StemCell Therapy

Kangstem Biotech said Monday that it has voluntarily withdrawn a phase 1 and 2a clinical trial investigational new drug (IND) approval for "FURESTEM-OA Kit Inj.," a candidate material for stem cell-based osteoarthritis (OA) treatment.

The company decided to withdraw its plans after determining that it required further data reinforcement concerning establishing a cell bank for clinical trial drugs after the government started enforcing the "Advanced Regenerative Medicine and Advanced Biopharmaceuticals Safety and Support Act."

The Ministry of Food and Drug Safety had requested the results of the adventitious virus-negative test from Kangstem Biotech. The test proves that even when the test drug used in clinical trials is manufactured using a cell bank, the quality and safety are the same, and there is no scientific risk factor.

Accordingly, the company confirmed that there is no adventitious virus by completing the virus test by the qPCR test method following the ICH (International Council for Harmonisation of Technical Requirements for Pharmaceuticals for Human Use) regulations at Korean institutions.

Also, the company entrusted the test to the additional culture method of Charles River, an American consignment testing institution.

However, the company decided to voluntarily withdraw its IND approval, confirming it would be difficult to complete the test and analysis to secure additional data within the administrative processing period required for review of the clinical trial plan approval period.

"The IND application for the FURESTEM-OA Kit was for the first clinical trial for a stem cell-based fusion drug under the Advanced Regenerative Medicine and Advanced Biopharmaceuticals Safety and Support Act," Kangstems Clinical Development Division Director Bae Yo-han said. "Therefore, the IND approval process was somewhat delayed as the Ministry of Food and Drug Safety had to review its safety from various angles thoroughly."

During the delay period, additional test data that did not need to be initially submitted became a requirement, Bae added.

However, Bae stressed that the Ministry of Food and Drug Safety also believes that there are no additional problems in the clinical trial plan itself, other than a review on securing safety related to adventitious factors by ingredients used in the manufacturing process of the drug.

"Therefore, the company is aiming to re-apply for the phase 1 and 2a IND of the FURESTEM-OA Kit in July at the earliest and get approval within October," he said.

Due to the company's explanation, the company's shares rebounded on Wednesday after dropping about 5 percent the previous day.

As of 1:40 p.m. Tuesday, the company's stock price stood at 2,860 won ($2.22) per share, up 2.33 percent from the previous trading day.

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Kangstem Biotech withdraws trial application for stem cell-based osteoarthritis treatment - KBR

SEATTLE, June 13, 2022 (GLOBE NEWSWIRE) -- Sana Biotechnology, Inc. ( SANA), a company focused on creating and delivering engineered cells as medicines, today announced that the company will present data from its hypoimmune platform at the International Society for Stem Cell Research (ISSCR) 2022 Annual Meeting taking place from Wednesday, June 15 through Sunday, June 19 in San Francisco.

About Sana BiotechnologySana Biotechnology, Inc. is focused on creating and delivering engineered cells as medicines for patients. We share a vision of repairing and controlling genes, replacing missing or damaged cells, and making our therapies broadly available to patients. We are a passionate group of people working together to create an enduring company that changes how the world treats disease. Sana has operations in Seattle, Cambridge, South San Francisco, and Rochester.

Cautionary Note Regarding Forward-Looking StatementsThis press release contains forward-looking statements about Sana Biotechnology, Inc. (the Company, we, us, or our) within the meaning of the federal securities laws, including those related to the companys vision, progress, and business plans, the Companys participation at the ISSCR Annual Meeting, and the subject matter of the Companys presentations and data being presented at ISSCR Annual Meeting. All statements other than statements of historical facts contained in this press release, including, among others, statements regarding the Companys strategy, expectations, cash runway and future financial condition, future operations, and prospects, are forward-looking statements. In some cases, you can identify forward-looking statements by terminology such as aim, anticipate, assume, believe, contemplate, continue, could, design, due, estimate, expect, goal, intend, may, objective, plan, positioned, potential, predict, seek, should, target, will, would and other similar expressions that are predictions of or indicate future events and future trends, or the negative of these terms or other comparable terminology. The Company has based these forward-looking statements largely on its current expectations, estimates, forecasts and projections about future events and financial trends that it believes may affect its financial condition, results of operations, business strategy and financial needs. In light of the significant uncertainties in these forward-looking statements, you should not rely upon forward-looking statements as predictions of future events. These statements are subject to risks and uncertainties that could cause the actual results to vary materially, including, among others, the risks inherent in drug development such as those associated with the initiation, cost, timing, progress and results of the Companys current and future research and development programs, preclinical and clinical trials, as well as the economic, market and social disruptions due to the ongoing COVID-19 public health crisis. For a detailed discussion of the risk factors that could affect the Companys actual results, please refer to the risk factors identified in the Companys SEC reports, including but not limited to its Quarterly Report on Form 10-Q dated May 10, 2022. Except as required by law, the Company undertakes no obligation to update publicly any forward-looking statements for any reason.

Investor Relations & Media:Nicole Keith[emailprotected][emailprotected]

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Sana Biotechnology Announces Multiple Preclinical Data Presentations to Showcase Its Hypoimmune Platform, Including in Type 1 Diabetes, at the...

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Efficient terminal erythroid differentiation requires the APC/C cofactor Cdh1 to limit replicative stress in erythroblasts | Scientific Reports -...

MELBOURNE, Australia--(BUSINESS WIRE)--Propanc Biopharma, Inc. (OTCQB: PPCB) (Propanc or the Company), a biopharmaceutical company developing novel cancer treatments for patients suffering from recurring and metastatic cancer, today announced that the results from a small trial of just 18 rectal cancer patients in complete remission using an immunotherapy called dostarlimab are impressive, whilst acknowledging theres more work to be done. Chief Scientific Officer and Co-Founder, Dr Julian Kenyon MD, MB, ChB, believes that the fields biggest challenge remains that immunotherapies work inconsistently across cancers. Oncologists estimate a response rate of 20% across cancer types, according to the Wall Street Journal (WSJ). The drugs can wipe out cancers from some people, but fail to work for others. It is also uncertain whether the cancer may eventually return once a patient is in remission, even after a prolonged period of time.

