack of efficacy and toxicity studies in humans. In an interview with Rheumatology Advisor, Christine Pham, MD, chief of the Division of Rheumatology at the Washington University School of Medicine in St Louis, discussed the advantages and challenges of applying nanotherapies in RA.

RheumatologyAdvisor: How can nanotechnology be applied in the treatment of RA?

ChristinePham, MD: Nanotechnology is a multidisciplinary approach aimed at the deliveryof therapeutic agents using submicron nanocarriers. In RA, the vessels at the siteof inflammation are leaky, allowing passage of these nanocarriers from the circulationto specific target sites in the joint environment.

RheumatologyAdvisor: Which RA drugs are suitable forthis approach?

DrPham: Many conventionalantirheumatic drugs such as methotrexate, glucocorticoids, and NSAIDs have beensuccessfully delivered by nanocarriers to mitigate inflammatory arthritis in experimentalmodels.

RheumatologyAdvisor: Whatare the main advantages of using nanotherapy/nanocarriers, as opposed to systemictherapy, in the treatment of RA?

DrPham: The mainadvantages are selective drug delivery to desired sites of action through passiveor active targeting, which can lead to increased local bioavailability and potentiallycan reduce unwanted off-target side effects. In addition, nanocarriers may increasethe solubility of certain drugs and protect therapeutics against degradation inthe circulation.

RheumatologyAdvisor: Howfar has the medical community gotten in developing (and testing) nanotherapies forRA? Which nanotherapies have shown the most promise?

DrPham: A numberof nanotherapeutics have been developed and tested in animal models of RA. Mosthave shown disease mitigation, however, none has so far made it to the clinic.

RheumatologyAdvisor: Whatneeds to happen before nanotherapies can get fully integrated into clinical practiceand treatment of patients with RA?

DrPham: Insufficientdata regarding long-term toxicity and optimal therapeutic efficacy have hamperedtheir integration into clinical practice. Anticytokine biologics have been verysuccessful, so nanotherapeutics need to show clearly that they have higher efficacyand lower toxicity for pharmaceutical companies to invest in their development forthe clinic.

Rheumatology Advisor: Are any other promising treatment strategies for RA currently under investigation?

DrPham: RNA interference(RNAi) has recently emerged as a specific way to silence gene expression. The invivo delivery of small interfering RNA (siRNA), however, remains a significant hurdle,given the short half-life of the molecule in the circulation. We have used a self-assemblingpeptide-based nanosystem that protects the siRNA from degradation when injectedintravenously and which has shown to mitigate experimental RA.8,9 siRNAworks by knocking down NFkappaB p65, asubunit of NF-kappa-B transcription complex which plays acentral role in inflammation in general and in RA in particular. This platform promisesto have real translational potential.

References

1. Pham CTN. Nanotherapeutic approaches for the treatment of rheumatoid arthritis. Wiley Interdiscip Rev Nanomed Nanobiotechnol. 2011;3(6):607-619.

2. Dolati S, Sadreddini S, Rostamzadek D, Ahmadi M, Jadidi-Niaragh F, Yousefi M. Utilization of nanoparticle technology in rheumatoid arthritis treatment. Biomed Pharmacother. 2016;80:30-41.

3. Rubinstein I, Weinberg GL. Nanomedicine for chronic non-infectious arthritis: the clinicians perspective. Nanomedicine. 2012;8(Suppl 1):S77-S82.

4. Henderson CS, Madison AC, Shah A. Size matters nanotechnology and therapeutics in rheumatology and immunology. Curr Rheumatol Rev. 2014;10(1):11-21.

5. Srinath P, Chary MG, Vyas SP, Diwan PV. Long-circulating liposomes of indomethacin in arthritic ratsa biodisposition study. Pharm Acta Helv. 2000;74:399-404.

6. Metselaar JM, Wauben MH, Wagenaar-Hilbers JP, Boerman OC, Storm G. Complete remission of experimental arthritis by joint targeting of glucocorticoids with long-circulating liposomes. Arthritis Rheum. 2003;48:2059-2066.

7. Koo OM, Rubinstein I, nyuksel H. Actively targeted low-dose camptothecin as a safe, long-acting, disease-modifying nanomedicine for rheumatoid arthritis. Pharm Res. 2011;28:776-787.

8. Zhou H-F, Yan H, Pan H, et al. Peptide-siRNA nanocomplexes targeting the NF-kB subunit p65 suppress nascent experimental arthritis. J Clin Invest. 2014;124:4363-4374.

9. Rai MF, Pan H, Yan H, Sandell L, Pham C, Wickline SA. Applications of RNA interference in the treatment of arthritis. Transl Res. 2019;214:1-16.

Link:
Nanotherapies for Rheumatoid Arthritis: Advantages, Challenges, and Future Direction - Rheumatology Advisor

Psoriasis in ankylosing spondylitis (AS) is not related to axial psoriatic arthritis (PsA), a type of psoriasis that causes lower back inflammation and pain similar to AS, according to a study published in Rheumatology.

The study included approximately 1303 patients with PsA and 766 patients with AS from 2 Canadian clinics. Of the patients with PsA, 477 had axial PsA and 826 had peripheral PsA. In the AS group, 91 participants had psoriasis and 675 did not.

Patients at both clinics were followed and assessed using a variety of diagnostic tools, with visits every 6 to 12 months for an average of 12.6 years for patients with axial PsA and 6.7 years for the patients with peripheral PsA. The average follow-up for AS with psoriasis was 5.4 years and 3.5 years for those without psoriasis.

The analysis showed that overall, patients with AS were younger at diagnosis, with an average age of 21.3 years in patients with psoriasis and 22.9 years in those without psoriasis compared with axial patients with PsA who had an average age at diagnosis of 34.4 years. There were also more males in both AS groups compared with the axial PsA group.

Spondyloarthritis is a family of inflammatory diseases causing arthritis and involves areas where ligaments and tendons attach to bones. AS is the most common form of spondyloarthritis and mainly affects the joints at the base of the spine where it meets the pelvis.

More patients in both AS groups tested positive for HLA-B27, a genetic marker for inflammatory arthritis of the spine and joints. Of the AS patients with psoriasis, 82% tested positive, while 75% of those without psoriasis tested positive. In the axial PsA group, only 19% tested positive.

Approximately 90% of patients with AS with psoriasis and 92% without psoriasis reported back pain compared with only 21% of patients with axial PsA. Furthermore, compared with patients with axial PsA, patients with AS and with and without psoriasis had a higher grade of sacroiliitis, or inflammation of the joints connecting the lower spine to the pelvis.

When the data were analyzed over time, there was also an increase in joint swelling in both patients with axial PsA and patients with peripheral PsA, whereas patients with AS with or without psoriasis were more likely to have back pain and a higher BASMI, or Bath Ankylosing Spondylitis Metrology Index, a measure of AS disease severity.

The study reveals that axial PsA and AS with psoriasis are 2 different diseases with different genetics, demographics, and disease expression, according to the study authors.

Reference

Excerpt from:
Ankylosing Spondylitis Not Linked to Axial Psoriatic Arthritis - Pharmacy Times

In rheumatoid arthritis patients in sustained remission on conventional synthetic disease modifying anti-rheumatic drugs (csDMARDs), continued csDMARD therapy with stable doses led to fewer disease activity flares and less frequent radiographic joint damage progression than tapered csDMARD treatment, according to a study presented at annual meeting of the American College of Rheumatology in Atlanta on November 12.

More patients with rheumatoid arthritis reach and maintain sustained remission on csDMARDs after the implementation of treat-to-target strategies. However, the knowledge about whether csDMARDs can be tapered in rheumatoid arthritis remission is limited.

The primary objective of the ARCTIC REWIND trial was to assess the effect of tapering of csDMARDs on the risk of flares in rheumatoid arthritis patients in sustained clinical remission.

In the trial, 155 rheumatoid arthritis patients (mean age 55 years) in clinical remission, as measured by the Disease Activity Score (DAS) for 44 joint counts, for at least 12 months on stable csDMARD therapy were randomly assigned to continued stable csDMARD (n=78, 64 percent female, 78.2 percent methotrexate monotherapy users) or half dose csDMARD (n=77, 69 percent female, 84.4 percent methotrexate monotherapy users), with visits every four months. The primary endpoint was the proportion of patients with a disease flare during the 12-month study period (a combination of DAS > 1.6, a change in DAS > 0.6 and at least two swollen joints, or both the physician and patient agreed that a clinically significant flare had occurred). Radiographic joint damage at baseline and 12 months was scored by van der Heijde modified Sharp score (progression: 1 unit change/year).

In an interview with Rheumatology Network, Siri Lillegraven, M.D., M.P.H, Ph.D., of Diakonhjemmet Hospital in Oslo, Norway, said the study aimed to include patients in deep remission, who had been in remission for at least a year. The study was designed as a non-inferiority study, based on the hypothesis that csDMARDs could be tapered in such a patient cohort. We were thus somewhat surprised by the clear difference in flare rates and by the difference in radiographic progression that was observed.

In the primary analysis, 6.4 percent of patients in the stable csDMARD group experienced a flare during the 12 months, compared to 24.7 percent in the half-dose csDMARD group, giving a risk difference (95% confidence interval [CI]) of 18.3 percent (7.2 percent to 29.3 percent). Non-inferiority, with a margin of 20 percent, could not be claimed.

In the stable group, 40 percent adjusted DMARD medication following the flares, compared to 94.7 percent in the half-dose group. No progression of radiographic joint damage was observed in 79.5 percent of patients on stable DMARDs and 62.7 percent in the half-dose group, difference (95% CI) -17.7 percent (-33 percent, -2.3 percent). At 12 months, 91.8 percent of patients in the stable arm and 85.1 percent of patients in the half-dose arm were in DAS remission, with similar results for other remission definitions.

A total of 75 and 53 adverse events occurred in the stable and tapered groups, respectively, with serious adverse events in 2.6 percent of patients in the stable group and in 5.1 percent, including two serious infections, of patients in the tapered group.

The results support that if a patient reaches sustained remission in RA on csDMARDs, flares are very rare if stable DMARD dose is continued, and that stable csDMARD therapy should be the preferred choice for these patients.

We find it interesting that very few disease activity flares occurred if patients in sustained remission received stable treatment, illustrating that the RA disease course can have a favorable outcome, even with the cheapest and globally most available DMARDs, Dr. Lillegraven said.

REFERENCE

LO8 - Tapering of Conventional Synthetic Disease Modifying Anti-Rheumatic Drugs in Rheumatoid Arthritis Patients in Sustained Remission: Results from a Randomized Controlled Trial. Siri Lillegraven, M.D., M.P.H, Ph.D., 9 a.m., Tuesday, Nov. 12. 2019 ACR/ARP Annual Meeting, Atlanta

More:
Conventional Therapy Bests Tapered Therapy in Rheumatoid Arthritis - Rheumatology Network

Racers of all ages will soon be gearing up in their favorite holiday costumes, along with lacing up their sneakers as they aim to cross the finish line during the Arthritis Foundations annual Jingle Bell Run on Saturday, December 7, at George M. Steinbrenner Field.

With this fundraising event, individuals can participate in the 5K untimed, 5K chip-timed, a Kids Run and a 1-Mile Fun Run or Walk. Besides the race, other festivities will also be available, such as entertainment, a kids zone, food and beverages and more.

Arthritis Foundation Development Director of Tampa Sherry Yagovane explained where 100 percent of these proceeds go to.

The funds raised will support our Live Yes! Network events, educational programs and send children to summer camp, Yagovane said. We also fund research for better treatments, cures and assist patients with access to treatments through advocacy on a state and federal level.

In 1948, the Arthritis Foundation became established. Arthritis, also known as joint disease or joint pain, can affect individuals of all ages. In fact, 300,000 children and more than 50 million Americans are diagnosed with it, according to the Arthritis Foundation. To add, arthritis is considered the leading cause of disability in America.

A couple of families shared how the Arthritis Foundation assisted them and their loved ones. For example, Tracey Corns two daughters suffer from rheumatoid arthritis. She also has volunteered with the Arthritis Foundation for more than 10 years.

This foundation means so much to our family as it provided educational resources and more, Corn said.

Carrie Shank also stated her appreciation for the foundation, as her daughter, Aubriana Gonzalez, has suffered from JIA (Juvenile Idiopathic Arthritis) since the age of 2. Gonzalez was selected to be this years Jingle Bell Run Youth Honoree.

I am passionate about this cause, and as a parent I do not feel alone on this journey with the foundation being such a great educational tool for myself, family and friends, Shank said.

To register for the walk, visit https://events.arthritis.org/index.cfm?fuseaction=donorDrive.event&eventID=930.

For more information, contact Yagovane at 467-7520.

View original post here:
Upcoming Jingle Bell Run Benefits The Arthritis Foundation - Osprey Observer

Women with rheumatoid arthritis (RA) and other rheumatic conditions who want to breastfeed their newborns are generally able to so. Thats the finding from research presented at the 2019 annual meetingof the American College of Rheumatology in Atlanta on November 11, 2019.

Related: Can a Woman Who Has Rheumatoid Arthritis Have Kids?

Still, not every woman living with rheumatic disease with this desire does follow through, in some cases because of unfounded concerns about the safety of medicines they may be taking, says study coauthor Megan Clowse, MD, director of the Duke Autoimmunity in Pregnancy Clinic and associate professor of medicine at Duke University in Durham, North Carolina.

The good news is we found quite high levels of women desiring to breastfeed, and high numbers of those successfully doing so, Dr. Clowse says.

The 265 women in the study were part of a pregnancy registry Clowse set up for her practice a decade ago. There are a lot of women with rheumatic diseases who want to breastfeed, but there was very little data about this. When I set up the registry, I made sure we asked about breastfeeding, she says.

Related: People Living With Rheumatoid Arthritis Develop Resilience by Dealing With Disease Challenges

Before they delivered, 79 percent of the pregnant women indicated their desire to nurse. By the time of their postpartum visit an average of 7.5 weeks after delivering, three-quarters of these women were in fact doing so.

This means 25 percent of the women who had hoped to breastfeed were not. Some had tried but stopped, in some cases because they couldnt develop a milk supply or because their baby had health issues.

Other women said they gave up breastfeeding because they worried that the medicines they were taking might possibly pass through to the baby.

This mindset echoes the results of a survey conducted among members of the arthritis community CreakyJoints, presented at the American College of Rheumatology meeting in September 2017.

In that survey, 86 percent of women said they had either avoided taking medicines while breastfeeding, or they stopped nursing prematurely in order to resume the drugs needed to avoid postpartum flares.