Immunotherapies like dostarlimab, known as a checkpoint inhibitor, seek to inhibit key regulators of the immune system that when stimulated, reduces the bodys immune response to fight cancer. Given that immunotherapies target specific gene sequences, it often means they can encounter resistance, due to mutations that occur and genetic variation even within the primary tumor of a patient. As a result, Dr Cercek, from Memorial Sloan Kettering, who conducted the study for dostarlimab, estimates only 10% of rectal cancer patients and about 4% of all cancers will respond to treatment, according to the WSJ.

For many cancers, multiple factors can drive growth, making it hard to effectively match one biomarker, or a particular gene sequence, to a single drug. On the other hand, a therapeutic approach like our lead product candidate, PRP, which alters the characteristics of the cancer cell, by enforcing it to express proteins it normally wouldnt, means the treatment is less likely to encounter resistance through mutations, which is what we have observed in the lab as well as in clinical practice, said Dr Julian Kenyon.

In addition to specifically selecting the 18 rectal cancer patients according to their genetic biomarker, the trial included patients that were pre-metastatic, where tumors were locally advanced in one area, but not spread to other organs. This means patients identified with metastatic cancer were excluded from the trial. Therefore, the treatment and prevention of metastatic cancer, the main cause of patient death for sufferers, still remains the unsolved, final frontier. Cancer stem cells, which are the cells responsible for spreading to other parts of the body, remains a key focus for Dr Kenyon.

Dr Kenyon said, PRP is a proenzyme treatment that targets and eradicates cancer stem cells by altering multiple pathways of a cancerous cell rather than a single genetic sequence. Weve observed that once they are treated with PRP, the effects are irreversible and are more easily recognizable by the immune system, therefore potentially improving the response rates of standard approaches like immunotherapy, to overcome advanced cancers. We look forward to testing the utility of PRP with these approaches as we further advance into the clinic.

PRP is a mixture of two proenzymes, trypsinogen and chymotrypsinogen from bovine pancreas administered by intravenous injection. A synergistic ratio of 1:6 inhibits growth of most tumor cells. Examples include kidney, ovarian, breast, brain, prostate, colorectal, lung, liver, uterine and skin cancers.

About Propanc Biopharma, Inc.

Propanc Biopharma, Inc. (the Company) is developing a novel approach to prevent recurrence and metastasis of solid tumors by using pancreatic proenzymes that target and eradicate cancer stem cells in patients suffering from pancreatic, ovarian and colorectal cancers. For more information, please visit http://www.propanc.com.

The Companys novel proenzyme therapy is based on the science that enzymes stimulate biological reactions in the body, especially enzymes secreted by the pancreas. These pancreatic enzymes could represent the bodys primary defense against cancer.

To view the Companys Mechanism of Action video on its anti-cancer lead product candidate, PRP, please click on the following link: http://www.propanc.com/news-media/video

Forward-Looking Statements

All statements other than statements of historical facts contained in this press release are forward-looking statements, which may often, but not always, be identified by the use of such words as may, might, will, will likely result, would, should, estimate, plan, project, forecast, intend, expect, anticipate, believe, seek, continue, target or the negative of such terms or other similar expressions. These statements involve known and unknown risks, uncertainties and other factors, which may cause actual results, performance or achievements to differ materially from those expressed or implied by such statements. These factors include uncertainties as to the Companys ability to continue as a going concern absent new debt or equity financings; the Companys current reliance on substantial debt financing that it is unable to repay in cash; the Companys ability to successfully remediate material weaknesses in its internal controls; the Companys ability to reach research and development milestones as planned and within proposed budgets; the Companys ability to control costs; the Companys ability to obtain adequate new financing on reasonable terms; the Companys ability to successfully initiate and complete clinical trials and its ability to successful develop PRP, its lead product candidate; the Companys ability to obtain and maintain patent protection; the Companys ability to recruit employees and directors with accounting and finance expertise; the Companys dependence on third parties for services; the Companys dependence on key executives; the impact of government regulations, including FDA regulations; the impact of any future litigation; the availability of capital; changes in economic conditions, competition; and other risks, including, but not limited to, those described in the Companys periodic reports that are filed with the Securities and Exchange Commission and available on its website at http://www.sec.gov. These forward-looking statements speak only as of the date hereof and the Company disclaims any obligations to update these statements except as may be required by law.

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Propanc Biopharma's CSO Hails Dostarlimab's Impressive Results Whilst Acknowledging More Work to Be Done in the Fight Against Cancer - Business Wire

DURHAM, N.C.--(BUSINESS WIRE)--Precision BioSciences, Inc. (Nasdaq: DTIL), a clinical stage gene editing company developing ARCUS-based ex vivo allogeneic CAR T and in vivo gene editing therapies, today announced it has entered into an exclusive worldwide in vivo gene editing research and development collaboration and license agreement with Novartis Pharma AG (the Agreement). As part of the Agreement, Precision will develop a custom ARCUS nuclease that will be designed to insert, in vivo, a therapeutic transgene at a safe harbor location in the genome as a potential one-time transformative treatment option for diseases including certain hemoglobinopathies such as sickle cell disease and beta thalassemia.

Under the terms of the Agreement, Precision will develop an ARCUS nuclease and conduct in vitro characterization, with Novartis then assuming responsibility for all subsequent research, development, manufacturing and commercialization activities. Novartis will receive an exclusive license to the custom ARCUS nuclease developed by Precision for Novartis to further develop as a potential in vivo treatment option for sickle cell disease and beta thalassemia. Precision will receive an upfront payment of $75 million and is eligible to receive up to an aggregate amount of approximately $1.4 billion in additional payments for future milestones. Precision is also eligible to receive certain research funding and, should Novartis successfully commercialize a therapy from the collaboration, tiered royalties ranging from the mid-single digits to low-double digits on product sales.