Related: Rheumatoid Arthritis: Anatomy of a Flare

But for almost all rheumatoid arthritismedication, this concern is unfounded, Clowse says. New mothers can safely nurse on nearly all RA drugs in use today, she says.

Thats because medicines like Enbrel (etanercept) and Remicade (infliximab) dont readily pass to a baby through mothers milk, and any that do get through, especially with full-term infants, are not well absorbed by their gut, according to Mother to Baby, a website created by experts on birth defect risks.

Related: Rheumatoid Arthritis Medication

Clowse even tells patients they can nurse while taking methotrexate, a medicine that women must avoid while pregnant. Breastfeeding is a different biology from pregnancy. There is very minimal transfer in breast milk, she says.

The one type of medicine Clowse does restrict from nursing mothers is small-molecule Janus kinase (JAK) inhibitors, such as Xeljanz (tofacitinib), primarily because they are so new that there is not enough data on its nursing safety.

Clowse admits that she is especially enthusiastic about allowing patients to breastfeed, because she knows first hand that it can be an important part of a mothers experience.

Plus, breast milk is so healthy. According to the American College of Obstetricians and Gynecologists (ACOG), breast milk contains antibodies that protect infants from ear infections, diarrhea, respiratory illnesses, and allergies. It also can make it easier for moms to lose pregnancy weight, and it may reduce her risks of breast cancer and ovarian cancer. This is why ACOG recommends exclusive breastfeeding for the first 6 months of life, or longer if it is mutually desired by the mother and baby.

Related: How to Find a Rheumatologist

Clowse knows that her encouragement is likely more pronounced than that of other rheumatologists, and likely explains the high numbers she found in her study, she says.

In this research, women who exclusively formula-fed babies were likely to be younger and have less education and lower incomes than nursing mothers. Although black women in her study were less likely to nurse than whites, Clowse says that was related more to the education levels of the women in her registry than their race.

If your doctor erroneously tells you that you cannot nurse on any of the medicines you are taking, you can show them the information from Mother to Baby. Theres actual data, so you dont have to base the decision on myth, Clowse says.

The reality is you can breastfeed on almost all RA medication. You dont have to pick between taking care of your disease and breastfeeding your baby, she asserts.

Aimee Matsumoto, a public relations professional in Pasadena, California,who blogs about her experience having RA, is a new mom who is determined to nurse her infant. Matsumoto is not on any medicines, having had bad reactions to those she has previously tried.

Related: Home Remedies and Alternative Therapies for Rheumatoid Arthritis

Matsumoto was fortunate to go into remission during her pregnancy, but since her baby was born 9 months ago, her pain has come back with a vengeance. When her joints flare, it can be hard to breastfeed because of the challenges of holding the baby in a nursing position, she says.

Matsumoto overcomes this by using a nursing pillow, such as My Brest Friend, to take the weight off her hands. Other time she feeds her baby while both are lying down.

Related: Rheumatoid Arthritis: 20 Home Upgrades for Under $20

A lactation consultant is the best person to help you figure out ways you can nurse that protect your joints.

You can find one near you on the website of the International Lactation Consultant Association.

See the rest here:
Rheumatoid Arthritis and Breastfeeding: What Women With RA Need to Know - Everyday Health

Compared with seven other biologics and a phosphodiesterase-4 inhibitor, the anti-IL-12/23 biologic ustekinumab was associated with a generally lower risk of serious infection requiring hospitalization in patients with psoriasis or psoriatic arthritis, researchers reported on November 12 at the American College of Rheumatology annual meeting in Atlanta.

The study included 123,383 adults (mean age 48, 50% female) with psoriasis or psoriatic arthrits who started treatment with a biologic DMARD (ustekinumab, secukinumab, ixekizumab, or a TNFi (adalimumab, etanercept, infliximab, certolizumab, golimumab) or the oral phosphodiesterase inhibitorapremilast.

Of the patients included in the analysis, 61 percent had psoriasis, 22 percent had psoriatic arthritis and 17 percent had both."Of 123,383 PsO or PsA patients, ustekinumab initiators had a generally lower risk of hospitalized serious infection compared to TNFi, IL-17 therapy, and apremilast initiators," reported Seoyoung C. Kim, M.D., of Brigham and Womens Hospital, Boston. Hospitalized serious infections were highest in patients who were prescribed infliximab and lowest in those who received ixekizumab and ustekinumab.

Ultimately, ustekinumab had a lower risk of hospitalized serious infection compared to other bDMARDs or apremilast. However, how well ustekinumab performed as compared to certolizumab and golimumab could not be determined due to the small sample size.Overall, data was consistent across all eight agents, though statistically weaker for certolizumab and golimumab.

The primary outcome was a composite endpoint of hospitalized serious bacterial, viral, or opportunistic infection. Follow-up started the first day a drug was dispensed and ran until the outcome was met, the database ended, or a patient left the study, died, or discontinued or switched drugs.

Having rigorous real-world based safety data directly comparing several drugs with a similar clinical indication is important when discussing a treatment option with patients and making a better-informed medical decision, Dr. Kim reported.

REFERENCEL01 - Comparative Risk of Hospitalized Serious Infection in Patients with Psoriasis and Psoriatic Arthritis: A Population-Based Multi-Database Study, Seoyoung C. Kim, MD, ScD, MSCE, 9 a.m., Tuesday, Nov 12. American College of Rheumatology 2019 annual meeting, Atlanta.

Follow this link:
Ustekinumab Linked to Lower Serious Infection Rates in Psoriasis and Psoriatic Arthritis - Rheumatology Network

The company said its RA 360 solution will support employees to reduce or maintain their current level of drug use

eWellness Healthcare Corporation (), the pioneer in physical therapy telehealth treatments, announced Tuesday that it is developing a new rheumatoid arthritis treatment platform called RA360.

In a statement, the Culver City, California-based company, said the new platform is expected to be available in the first quarter of 2020.

Rheumatoid arthritis and related autoimmune disorders are the leading cause of illness and disability in the US.

In 2019, one in four Americans has arthritis, or one of its 100 related autoimmune disorders, according to the company.

Those with rheumatoid arthritis will need to go on disability or stop work entirely within 2 years of onset, the group added.

However, the company said that its innovative RA360 solution will support employees to reduce or maintain their current level of theraputic drug use.

The company notes that costs associated with arthritis hit $128 billion in 2005, while other studies put the cost closer to $353 billion when payouts, lost wages and other associated medical costs were stacked up.

According to eWellness Healthcare, a reduction in symptoms will alleviate stress on the health care system and the employer.

Arthritis isnt an individual problem, its everyones problem. The damage cannot be undone but can be managed, the company added, while making the case that its new rheumatoid arthritis treatment platform RA360 was part of the solution.

eWellness Healthcare is the first physical therapy telehealth company to offer real-time distance monitored assessments and treatments.

Contact Uttara Choudhury at[emailprotected]

Follow her onTwitter:@UttaraProactive

Continued here:
eWellness Healthcare developing new rheumatoid arthritis treatment platform RA360 - Proactive Investors USA & Canada

BACKGROUND:

Recent studies have demonstrated patients with rheumatoid arthritis (RA) have deranged coagulation parameters predisposing them to venous thromboembolisms (VTEs). Therefore, the purpose of this study was to investigate whether patients who have RA undergoing primary TKA have higher rates of (1) VTEs; (2) readmission rates; and (3) costs of care.