We are excited to collaborate with Novartis to bring together the precision and versatility of ARCUS genome editing with Novartis gene therapy expertise and commitment to developing one-time, potentially transformative treatment for hard-to-treat inherited blood disorders, said Michael Amoroso, Chief Executive Officer at Precision BioSciences. This collaboration will build on the unique gene insertion capabilities of ARCUS and illustrates its utility as a premium genome editing platform for potential in vivo drug development. With this Agreement, Precision, either alone or with world-class partners, will have active in vivo gene editing programs for targeted gene insertion and gene deletions in hematopoietic stem cells, liver, muscle and the central nervous system showcasing the distinctive versatility of ARCUS.

We identify here a collaborative opportunity to imagine a unique therapeutic option for patients with hemoglobinopathies, such as sickle cell disease and beta thalassemia a potential one-time treatment administered directly to the patient that would overcome many of the hurdles present today with other therapeutic technologies, said Jay Bradner, President of the Novartis Institutes for Biomedical Research (NIBR), the Novartis innovation engine. We look forward to working with Precision and leveraging the ARCUS technology platform, which could bring a differentiated approach to the treatment of patients with hemoglobinopathies."

The in vivo gene editing approach that we are pursuing for sickle cell disease could have a number of significant advantages over other ex vivo gene therapies currently in development, said Derek Jantz, Ph.D., Chief Scientific Officer and Co-Founder of Precision BioSciences. Perhaps most importantly, it could open the door to treating patients in geographies where stem cell transplant is not a realistic option. We believe that the unique characteristics of the ARCUS platform, particularly its ability to target gene insertion with high efficiency, make it the ideal choice for this project, and we look forward to working with our partners at Novartis to bring this novel therapy to patients.

Upon completion of the transaction, Precision expects that existing cash and cash equivalents, expected operational receipts, and available credit will be sufficient to fund its operating expenses and capital expenditure requirements into Q2 2024.

Precision BioSciences Conference Call and Webcast Information

Precision's management team will host a conference call and webcast tomorrow, June 22, 2022, at 8:00 AM ET to discuss the collaboration. The dial-in conference call numbers for domestic and international callers are (866)-996-7202 and (270)-215-9609, respectively. The conference ID number for the call is 6252688. Participants may access the live webcast on Precision's website https://investor.precisionbiosciences.com/events-and-presentations in the Investors page under Events and Presentations. An archived replay of the webcast will be available on Precision's website.

About ARCUS and Safe harbor ARCUS Nucleases

ARCUS is a proprietary genome editing technology discovered and developed by scientists at Precision BioSciences. It uses sequence-specific DNA-cutting enzymes, or nucleases, that are designed to either insert (knock-in), remove (knock-out), or repair DNA of living cells and organisms. ARCUS is based on a naturally occurring genome editing enzyme, I-CreI, that evolved in the algae Chlamydomonas reinhardtii to make highly specific cuts in cellular DNA. Precision's platform and products are protected by a comprehensive portfolio including nearly 100 patents to date.

Precision can use an ARCUS nuclease to add a healthy copy of a gene (or payload) to a persons genome. The healthy copy of the gene can be inserted at its usual site within the genome, replacing the mutated, disease-causing copy. Alternatively, an ARCUS nuclease can be used to insert a healthy copy of the gene at another site within the genome called a safe harbor that enables production of the healthy gene product without otherwise affecting the patients DNA of gene expression patterns.

About Sickle Cell Disease and Beta Thalassemia

Sickle cell disease (SCD) is a complex genetic disorder that affects the structure and function of hemoglobin, reduces the ability of red blood cells to transport oxygen efficiently and, early on, progresses to a chronic vascular disease.1-4 The disease can lead to acute episodes of pain known as sickle cell pain crises, or vaso-occlusive crises, as well as life-threatening complications.5-7 The condition affects 20 million people worldwide.8 Approximately 80% of individuals with SCD globally live in sub-Saharan Africa and it is estimated that approximately 1,000 children in Africa are born with SCD every day and more than half will die before they reach five.9,10 SCD is also a multisystem disorder and the most common genetic disease in the United States, affecting 1 in 500 African Americans. About 1 in 12 African Americans carry the autosomal recessive mutation, and approximately 300,000 infants are born with sickle cell anemia annually.11 Even with todays best available care, SCD continues to drive premature deaths and disability as this lifelong illness often takes an extreme emotional, physical, and financial toll on patients and their families.12,13

Beta thalassemia is also an inherited blood disorder characterized by reduced levels of functional hemoglobin.14 The condition has three main forms minor, intermedia and major, which indicate the severity of the disease.14 While the symptoms and severity of beta thalassemia varies greatly from one person to another, a beta thalassemia major diagnosis is usually made during the first two years of life and individuals require regular blood transfusions and lifelong medical care to survive.14 Though the disorder is relatively rare in the United States, it is one of the most common autosomal recessive disorders in the world.14 The incidence of symptomatic cases is estimated to be approximately 1 in 100,000 individuals in the general population.14, 15 The frequency of beta-thalassemia mutations varies by regions of the world with the highest prevalence in the Mediterranean, the Middle-East, and Southeast and Central Asia. Approximately 68,000 children are born with beta-thalassemia.16

About Precision BioSciences, Inc.

Precision BioSciences, Inc. is a clinical stage biotechnology company dedicated to improving life (DTIL) with its novel and proprietary ARCUS genome editing platform. ARCUS is a highly precise and versatile genome editing platform that was designed with therapeutic safety, delivery, and control in mind. Using ARCUS, the Companys pipeline consists of multiple ex vivo off-the-shelf CAR T immunotherapy clinical candidates and several in vivo gene editing candidates designed to cure genetic and infectious diseases where no adequate treatments exist. For more information about Precision BioSciences, please visit http://www.precisionbiosciences.com.