Patients who have RA undergoing primary TKA were identified and matched to controls in a 1:5 ratio by age, sex, and comorbidities. Exclusions included patients with a history of VTEs and hypercoagulable states. Primary outcomes analyzed included rates of 90-day VTEs, along with lower extremity deep vein thromboses and pulmonary embolisms, 90-day readmission rates, in addition to day of surgery, and 90-day costs of care. A P-value less than .05 was considered statistically significant.

Patients who have RA were found to have significantly higher incidence and odds (OR) of VTEs (1.9 vs 1.3%; OR: 1.51, P < .0001), deep vein thromboses (1.6 vs 1.1%; OR: 1.55, P < .0001), and pulmonary embolisms (0.4 vs 0.3%; OR: 1.26, P= .0001). Study group patients also had significantly higher incidence and odds of readmissions (21.6 vs 14.1%; OR: 1.67, P < .0001) compared to controls. In addition, RA patients incurred significantly higher day of surgery ($12,475.17 vs $11,428.96; P < .0001) and 90-day costs of care ($15,937.34 vs $13,678.85; P < .0001).

After adjusting for age, sex, and comorbidities, the study found patients who have RA undergoing primary TKA had significantly higher rates of VTEs, readmissions, and costs.

Read the original:
Rheumatoid Arthritis Increases Venous Thromboemboli, Readmissions, and Costs of Care After Primary Total Knee Arthroplasty: A Matched-Control Analysis...

NEW YORK--(BUSINESS WIRE)--Pfizer Inc. (NYSE: PFE) announced today that positive results from a Phase 3 investigational study of tofacitinib in children and adolescents aged two to less than 18 with juvenile idiopathic arthritis (JIA) will be presented for the first time during a late-breaking oral presentation at the American College of Rheumatology (ACR)/Association of Rheumatology Professionals (ARP) Annual Meeting (November 8-13, Atlanta, GA). The study of tofacitinib in JIA is investigative and JIA is not an FDA-approved indication for XELJANZ. Pfizer has plans to file for the indication in 2020.

The JIA study is a Phase 3, randomized, double-blind, placebo-controlled withdrawal study that included 225 patients with polyarticular course JIA (n=184), psoriatic arthritis (n=20) or enthesitis related arthritis (n=21). The study evaluated the efficacy and safety of tofacitinib taken as either a 5 mg tablet or as a 1 mg/mL oral solution twice daily based on the subjects body weight.

The trial met its primary endpoint showing that in patients with polyarticular JIA, the occurrence of disease flare in patients treated with tofacitinib was significantly lower than patients treated with placebo at week 44. In this study, disease flare was defined as a 30 percent or more worsening in at least three of the six variables of the JIA core set (outcome measures used in JIA clinical trials).

The most common adverse events in this study of any treatment group were upper respiratory tract infection, headache, nasopharyngitis, nausea, pyrexia, disease progression, vomiting and JIA. There were no cases of death, major adverse cardiovascular events (MACE), malignancies, thrombosis, opportunistic infection or tuberculosis. There were two patients with herpes zoster and four patients with serious infections in the tofacitinib treatment arm throughout the course of the study.

Pediatric patients living with juvenile idiopathic arthritis need additional options, including oral therapies, to treat this chronic inflammatory disease, said Michael Corbo, Chief Development Officer, Inflammation & Immunology, Pfizer Global Product Development. We are encouraged by the results from our pivotal Phase 3 investigational study of tofacitinib in patients with polyarticular juvenile idiopathic arthritis and look forward to filing for this indication with the FDA in 2020.

About the JIA Study

The A3921104 Phase 3 study had two phases. During the run-in phase, all subjects enrolled in the study received open-label tofacitinib for 18 weeks. At the end of the 18-week run in phase, only subjects who achieved at least a JIA ACR30 response were randomized into the 26-week, double-blind, placebo-controlled, withdrawal phase to receive either tofacitinib or placebo through the end of the study duration at week 44. For more information about study A3921104, please visit https://www.clinicaltrials.gov.

About XELJANZ (tofacitinib)

XELJANZ (tofacitinib) is approved in the U.S. for adult patients in three indications: moderately to severely active rheumatoid arthritis (RA) after methotrexate failure, active psoriatic arthritis (PsA) after disease modifying antirheumatic drug (DMARD) failure and moderately to severely active ulcerative colitis (UC) after tumor necrosis factor inhibitor (TNFi) failure. XELJANZ has been studied in more than 50 clinical trials worldwide, including more than 20 trials in RA patients, and prescribed to over 208,000 adult patients (the majority of whom were RA patients) worldwide in the last seven years. 1,2,3

As the developer of tofacitinib, Pfizer is committed to advancing the science of JAK inhibition and enhancing understanding of tofacitinib through robust clinical development programs in the treatment of immune-mediated inflammatory conditions.

FDA APPROVED INDICATIONS

Rheumatoid Arthritis

Psoriatic Arthritis

It is important to note that a dosage of Xeljanz 10 mg twice daily is not recommended for the treatment of rheumatoid arthritis or psoriatic arthritis.

Ulcerative Colitis

IMPORTANT SAFETY INFORMATION

SERIOUS INFECTIONS

Patients treated with XELJANZ/XELJANZ XR are at increased risk for developing serious infections that may lead to hospitalization or death. Most patients who developed these infections were taking concomitant immunosuppressants, such as methotrexate or corticosteroids.

If a serious infection develops, interrupt XELJANZ/XELJANZ XR until the infection is controlled.

Reported infections include:

The most common serious infections reported with XELJANZ included pneumonia, cellulitis, herpes zoster, urinary tract infection, diverticulitis, and appendicitis. Avoid use of XELJANZ/XELJANZ XR in patients with an active, serious infection, including localized infections, or with chronic or recurrent infection.

In the UC population, XELJANZ 10 mg twice daily was associated with greater risk of serious infections compared to 5 mg twice daily. Opportunistic herpes zoster infections (including meningoencephalitis, ophthalmologic, and disseminated cutaneous) were seen in patients who were treated with XELJANZ 10 mg twice daily.

The risks and benefits of treatment with XELJANZ/XELJANZ XR should be carefully considered prior to initiating therapy in patients with chronic or recurrent infection, or those who have lived or traveled in areas of endemic TB or mycoses. Viral reactivation including herpes virus and Hepatitis B reactivation have been reported. Screening for viral hepatitis should be performed in accordance with clinical guidelines before starting therapy.

Patients should be closely monitored for the development of signs and symptoms of infection during and after treatment with XELJANZ/XELJANZ XR, including the possible development of tuberculosis in patients who tested negative for latent tuberculosis infection prior to initiating therapy.

Caution is also recommended in patients with a history of chronic lung disease, or in those who develop interstitial lung disease, as they may be more prone to infection.

MORTALITY

Rheumatoid arthritis patients 50 years of age and older with at least one cardiovascular (CV) risk factor treated with XELJANZ 10 mg twice a day had a higher rate of all-cause mortality, including sudden CV death, compared to those treated with XELJANZ 5 mg given twice daily or TNF blockers in a large, ongoing, postmarketing safety study.

XELJANZ 10mg twice daily or XELJANZ XR 22mg once daily is not recommended for the treatment of RA or PsA. For UC, use XELJANZ at the lowest effective dose and for the shortest duration needed to achieve/maintain therapeutic response.