Forward-Looking Statements

This press release contains forward-looking statements, as may any related presentations, within the meaning of the Private Securities Litigation Reform Act of 1995. All statements contained in this herein and in any related presentation that do not relate to matters of historical fact should be considered forward-looking statements, including, without limitation, statements regarding the goal of providing a one time, potentially curative treatment for certain hemoglobinopathies, the success of the collaboration with Novartis, including the receipt of any milestone, royalty, or other payments pursuant to and the satisfaction of obligations under the Agreement, clinical and regulatory development and expected efficacy and benefit of our platform and product candidates, expectations about our operational initiatives and business strategy, expectations about achievement of key milestones, and expected cash runway. In some cases, you can identify forward-looking statements by terms such as aim, anticipate, approach, believe, contemplate, could, estimate, expect, goal, intend, look, may, mission, plan, potential, predict, project, should, target, will, would, or the negative thereof and similar words and expressions. Forward-looking statements are based on managements current expectations, beliefs and assumptions and on information currently available to us. Such statements are subject to a number of known and unknown risks, uncertainties and assumptions, and actual results may differ materially from those expressed or implied in the forward-looking statements due to various important factors, including, but not limited to: our ability to become profitable; our ability to procure sufficient funding and requirements under our current debt instruments and effects of restrictions thereunder; risks associated with raising additional capital; our operating expenses and our ability to predict what those expenses will be; our limited operating history; the success of our programs and product candidates in which we expend our resources; our limited ability or inability to assess the safety and efficacy of our product candidates; our dependence on our ARCUS technology; the initiation, cost, timing, progress, achievement of milestones and results of research and development activities, preclinical studies and clinical trials; public perception about genome editing technology and its applications; competition in the genome editing, biopharmaceutical, and biotechnology fields; our or our collaborators ability to identify, develop and commercialize product candidates; pending and potential liability lawsuits and penalties against us or our collaborators related to our technology and our product candidates; the U.S. and foreign regulatory landscape applicable to our and our collaborators development of product candidates; our or our collaborators ability to obtain and maintain regulatory approval of our product candidates, and any related restrictions, limitations and/or warnings in the label of an approved product candidate; our or our collaborators ability to advance product candidates into, and successfully design, implement and complete, clinical or field trials; potential manufacturing problems associated with the development or commercialization of any of our product candidates; our ability to obtain an adequate supply of T cells from qualified donors; our ability to achieve our anticipated operating efficiencies at our manufacturing facility; delays or difficulties in our and our collaborators ability to enroll patients; changes in interim top-line and initial data that we announce or publish; if our product candidates do not work as intended or cause undesirable side effects; risks associated with applicable healthcare, data protection, privacy and security regulations and our compliance therewith; the rate and degree of market acceptance of any of our product candidates; the success of our existing collaboration agreements, and our ability to enter into new collaboration arrangements; our current and future relationships with and reliance on third parties including suppliers and manufacturers; our ability to obtain and maintain intellectual property protection for our technology and any of our product candidates; potential litigation relating to infringement or misappropriation of intellectual property rights; our ability to effectively manage the growth of our operations; our ability to attract, retain, and motivate key executives and personnel; market and economic conditions; effects of system failures and security breaches; effects of natural and manmade disasters, public health emergencies and other natural catastrophic events; effects of COVID-19 pandemic and variants thereof, or any pandemic, epidemic or outbreak of an infectious disease; insurance expenses and exposure to uninsured liabilities; effects of tax rules; risks related to ownership of our common stock and other important factors discussed under the caption Risk Factors in our Quarterly Report on Form 10-Q for the quarterly period ended March 31, 2022, as any such factors may be updated from time to time in our other filings with the SEC, which are accessible on the SECs website at http://www.sec.gov and the Investors page of our website under SEC Filings at investor.precisionbiosciences.com.

References

1 Saraf SL, et al. Paediatr Respir Rev. 2014;15(1):4-12.2 Stuart MJ, et al. Lancet. 2004;364(9442):1343-1360.3 National Institutes of Health (NIH). Sickle cell disease. Bethesda, MD. U.S. National Library of Medicine. 2018:1-7.4 Conran N, Franco-Penteado CF, Costa FF. Hemoglobin. 2009;33(1):1-16.5 Ballas SK, et al. Blood. 2012;120(18):3647-3656.6 Elmariah H, et al. Am J Hematol. 2014(5):530-535.7 Steinberg M. Management of sickle cell disease. N Engl J Med. 1999;340(13):1021-1030.8 National Heart Lung and Blood Institute: What Is Sickle Cell Disease? 9 Odame I. Perspective: We need a global solution. Nature. 2014 Nov;515(7526):S1010 Scott D. Grosse, Isaac Odame, Hani K. Atrash, et al. Sickle Cell Disease in Africa: A Neglected Cause of Early Childhood Mortality. American Journal of Preventive Medicine 41, no. S4 (December 2011): S398-40511 Sedrak A, Kondamudi NP. Sickle Cell Disease. [Updated 2021 Nov 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.12 Sanger M, Jordan L, Pruthi S, et al. Cognitive deficits are associated with unemployment in adults with sickle cell anemia. Journal of Clinical and Experimental Neuropsychology. 2016;38(6):661-671.13 Anim M, Osafo J, Yirdong F. Prevalence of psychological symptoms among adults with sickle cell disease in Korie-Bu Teaching Hospital, Ghana. BMC Psychology. 2016;4(53):1-9.14 NORD Rare Disease Database: Beta Thalassemia 15 Galanello R, Origa R. Orphanet J Rare Dis. 2010;5:1116 Needs T, Gonzalez-Mosquera LF, Lynch DT. Beta Thalassemia. [Updated 2022 May 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.

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Precision BioSciences Announces In Vivo Gene Editing Collaboration with Novartis to Develop Potentially Curative Treatment for Disorders Including...