MALIGNANCIES

Lymphoma and other malignancies have been observed in patients treated with XELJANZ. Epstein Barr Virus-associated post-transplant lymphoproliferative disorder has been observed at an increased rate in renal transplant patients treated with XELJANZ and concomitant immunosuppressive medications.

Consider the risks and benefits of XELJANZ/XELJANZ XR treatment prior to initiating therapy in patients with a known malignancy other than a successfully treated non-melanoma skin cancer (NMSC) or when considering continuing XELJANZ/XELJANZ XR in patients who develop a malignancy.

Malignancies (including solid cancers and lymphomas) were observed more often in patients treated with XELJANZ 10 mg twice daily dosing in the UC long-term extension study.

Other malignancies were observed in clinical studies and the post-marketing setting including, but not limited to, lung cancer, breast cancer, melanoma, prostate cancer, and pancreatic cancer. NMSCs have been reported in patients treated with XELJANZ. In the UC population, treatment with XELJANZ 10 mg twice daily was associated with greater risk of NMSC. Periodic skin examination is recommended for patients who are at increased risk for skin cancer.

THROMBOSIS

Thrombosis, including pulmonary embolism, deep venous thrombosis, and arterial thrombosis, has been observed at an increased incidence in RA patients who were 50 years of age and older with at least one CV risk factor treated with XELJANZ 10 mg twice daily compared to XELJANZ 5 mg twice daily or TNF blockers in a large, ongoing postmarketing safety study. Many of these events were serious and some resulted in death. Avoid XELJANZ/XELJANZ XR in patients at risk. Discontinue XELJANZ/XELJANZ XR and promptly evaluate patients with symptoms of thrombosis. For patients with UC, use XELJANZ at the lowest effective dose and for the shortest duration needed to achieve/maintain therapeutic response. XELJANZ 10 mg twice daily or XELJANZ XR 22 mg once daily is not recommended for the treatment of RA or PsA. In a long-term extension study in UC, four cases of pulmonary embolism were reported in patients taking XELJANZ 10 mg twice a day, including one death in a patient with advanced cancer.

GASTROINTESTINAL PERFORATIONS

Gastrointestinal perforations have been reported in XELJANZ clinical trials, although the role of JAK inhibition is not known. In these studies, many patients with rheumatoid arthritis were receiving background therapy with Nonsteroidal Anti-Inflammatory Drugs (NSAIDs). There was no discernable difference in frequency of gastrointestinal perforation between the placebo and the XELJANZ arms in clinical trials of patients with UC, and many of them were receiving background corticosteroids. XELJANZ/XELJANZ XR should be used with caution in patients who may be at increased risk for gastrointestinal perforation (e.g., patients with a history of diverticulitis or taking NSAIDs).

HYPERSENSITIVITY

Angioedema and urticaria that may reflect drug hypersensitivity have been observed in patients receiving XELJANZ/XELJANZ XR some events were serious. If a serious hypersensitivity reaction occurs, promptly discontinue tofacitinib while evaluating the potential cause or causes of the reaction.

LABORATORY ABNORMALITIES

Lymphocyte Abnormalities: Treatment with XELJANZ was associated with initial lymphocytosis at one month of exposure followed by a gradual decrease in mean lymphocyte counts. Avoid initiation of XELJANZ/XELJANZ XR treatment in patients with a count less than 500 cells/mm3. In patients who develop a confirmed absolute lymphocyte count less than 500 cells/mm3, treatment with XELJANZ/XELJANZ XR is not recommended. Risk of infection may be higher with increasing degrees of lymphopenia and consideration should be given to lymphocyte counts when assessing individual patient risk of infection. Monitor lymphocyte counts at baseline and every 3 months thereafter.

Neutropenia: Treatment with XELJANZ was associated with an increased incidence of neutropenia (less than 2000 cells/mm3) compared to placebo. Avoid initiation of XELJANZ/XELJANZ XR treatment in patients with an ANC less than 1000 cells/mm3. For patients who develop a persistent ANC of 500-1000 cells/mm3, interrupt XELJANZ/XELJANZ XR dosing until ANC is greater than or equal to 1000 cells/mm3. In patients who develop an ANC less than 500 cells/mm3, treatment with XELJANZ/XELJANZ XR is not recommended. Monitor neutrophil counts at baseline and after 4-8 weeks of treatment and every 3 months thereafter.

Anemia: Avoid initiation of XELJANZ/XELJANZ XR treatment in patients with a hemoglobin level less than 9 g/dL. Treatment with XELJANZ/XELJANZ XR should be interrupted in patients who develop hemoglobin levels less than 8 g/dL or whose hemoglobin level drops greater than 2 g/dL on treatment. Monitor hemoglobin at baseline and after 4-8 weeks of treatment and every 3 months thereafter.

Liver Enzyme Elevations: Treatment with XELJANZ was associated with an increased incidence of liver enzyme elevation compared to placebo. Most of these abnormalities occurred in studies with background DMARD (primarily methotrexate) therapy. If drug-induced liver injury is suspected, the administration of XELJANZ/XELJANZ XR should be interrupted until this diagnosis has been excluded. Routine monitoring of liver tests and prompt investigation of the causes of liver enzyme elevations is recommended to identify potential cases of drug-induced liver injury.

Lipid Elevations: Treatment with XELJANZ was associated with dose-dependent increases in lipid parameters, including total cholesterol, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol. Maximum effects were generally observed within 6 weeks. There were no clinically relevant changes in LDL/HDL cholesterol ratios. Manage patients with hyperlipidemia according to clinical guidelines. Assessment of lipid parameters should be performed approximately 4-8 weeks following initiation of XELJANZ/XELJANZ XR therapy.

VACCINATIONS

Avoid use of live vaccines concurrently with XELJANZ/XELJANZ XR. The interval between live vaccinations and initiation of tofacitinib therapy should be in accordance with current vaccination guidelines regarding immunosuppressive agents. Update immunizations in agreement with current immunization guidelines prior to initiating XELJANZ/XELJANZ XR therapy.

PATIENTS WITH GASTROINTESTINAL NARROWING

Caution should be used when administering XELJANZ XR to patients with pre-existing severe gastrointestinal narrowing. There have been rare reports of obstructive symptoms in patients with known strictures in association with the ingestion of other drugs utilizing a non-deformable extended release formulation.

HEPATIC and RENAL IMPAIRMENT

Use of XELJANZ/XELJANZ XR in patients with severe hepatic impairment is not recommended.

For patients with moderate hepatic impairment or with moderate or severe renal impairment taking XELJANZ 5 mg twice daily, reduce to XELJANZ 5 mg once daily.

For UC patients with moderate hepatic impairment or with moderate or severe renal impairment taking XELJANZ 10 mg twice daily, reduce to XELJANZ 5 mg twice daily.

ADVERSE REACTIONS

The most common serious adverse reactions were serious infections. The most commonly reported adverse reactions during the first 3 months in controlled clinical trials in patients with rheumatoid arthritis (RA) with XELJANZ 5 mg twice daily and placebo, respectively, (occurring in greater than or equal to 2% of patients treated with XELJANZ with or without DMARDs) were upper respiratory tract infection, nasopharyngitis, diarrhea, headache, and hypertension. The safety profile observed in patients with active psoriatic arthritis treated with XELJANZ was consistent with the safety profile observed in RA patients.