The last decade of immunotherapy progress was based on decades of prior research, including other forms of immunotherapy.

Until recent years, cancer treatment revolved around surgery, chemotherapy, and radiation. But the FDA approval of ipilimumab (Yervoy) in 2011 led to a fourth leg of that treatment stool: immunotherapy. This enabled new treatment paradigms, sometimes with shocking levels of success.

The types of immunotherapy treatments available are proliferating, with approved immune checkpoint inhibitors (ICIs) and cellular therapies like chimeric antigen receptor (CAR) T cells as well as other modalities in the research and discovery phases. Some even include more established approaches like vaccines that are being revisited with new information and iterations.

The last decade of immunotherapy progress was based on decades of prior research, including other forms of immunotherapy. The Bacillus Calmette-Gurin vaccine, used to prevent tuberculosis for a century, has also been used as an immunotherapy to treat nonmuscle invasive bladder cancer since 1990.1 And rituximab (Rituxan), a monoclonal antibody therapy approved in 1997 for B-cell malignancies, is seen by some as an early immunotherapy as well.2

What many clinicians think of in terms of immunotherapy, however, are treatments targeting CTLA-4 and PD-1/PD-L1 pathways, brought from the bench by James P. Allison, PhD, and Tasuku Honjo, PhD, respectively, leading to a Nobel Prize awarded jointly to them in 2018.3

Immune responses are tightly controlled by T cells, and these T cells have on/off switches that help control their responses, according to Padmanee Sharma, MD, PhD, a professor in the Department of Genitourinary Medical Oncology in the Division of Cancer Medicine and the scientific director of the James P. Allison Institute at The University of Texas MD Anderson Cancer Center in Houston. Previously, she said, clinicians were not aware of the off switches. Allison showed that CTLA-4 was an inhibitory pathway and that by blocking it, the T cells could stay longer to eradicate the tumors.

With 8 ICIs approved for immunotherapy in hematological and solid tumors,4 researchers are not only investigating newer forms of therapy, but also combining them to fi nd more effective and durable treatments and introducing them into earlier lines of treatment (TIMELINE). Current research is also attempting to predict who will respond to which therapy based on current and emerging biomarkers.

Ipilimumab, which kicked off the current era of cancer immunotherapy treatment with FDA approval in 2011, targets CTLA-4 for newly diagnosed or previously treated unresectable or metastatic melanoma.5 Ipilimumab blocks CTLA-4, removing its inhibitory signals. This allows the T cells to activate and launch an immune response to the tumors antigens.

CTLA-4 is basically the fi rst inhibitory pathway that comes up on the T cells, Sharma said. CTLA-4 is a member of an immunoglobulin-related receptor family responsible for some immune regulation aspects of T cells.6 It is thought to regulate T-cell proliferation mostly in lymph nodes, early in an immune response, by having an inhibitory role.7

What ipilimumab really did and what the immune checkpoint inhibitors really did is they opened up this whole different way to approach the immune system, Elizabeth Buchbinder, MD, a medical oncologist at Dana-Farber Cancer Institute and an assistant professor of medicine at Harvard Medical School in Boston, Massachusetts, said. Ipilimumab provided amazing durable responses in patients with melanoma with widely metastatic disease, some of whom were alive 10 years later, she said.

The PD-1 and PD-L1 blockades build on ipilimumabs success. Like CTLA-4, PD-1 is a negative regulator of T-cell immune function, inhibiting the target to increase immune system activation. PD-1 suppresses T cells mostly in the peripheral tissues.7 As of November 2021, 8 ICIs have been approved that target CTLA-4, PD-1, and PD-L1 pathways and treat 18 types of cancer.3

AntiPD-1 inhibitors

The percentage of people who benefi tted from ipilimumab was on the low side, Buchbinder said, with only an 11% response rate and 20% of people doing well long term in clinical trials. With PD-1 inhibition, however, there was approximately a 40% response rate and many more patients doing well long term, as demonstrated in clinical trials. So [PD-1 inhibition is] both far more effective and also less toxic, Buchbinder said.

When choosing an agent in the PD-1 class, we dont need to differentiate them. Theyre all antiPD-1, Sharma explained. There arent any data to indicate that patients will respond any differently to pembrolizumab [Keytruda] vs nivolumab [Opdivo]. The mechanism of action for both drugs [is] exactly the same.

Instead, clinicians should consider the FDA approvals for each drugs indications and combinations. But from a scientific standpoint, theres no distinguishing between [them], Sharma said.

AntiPD-L1 inhibitors

PD-1 and PD-L1 targeting drugs were found to work beyond melanoma and kidney cancer, the early indications for treatments targeting the CTLA-4 pathway, Buchbinder said. That was a huge opening up of this fi eld to all of these other cancers, like lung cancer, head and neck cancer, GI [gastrointestinal] cancer, breast [cancer], and beyond, she said.

Before receiving these immunotherapies, patients may need to show PD-1 or PD-L1 expression, although this may not identify all patients who can benefi t from the treatments. Researchers continue to try to identify additional and better biomarkers to indicate which patients may respond.13

In March, the FDA approved the newest ICI, nivolumab and relatlimab-rmbw (Opdualag), for adult and pediatric patients (12 years and older) with unresectable or metastatic melanoma. 3 Nivolumab is a PD-1 inhibitor, and relatlimab blocks LAG3 proteins on immune cells. It is being tested in a lot of other tumors, Buchbinder noted.

Another target in the discovery phase is T cell immunoglobulin and mucin domain 3, which is a checkpoint receptor expressed by many immune cells and leukemic stem cells.14 It is activated by several ligands and is being tested in different cancer types.

Also in clinical trials are tumor-infiltrating lymphocytes (TIL) that recognize cancer cells as abnormal, entering the tumor to kill the cells. TILs already recognize the targets because they originate from the tumor itself.15 Although they need to be expanded, they are not the same as CAR T cells, which must be engineered to recognize the targets.