Adverse reactions reported in 5% of patients treated with either 5 mg or 10 mg twice daily of XELJANZ and 1% greater than reported in patients receiving placebo in either the induction or maintenance clinical trials for UC were: nasopharyngitis, elevated cholesterol levels, headache, upper respiratory tract infection, increased blood creatine phosphokinase, rash, diarrhea, and herpes zoster.

USE IN PREGNANCY

Available data with XELJANZ/XELJANZ XR use in pregnant women are insufficient to establish a drug-associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes. There are risks to the mother and the fetus associated with rheumatoid arthritis and UC in pregnancy. In animal studies, tofacitinib at 6.3 times the maximum recommended dose of 10 mg twice daily demonstrated adverse embryo-fetal findings. The relevance of these findings to women of childbearing potential is uncertain. Consider pregnancy planning and prevention for females of reproductive potential.

Please see full Prescribing Information, including BOXED WARNING for XELJANZ/XELJANZ XR available at: http://labeling.pfizer.com/ShowLabeling.aspx?id=959.

Pfizer Inc.: Breakthroughs that change patients lives

At Pfizer, we apply science and our global resources to bring therapies to people that extend and significantly improve their lives. We strive to set the standard for quality, safety and value in the discovery, development and manufacture of health care products, including innovative medicines and vaccines. Every day, Pfizer colleagues work across developed and emerging markets to advance wellness, prevention, treatments and cures that challenge the most feared diseases of our time. Consistent with our responsibility as one of the world's premier innovative biopharmaceutical companies, we collaborate with health care providers, governments and local communities to support and expand access to reliable, affordable health care around the world. For more than 150 years, we have worked to make a difference for all who rely on us. We routinely post information that may be important to investors on our website at http://www.pfizer.com. In addition, to learn more, please visit us on http://www.pfizer.com and follow us on Twitter at @Pfizer and @Pfizer_News, LinkedIn, YouTube and like us on Facebook at Facebook.com/Pfizer.

DISCLOSURE NOTICE: The information contained in this release is as of November 12, 2019. Pfizer assumes no obligation to update forward-looking statements contained in this release as the result of new information or future events or developments.

This release contains forward-looking information about XELJANZ (tofacitinib) and a potential new indication for the treatment of juvenile idiopathic arthritis, including their potential benefits, that involves substantial risks and uncertainties that could cause actual results to differ materially from those expressed or implied by such statements. Risks and uncertainties include, among other things, the uncertainties inherent in research and development, including the ability to meet anticipated clinical endpoints, commencement and/or completion dates for our clinical trials, as well as the possibility of unfavorable new clinical data and further analyses of existing clinical data; risks associated with interim data; the risk that clinical trial data are subject to differing interpretations and assessments by regulatory authorities; whether regulatory authorities will be satisfied with the design of and results from our clinical studies; uncertainties regarding the commercial success of XELJANZ and XELJANZ XR; uncertainties regarding the commercial impact of the update to the U.S. prescribing information for XELJANZ and XELJANZ XR; uncertainties regarding the commercial impact of any potential actions by other regulatory authorities, including as a result of the ongoing review by the European Medicines Agencys scientific committee, based on analysis of clinical trial A3921133 or other data, which will depend, in part, on labeling determinations; whether and when any applications for the potential new indication for XELJANZ may be filed in any jurisdictions; whether and when any applications that may be filed for the potential new indication or that may be pending or filed for any other potential indications for XELJANZ or XELJANZ XR in any jurisdictions may be approved by regulatory authorities, which will depend on myriad factors, including making a determination as to whether the products benefits outweigh its known risks and determination of the products efficacy, and, if approved, whether they will be commercially successful; decisions by regulatory authorities impacting labeling, safety, manufacturing processes and/or other matters that could affect the availability or commercial potential of XELJANZ and XELJANZ XR; and competitive developments.

A further description of risks and uncertainties can be found in Pfizers Annual Report on Form 10-K for the fiscal year ended December 31, 2018 and in its subsequent reports on Form 10-Q, including in the sections thereof captioned Risk Factors and Forward-Looking Information and Factors That May Affect Future Results, as well as in its subsequent reports on Form 8-K, all of which are filed with the U.S. Securities and Exchange Commission and available at http://www.sec.gov and http://www.pfizer.com.

_______________________1 Pfizer Data on File. XELJANZ Worldwide Registration Status.2 ClinicalTrials.gov. Tofacitinib RA Studies. https://clinicaltrials.gov/ct2/results?term=tofacitinib%2C+rheumatoid+arthritis%2C+ORAL&type=&rslt=&recr=&age_v=&gndr=&cond=Rheumatoid+Arthritis&intr=&titles=&outc=&spons=&lead=&id=&state1=&cntry1=&state2=&cntry2=&state3=&cntry3=&locn=&rcv_s=&rcv_e=&lup_s=&lup_e=. Accessed August 1, 2019.3 Pfizer. Data on File. Tofa Counts. April 2019

Link:
Pfizer Announces Results of Phase 3 Study for XELJANZ (tofacitinib) in Juvenile Idiopathic Arthritis Ahead of Presentation at 2019 American College of...

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The sixth annual Arkansas Bioinformatics Consortium conference is set for Feb. 10-11 at the Wyndham Riverfront in North Little Rock. Its theme is Artificial Intelligence in Arkansas.

AR-BIC is an annual event, but its meant to be a collaborative community of research scientists and practitioners in this field of bioinformatics, said Jeremy Harper, director of communications for the Arkansas Research Alliance.

ARA, headquartered in Conway, is the lead organizer of the conference. The Food & Drug Administrations National Center for Toxicological Research in Jefferson County is a major sponsor.

Harper said conference registration is free and complementary lodging is available, thanks to a $15,000 grant from the FDA and sponsorships that cover what remains of its $40,000-$50,000 budget.

The conference will be held from 1-7:30 p.m. Feb. 10 and from 8:30 a.m.-4:30 p.m. Feb. 11.

AR-BIC was born out of a realization by the NCTRs Division of Bioinformatics & Biostatistics and others that we have a real developing, emerging competency in bioinformatics here in the state and it needed to be nurtured, Harper said. The objectives of AR-BIC, he said, are to:

The first conference attracted 90 attendees, and attendance has been growing since then, Harper said. More than 200 attended the 2019 conference.

The AR-BIC governing board oversees the conference. The board includes representatives from Arkansas State University, the University of Arkansas, the University of Arkansas at Little Rock, the University of Arkansas for Medical Sciences, the University of Arkansas at Pine Bluff, the NCTR and ARA. ARA President and CEO Jerry Adams chairs it. Entities represented on the board provide most of the conferences speakers.

Highlights of the 2020 conference include a new panel composed of ARA Academy scholars and fellows and a theme that is on point, Harper said.

This [upcoming] year is on AI, and theres just been an explosion of growth around AI, he said. The computational requirements of personalized medicine alone, not to mention things like driverless cars and all that, make it a pretty strategic theme.

Harper also said the FDA, a major sponsor, will need AI to do its job, which is to protect human health.

In addition, the topic is timely, he said, because ARA fellow Xiuzhen Huang of A-State recently founded the Arkansas AI-Campus. It is a virtual statewide interactive training program seven institutions are participating in. The program allows researchers to work with global and national experts in machine learning, artificial intelligence and deep learning. Deep learning is the practice of imitating the workings of the human brain in processing data and creating patterns for use in decision-making.