In addition, older therapies are experiencing a resurgence, with research underway to make interleukin 2 (IL-2) help cytokines function better. That work is trying to optimize what those cytokines do in the body and the immune system, Buchbinder said. There are so many areas where the goal of the therapy is activation of the immune system.

One of these areas includes a return to vaccines. In earlier vaccine therapy, We had no idea that while we were giving therapy to turn on the cells, we were also rapidly turning off the cells because an on switch will automatically drive an off switch for the immune system, Sharma said. The yin and the yang of the immune response is very important to understand because when the immune response is driven in one direction, it will always try to control itself. With that in mind, newer vaccines might work better if given in combination with an antiCTLA-4, for example, to block the inhibitory pathways, she said.

Vaccines are taking many forms, including the mRNA vaccine used for COVID-19, peptide vaccines that include a tiny bit of protein that is expected to be expressed on the tumor surface, and vaccines constructed from dendritic cells, which stimulate T cells, Buchbinder said.

There are also viral therapies injected directly into tumor vaccines, such as talimogene laherparepvec (Imlygic) approved in 2015 for the treatment of some patients with metastatic melanoma that cannot be surgically removed.16 It is a is a modifi ed herpes virus directly injected into the tumor to bring about a local immune response, Buchbinder said.

According to Sharma, approximately 60 targets are currently being evaluated for immunotherapy development.

The FDA has approved 2 CAR T-cell therapies, both in 2017: tisagenlecleucel (Kymriah) for patients 25 years and younger with relapsed B-cell precursor acute lymphoblastic leukemia17 and axicabtagene ciloleucel (Yescarta) for the treatment of adult patients with large B-cell lymphoma that is refractory to fi rst-line chemoimmunotherapy or that relapses within 12 months of fi rst-line chemoimmunotherapy.18 These treatments involve collecting T cells from the patient and engineering them to express CARs that recognize the patients cancer cells. The cells are then enlarged and infused back into the patient, where they can target the antigen- expressing cancer cells. CARs have been shown to greatly improve clinical response and disease remission in some patients.19

I think CAR T cells are clearly building on the concept that T cells are the soldiers of immune response. They are basically engineering the cell to have an antibody that recognizes a specifi c antigen, Sharma said, adding that its important to ensure the targeted antigen is part of the cancer.

CAR T cells have had limited effectiveness in treating solid tumors, given the low T-cell infiltration and immunosuppressive environment that challenges the immune system from successfully reaching and killing solid tumor cancer cells.20

Natural killer (NK) cells are another cell type being researched to attempt tumor eradication, and this therapy is in the early stages, according to Sharma. CAR NK cells can be generated from allogenic donors, making them more attractive as off the shelf treatments compared with CAR T cells, which are collected from the patient. As of early 2021, more than 500 CAR T-cell trials and 17 CAR T-cell/NK-cell trials were in the works globally.21

A major consideration when choosing any treatment, including immunotherapies, is the adverse event (AE) profile. Immunotherapy drugs have different AEs than oncology treatments like chemotherapy or radiation. [With immunotherapy,] what we see is infl ammation because youre turning on the immune system in such a powerful way, Sharma said. Inflammatory reactions include a skin rash or dermatitis, infl ammation in the colon (colitis and diarrhea), and/or infl ammation in the lung with pneumonitis. Clinicians are now aware of these AEs and can monitor them closely, stopping therapy if needed to control them before they become severe, Sharma said.

Toxicities with ipilimumab can be severe, and patients requiring hospital admission might need high-dose steroids, Buchbinder noted. Common AEs for the CTLA-4 inhibitor are typically GI related, including diarrhea, colitis, and hepatitis. Some patients may experience fatigue or a small rash, but most generally make it through treatment with minimal AEs.

The stronger AEs with ipilimumab can be seen from a trial comparing ipilimumab plus nivolumab to nivolumab and relatlimab. Almost 60% of patients experienced AEs with the ipilimumab combination vs 20% in the latter group.17

PD-1 and PD-L1 inhibition typically involve AEs that cause lung issues rather than GI. The types of organ systems affected by immunotherapy AEs can vary based upon which checkpoint inhibitor you use but in some ways, the mechanism by which these occur is very similar, Buchbinder said. Its all an overactivation of the immune system leading to infl ammation in an organ, and there are very few organs that we have not seen toxicity from immunotherapy.

Buchbinder noted that cellular therapies can cause more severe AEs, such as cytokine release syndrome (CRS). Patients can get very sick very quickly, she said, because the therapies given with the cellsincluding the chemotherapy given before and the IL-2 given aftercause most of the AEs. With a lot of the injection therapies, the AEs are related to delivery method, like injection-site issues, but there are also potential systemic AEs like fever, chills, and reactions someone would get to a virus. Its really a huge range in terms of the different [adverse] effects, Buchbinder said.

CRS is the most common AE of CAR T-cell therapy, and it is caused by large numbers of T cells activating, which releases inflammatory cytokines. Although this demonstrates that the therapy is working, it can cause worrisome symptoms. The CRS and the related neurotoxicity can be treated with tocilizumab (Actemra).

One question in the immunotherapy world is whether the development of immune-related AEs predicts a positive or negative response to treatment. With melanoma, we think the data have been very tricky, Buchbinder said. Early trials appeared to show a higher response rate for patients who developed severe symptoms, but as trials developed, that signal was not always there. I think the overall impression is that yes, severe AEs are associated with a better response, she said. A cosmetic AE that clinicians who treat melanoma are excited to see, she said, is vitiligo. It suggests that the immune system is attacking normal melanocytes and that it is attacking cancer cells as well. Those patients generally do far better than patients who dont get vitiligo.