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Conference to Focus on AI in Arkansas - Arkansas Business Online

SOUTH SAN FRANCISCO, Calif.--(BUSINESS WIRE)--Nov 18, 2019--

Genentech, a member of the Roche Group (SIX: RO, ROG; OTCQX: RHHBY), today announced that results from a number of studies across its growing breast cancer portfolio will be presented at the San Antonio Breast Cancer Symposium (SABCS) on December 10-14, 2019. These data include new results in HER2-positive breast cancer and studies of new molecules in hormone receptor-positive (HR-positive) breast cancer.

For the past three decades, we have remained dedicated to improving outcomes for people with breast cancer, said Levi Garraway, M.D., Ph.D., chief medical officer and head of Global Product Development. This sustained commitment is exemplified by new data for our approved and investigational medicines across the spectrum of breast cancer being presented at SABCS this year.

Key presentations

New data will be presented from a second interim overall survival (OS) analysis of the Phase III APHINITY trial evaluating Perjeta (pertuzumab) and Herceptin (trastuzumab) plus chemotherapy (the Perjeta-based regimen), compared to Herceptin and chemotherapy, as an adjuvant treatment for HER2-positive early breast cancer (eBC). This latest interim OS analysis also includes updated descriptive invasive disease-free survival and cardiac safety data.

Genentech will also present data from the primary analysis of the Phase III FeDeriCa study which evaluated a new investigational fixed-dose combination (FDC) of Perjeta and Herceptin administered as a single subcutaneous formulation in combination with intravenous chemotherapy. The FDC is administered under the skin in just minutes, significantly reducing the time spent receiving treatment and providing people with HER2-positive breast cancer a potential new treatment option for faster delivery of the Perjeta-based regimen.

Data will also be presented from studies in HR-positive breast cancer, including findings from early studies investigating Genentechs pipeline molecules GDC-9545, a selective estrogen receptor degrader, and GDC-0077, a mutant selective PI3K inhibitor.

Overview of Genentech studies to be presented at SABCS 2019

Medicine(s)

Abstract title

Abstract number

(date, time, location of presentation)

HER2-positive breast cancer

Perjeta and Herceptin

Interim OS analysis of APHINITY (BIG 4-11): a randomized multicenter, double-blind, placebo-controlled trial comparing chemotherapy plus trastuzumab plus pertuzumab versus chemotherapy plus trastuzumab plus placebo as adjuvant therapy in patients with operable HER2-positive eBC

Abstract GS1-04

(Oral)

Wednesday, December 119:30 9:45 AM CST

Hall 3

Perjeta and Herceptin

Subcutaneous trastuzumab and hyaluronidase-oysk with intravenous pertuzumab and docetaxel in HER2-positive advanced breast cancer: final analysis of the Phase IIIb, multicenter, open-label, single-arm MetaPHER study

Abstract P1-18-05

(Poster)

Wednesday, December 115:00 7:00 PM CST

Hall 1

Perjeta and Herceptin

Risk of recurrence and death in patients with early HER2-positive breast cancer who achieve a pathological complete response (pCR) after different types of HER2-targeted therapy: a retrospective exploratory analysis

Abstract P1-18-01

(Poster)

Wednesday, December 115:00 7:00 PM CST

Hall 1

Perjeta and Herceptin

Use of pertuzumab in combination with taxanes for HER2-positive metastatic breast cancer (MBC): analysis of United States electronic health records

Abstract P1-18-14

(Poster)

Wednesday, December 115:00 7:00 PM CST

Hall 1

Kadcyla (ado-trastuzumab emtansine)

Cardiac events in patients with HER2-positive MBC who have low left ventricular ejection fraction prior to initiating treatment with ado-trastuzumab emtansine: a retrospective cohort study using electronic health record data

Abstract P1-18-11

(Poster)

Wednesday, December 115:00 7:00 PM CST

Hall 1

Tecentriq (atezolizumab), Kadcyla, Perjeta and Herceptin

Atezolizumab in combination with ado-trastuzumab emtansine or with trastuzumab and pertuzumab in patients with HER2-positive breast cancer and atezolizumab with doxorubicin and cyclophosphamide in HER2-negative breast cancer: safety and biomarker outcomes from a multi-cohort Phase Ib study

Abstract PD1-05

(Poster discussion)

Wednesday, December 115:00 7:00 PM CST

Hemisfair Ballroom

Perjeta and Herceptin

Subcutaneous administration of the fixed-dose combination of trastuzumab and pertuzumab in combination with chemotherapy in HER2-positive eBC: primary analysis of the Phase III, multicenter, randomized, open-label, two-arm FeDeriCa study

Abstract PD4-07

(Poster discussion)

Thursday, December 12

7:00 9:00 AM CST

Stars at Night Ballroom 1&2

Kadcyla and Perjeta

Association of immune gene expression with outcome in the MARIANNE Phase III clinical trial in HER2-positive MBC

Abstract PD5-11

(Poster discussion)

Thursday, December 12

7:00 9:00 AM CST

Stars at Night Ballroom 3&4

Kadcyla and Herceptin

Adjuvant ado-trastuzumab emtansine versus trastuzumab in patients with residual invasive disease after neoadjuvant therapy for HER2-positive breast cancer: KATHERINE subgroup analysis

Abstract P3-14-01

(Poster)

Thursday, December 12

5:00 7:00 PM CST

Hall 1

Herceptin

Palbociclib in combination with trastuzumab and endocrine therapy versus treatment of physician's choice in metastatic HER2-positive and HR-positive breast cancer with PAM50 luminal intrinsic subtype (SOLTI-1303 PATRICIA II): a multi-center, randomized, open-label, Phase II trial

Abstract OT2-02-06

(Poster)

Thursday, December 12

5:00 7:00 PM CST

Hall 1

Kadcyla and Herceptin

Cost-effectiveness of ado-trastuzumab emtansine versus trastuzumab for the adjuvant treatment of patients with residual invasive HER2-positive eBC in the United States

Abstract P6-13-01

(Poster)

Saturday, December 14

7:00 9:00 AM CST

Hall 1

Hormone receptor-positive

GDC-0077

A first-in-human Phase Ia dose escalation study of GDC-0077, a p110a-selective and mutant-degrading PI3K inhibitor, in patients with PIK3CA-mutant solid tumors

Abstract OT1-08-04

(Poster)

Wednesday, December 11

5:00 7:00 PM CST

Hall 1

GDC-0077

A Phase Ib dose escalation study evaluating the mutant selective PI3K-alpha inhibitor GDC-0077 in combination with letrozole with and without palbociclib in patients with PIK3CA-mutant HR-positive, HER2-negative breast cancer

Abstract P1-19-46

(Poster)

Wednesday, December 11

5:00 7:00 PM CST

Hall 1

GDC-9545

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Genentech to Present New and Updated Data for Seven Approved and Investigational Medicines Across Multiple Types of Breast Cancer at the 2019 San...

Why has nobody really 3D printed a heart yet? Will animals also benefit from 3D printing in the veterinary field? How to start a 3D printing lab in a public hospital? And who is Gary? These are just a few of the proposals answered at the latest and fifth edition of the 3D Med Australia Conference, which concluded last Saturday after three days of workshops, lab tours, and lectures at the AAMI Park, a huge Stadium in Melbourne. The event highlighted 3D printing applications in various health areas like presurgical planning in adult and pediatric fields, bioprinting, medical device design, prosthetic and implantable device design, education of trainees and medical students, as well as patient experience, and even 3D printing to support longevity of equipment for helicopter retrieval (from blood warmers to vial containment).It is the largest 3D technologies in medicine conference in Australasia, convened by Jason Chuen, Associate Professor at The University of Melbourne and Director of Vascular Surgery at Austin Health, in Melbourne, and Jasamine Coles-Black, doctor and vascular researcher at the Department of Vascular Surgery at Austin Health and Austin 3D Medical Printing Laboratory (Austin 3D Med Lab). Apart from featuring frontier health innovation in 3D printing, it was attended by most major labs and scientists in this space.

The highly awaited experience showcased The University of Melbournes experience in this space, as a recognized hotspot of medical device innovation. The multidisciplinary nature of frontier technologies in health meant the work presented is a result of the collaboration between doctors, engineers, veterinarians, cell biologists, industrial designers, lawyers, and policymakers.

3D technologies, including 3D printing and augmented reality, are set to radically transform the way we teach, train, plan, rehearse, and perform surgery; and Australia is lining up to be one of the leaders in the field, said Chuen. We are proud to support this by bringing together all of these great minds: from what I can see, Australia, and Melbourne, in particular, will be a major hub of medical technology development, and 3D related technologies will be a key part of this.

Atandrila Das, General Surgeon at Northern Health, Melbourne, presented a world-first case combining 3D visualization with robotic cancer surgery, which was a result of a collaboration between Austin Health and the Peter MacCallum Cancer Centers Department of Surgery doctoral students and surgeons. In addition, Claudia di Bella, Orthopaedic Surgeon, and researcher at Biofab3D in St Vincents Hospitalat The University of Melbourne exhibited her robotics and tissue engineering work.

Additionally, ethics and regulation were a big part of the event, with attendees getting updates from Australian governing bodies like the Therapeutic Goods Administration (TGA), the Department of Health and Human Services (DHHS), and Medical Device Innovation. The TGAs John Skerritt provided leading researchers with an update on the current changes to custom medical device and implant regulations coming in late November. Some of the proposals for change include a medical device production system framework to allow healthcare providers to produce lower risk personalized devices without manufacturing certification and regulation of medical devices with a human origin component as medical devices with a biological component rather than biologicals.

What is wrong with this image? OConnell explains why nobody has really 3D printed a heart yet (Image Credit: Cathal OConnell)

During the talk Dont Print Your Heart Out, facility manager at BioFab3D, Cathal OConnell, dissected the hype from reality and explained why nobody has really 3D printed a heart yet, suggesting it is dangerous to provoke so much buildup in platform technologies and how clinicians, scientists, and reporters need to be careful when delivering their message on medical technologies.

In the original printed heart scientific paper, Israeli scientists describe [] the main focus was to print a square patch of heart cells and blood vessels using a personalized bioink. As a final flourish, the team also printed the cells into a thumbnail-sized, heart shape. The text of the original paper clearly states the printed heart-shaped structure is not a real heart and lacks most of the features required to make a heart work. This is impressive work the cardiac patches may indeed turn out to be an important development in the field. Im more worried about media reports giving the impression that our field of research is far more advanced than it is, said OConnell.

Elizabeth Sigston at the Women in 3D Med Event (Image Credit: Austin 3D Med Lab)

While Blake Cochran, from the University of New South Wales (UNSW), Sydney, introduced Gary, a 3D printed radiologically realistic skull, and Stewart Ryan, from The University of Melbourne Universitys vet school, explored the importance of 3D printing for the training of veterinary surgeons for all creatures great and small, and Ryan should know, he has even performed surgery for a 14-year old tiger at the Melbourne Zoo to remove a cancerous tumor.

As part of the event, the inaugural Women in 3D Technologies networking drinks were held in partnership with the Commonwealth Scientific and Industrial Research Organisation (CSIRO), with Elizabeth Sigston (a leading head and neck cancer surgeon) giving the keynote speech. The conference proved that there is a strong representation of women in STEMM careers across Medicine, Dentistry and Health Sciences (MDHS) in Melbourne.

3D technologies are the natural next steppingstone in the era of personalised medicine, said Coles-Black. Australian doctors, engineers and other researchers need to come together in order to make the most of this new frontier in medicine. Our conference provides a collegiate environment for much-needed multidisciplinary collaboration.

Jason Chuen, Elizabeth Sigston, Frank McGuire, and Jasamine Coles-Black at the 3D Med Conference (Image Credit: Austin 3D Med Lab)

Coles-Black also explained that this conference seeks to bring together experts to solve the often-quoted barriers to the adoption of 3D printing technologies in healthcare settings, such as the lack of technical and regulatory knowledge, perceived costs, and lack of expertise in implementation.

A tour of RMITs Additive Manufacturing Precinct (Image Credit: Austin 3D Med Lab)

In addition, the conference featured a tour of the new MDHS SBS Digital Learning Hub. Other University of Melbourne labs featured through hands-on tours included the Melbourne School of Designs NExT Lab and BioFab3d, Austin 3D Med Lab, and the Australian Research Council Training Centre for Medical Implant Technologies (ARC-CMIT)which launched on November 8. In addition, there was a significant focus on industry, startup and commercialization, and medical device development with representatives from the Medical Device Partnering Program, Stratasys, HP, Evok3D, Kyocera, Leapfrog, Gore, Global3D and Materialise.

Clinicians and engineers need to work together to develop this technology and find ways to implement it effectively and safely. Collaboration is key in this industry, claimed Chuen.

During the occasion, there was a lot of hype about the clinical uses of augmented and virtual reality in presurgical planning, medical student education, forensics, trauma simulation, and to improve hospital systems.

At the Anatomical 3D Segmentation Workshop, in collaboration with Evok3D, an HP 3D Partner in Australia, guests learned more about the end-to-end workflows for the production of 3D printed color anatomical models, which can be used to improve pre-surgical planning, patient consultation, and support medical education. Medical 3D technology for patient care is getting more and more accessible, every day, providing patients personalized treatment based on their scans as point-of-care 3D printing enables manufacturing directly on location.

Promotional booths were a big part of the event, with visitors looking into how Materialise solutions can provide personalized treatment to patients and guidance on setting up a 3D point-of-care facility at hospitals. And Stratasys even chose the 3D Med Conference to launch its J750 Digital Anatomy Printer in the Australasia region.

The last day of the event kicked off with Mia Woodruff, Professor of Biomedical Engineering at Queensland University of Technology (QUT), and Gordon Wallace, a distinguished professor at theUniversity of Wollongong (UOW), talking about the future of bioprinting. Woodruff shared challenges and motivations to translate biofabrication in the hospital of the future, and along with Wallace announced the Biofabrication 2020 event: Biofab by the Beach, set for September 27 through 30, in 2020, proving its all about teamwork, something Wallace was keen on emphasizing during his panel, claiming cross-disciplinary collaboration is key and Australia leads the way as Australians are collaborative by nature. Finally, rounding up the event was Peter Lee, Director of the ARC CMIT, focusing on building the multidisciplinary networks needed to train the new generation of implant engineers. Thats what it was all about at the 3D Med Conference, looking into the future for biotechnology and medical applications that will pave the way for future research and adoption of 3D printing technology.

The entrance to the 3D Med Conference (Image Credit: Austin 3D Med Lab)

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Australias 3D Printing Medical Conference: Focusing on Technology and Teamwork to Advance the Field - 3DPrint.com