A meta-analysis of 30 studies on the topic, including 4971 individuals, showed that patients who developed immune-related AEs experienced an overall survival benefi t and a progression-free survival benefi t using ICI therapy compared with those who did not. The authors stated that more studies are needed and that the results are controversial.22

Melanoma has been the proving ground for ICIs, Buchbinder said, But now the bar is higher in terms of immunotherapy.

ICIs are now being tested in more immuneresistant tumors. Although there are huge hurdles in terms of some cancers where its going to be hard for immune therapy to do muchlike pancreatic cancer or prostate cancerthere are still diseases where theres opportunity and a possibility that the correct approach or combination might get to some great therapy for those diseases, Buchbinder said

Immunotherapies are being combined with conventional therapies to better integrate treatment. We dont see cancer as a death sentence anymore, Sharma said. We really do see a lot of hope, [and patients with cancer] should be encouraged to discuss immunotherapy with their physician either in a clinical trial or an FDA-approved agent. If you do have a response, its a pretty phenomenal response.

REFERENCES:

1. Lobo N, Brooks NA, Zlotta AR, et al. 100 years of Bacillus Calmette- Gurin immunotherapy: from cattle to COVID-19. Nat Rev Urol. 2021;18(10):611-622. doi:10.1038/s41585-021-00481-1

2. Pierpont TM, Limper CB, Richards KL. Past, present, and future of rituximab-the worlds fi rst oncology monoclonal antibody therapy. Front Oncol. 2018;8:163. doi:10.3389/fonc.2018.00163

3. Kruger S, Ilmer M, Kobold S, et al. Advances in cancer immunotherapy 2019 - latest trends. J Exp Clin Cancer Res. 2019;38(1):268. doi:10.1186/s13046-019-1266-0

4. Lee JB, Kim HR, Ha SJ. Immune checkpoint inhibitors in 10 years: contribution of basic research and clinical application in cancer immunotherapy. Immune Netw. 2022;22(1):e2. doi:10.4110/in.2022.22.e2

5. FDA approves Yervoy (ipilimumab) for the treatment of patients with newly diagnosed or previously-treated unresectable or metastatic melanoma, the deadliest form of skin cancer. News release. Bristol Myers Squibb. March 25, 2011. Accessed May 11, 2022. https://bit.ly/3PFp7q2

6. Rowshanravan B, Halliday N, Sansom DM. CTLA-4: a moving target in immunotherapy. Blood. 2018;131(1):58-67. doi:10.1182/ blood-2017-06-741033

7. Buchbinder EI, Desai A. CTLA-4 and PD-1 pathways: similarities, differences, and implications of their inhibition. Am J Clin Oncol. 2016;39(1):98-106. doi:10.1097/COC.0000000000000239

8. Keown A. Keytruda approvals: a timeline. BioSpace. Aug 13, 2019. Accessed May 11, 2022. https://bit.ly/3yHvfrL

9. Stewart J. Opdivo FDA approval history. Drugs.com. Updated March 15, 2022. Accessed May 20, 2022. https://bit.ly/3lnmtar

10. Markham A, Duggan S. Cemiplimab: fi rst global approval. Drugs. 2018;78(17):1841-1846. doi:10.1007/s40265-018-1012-5

11. FDA grants accelerated approval to dostarlimab-gxly for dMMr endometrial cancer. FDA. Updated April 22, 2021. Accessed May 20, 2022. https://bit.ly/38BSJns

12. Pierpont TM, Limper CB, Richards KL. Past, present, and future of rituximab-the worlds first oncology monoclonal antibody therapy. Front Oncol. 2018;8:163. doi:10.3389/fonc.2018.00163

13. Opdualag becomes fi rst FDA-approved immunotherapy to target LAG-3. National Cancer Institute. April 6, 2022. Accessed May 11, 2022. https://bit.ly/3FZWaAp

14. Acharya N, Sabatos-Peyton C, Anderson AC. TIM-3 finds its place in the cancer immunotherapy landscape. J Immunother Cancer. 2020;8(1):e000911. doi:10.1136/jitc-2020-000911

15. Boldt C. TIL Therapy: 6 things to know. MD Anderson Cancer Center. April 15, 2021. Accessed May 11, 2022. https://bit.ly/3wmguJb

16. FDA approves talimogene laherparepvec to treat metastatic melanoma. National Cancer Institute. November 25, 2015. Accessed May 20, 2022. https://bit.ly/3woTDwA

17. OLeary MC, Lu X, Huang Y, et al. FDA approval summary: tisagenlecleucel for treatment of patients with relapsed or refractory B-cell precursor acute lymphoblastic leukemia. Clin Cancer Res. 2019;25(4):1142-1146. doi:10.1158/1078-0432.CCR-18-2035

18. FDA approves CAR-T cell therapy to treat adults with certain types of large B-cell lymphoma. News release. FDA. Oct. 18, 2017. Accessed May 11, 2022. https://bit.ly/3wpECL1

19. FDA approves fi rst CAR T-cell therapy the evolution of CAR T-cell therapy. Cell Culture Dish. October 24, 2017. Accessed May 10, 2022. https:// bit.ly/3LlDD2B

20. Albinger N, Hartmann J, Ullrich E. Current status and perspective of CAR-T and CAR-NK cell therapy trials in Germany. Gene Ther. 2021;28:513-527. doi:10.1038/s41434-021-00246-w

21. Ahmad A, Uddin S, Steinhoff M. CAR-T cell therapies: an overview of clinical studies supporting their approved use against acute lymphoblastic leukemia and large B-cell lymphomas. Int J Mol Sci. 2020;21(11):3906. doi:10.3390/ijms21113906

22. Zhou X, Yao Z, Yang H, Liang N, Zhang X, Zhang F. Are immune-related adverse events associated with the efficacy of immune checkpoint inhibitors in patients with cancer? a systematic review and meta-analysis. BMC Med. 2020;18(1):87. doi:10.1186/s12916-020-01549-2

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10 Years of Immunotherapy: Advances, Innovations, and Better Patient Outcomes - Targeted Oncology

Why do some heavy smokers never get lung cancer? And why do some people who never smoke get lung cancer? Answers are emerging for both of those questions. In both cases, much depends on our individual genetic make-up.

Lung cancer is the second most common cancer worldwide, accounting for2.2 million new cases and 1.8 million deaths in 2020. It is also the most commonly occurring cancer for which the major cause is both known and preventable. Yet there remain mysteries about causation of lung cancer. How do some heavy smokers manage to avoid lung cancer? And what accounts for the occurrence of lung cancer in people who have never smoked?

In a just-published study, researchers at the Albert Einstein College of Medicine in the Bronx have found that some smokers DNA appears to become accustomed to the cancer-causing agents in cigarettes. This may help prevent dangerous mutations that result in lung cancer.

The heaviest smokers did not have the highest mutation burden, lead study author Dr. Simon Spivack said in a statement. Our data suggests these individuals may have survived for so long in spite of their heavy smoking because they managed to suppress further mutation accumulation. This leveling off of mutations could stem from these people having very proficient systems for repairing DNA damage or detoxifying cigarette smoke.

While this explanation may account for one mystery, another remains: What about the hundreds of thousands of people throughout the world who get lung cancer every year but never so much as took a drag?

Cigarette smoking accounts for between 80 and 90 percent of lung cancer cases in the West. The vast majority of lung cancers in high-income countries could be prevented if all smokers gave up their habit. While this is not likely to happen, just noting this fact is a crucial starting point for any discussion of lung cancer.

The only other common non-skin cancer for which the predominant cause has been identified is cervical cancer, which is caused by the human papilloma virus (HPV), and which can be almost totally prevented by vaccination.

There are striking differences in the epidemiologic, clinical, and biological characteristics of lung cancer in different parts of the world. In the U.S., where nearly 240,000 cases of lung cancer are diagnosed each year and where there are 130,000 deaths annually from the disease, lung cancer rates are roughly comparable in men and women, and are decreasing in both sexes. In contrast, in China, lung cancer rates are increasing in both sexes, but are roughly twice as high in males compared to females.

While most lung cancer in the West is associated with smoking, worldwide, it has been estimated that 15 percent of men and 53 percent of all women with lung cancer worldwide are never smokers.

Lung cancer in never smokers (LCINS), which tends to be of the adenocarcinoma cell type, is found predominantly in women and in East Asians. In contrast, the most common cell types found in lung cancer occurring in smokers are squamous cell and small cell types.

When considered as a distinct disease entity, lung cancer in never smokers ranked as the 7th most common cause of cancer death and the 11th or 12th most common incident type of cancer.

For at least 40 years, we have tried to identify environmental risk factors that might explain the occurrence of lung cancer in people who have never smoked. Potential factors that have been studied include passive smoking; residential exposure to radon gas; exposure to cooking fumes from coal and other fuels (particularly, in low-income countries); general air pollution; pre-existing lung disease; hormonal/reproductive factors (that might help account for the more frequent occurrence in women who never smoked); and inherited susceptibility. Other potential risk factors include asbestos and oncogenic viruses.

Although numerous studies have examined these factors, they appear to have relatively weak effects and are unlikely to account for the majority of cases (here, here, and here).

A 2012 review of the epidemiology of lung cancer in never smokers concluded that, In any event, a large fraction of lung cancers occurring in never smokers cannot be definitively associated with established environmental risk factors, highlighting the need for additional epidemiologic research in this area.

If strong environmental risk factors that account for lung cancer in never smokers are lacking, research examining molecular markers and driver mutations has produced novel and potentially clinically actionable results. Current evidence indicates that LCINS is a distinct disease with unique molecular and genetic characteristics.

Cancer results from the binding of mutagens to the DNA of critical genes, including tumor suppressor genes, proto-oncogenes, and genes involved in DNA repair. If the damage is not repaired, the transformed cell can go on to produce a clone, which can go on to develop into a full-blown (i.e., clinical) cancer. Tobacco smoke contains more than 60 mutagens that bind to, and chemically modify, DNA, leaving a distinctive mutational imprint on the lung cancer genome.

However, identifying the specific mutations that account for the potent carcinogenic effect of smoking on lung cancer has proved a challenge. The recent study from Albert Einstein College of Medicine used a new method to identify mutations in the progenitor cells that give rise a cell type that is susceptible to lung cancer (basal lung epithelial cells).

The researchers examined normal lung tissue from 14 never smokers and 19 smokers. Only one of the former had lung cancer, whereas 13 of the latter had lung cancer. The number of mutations increased with age in both smokers and never smokers, and with increasing pack-years of smoking up to 23 pack-years among smokers, but with no further increase in heavy smokers. However, the one never smoker who developed lung cancer did not have more mutations in normal lung cells than the never smokers who were free of lung cancer.

Notably, the smokers who developed lung cancer did not have more mutations in their normal lung tissue than the smokers who did not develop lung cancer. Thus, it is not clear which mutations associated with smoking determine who goes on to develop lung cancer, or whether it is a matter of susceptibility factors or just bad luck.

Although smoking is a powerful risk factor for lung cancer, its also known that susceptibility genes also play a role in lung cancer, as well as in cancer generally. This is apparent from the fact that most smokers never develop lung cancer.

Its been long recognized that the pattern of lung cancer in Asia differs from that seen in the West. Smoking rates have been much lower in Asian women compared to Asian men, and women tend to develop the adenocarcinoma cell type, which occurs in the periphery of the lung, as opposed to squamous cell and small cell lung cancer, which occur in the main bronchi.

In the early 2000s it was noted that the response to treatment with epidermal growth factor receptor tyrosine kinase (EGFR-TK) inhibitors, such as gefitinib and erlotinib, among patients with non-small cell lung cancer (NSCLC) was markedly more effective in never smokers than in smokers. The benefit of treatment included statistically significant increased response rates, longer interval to progression, and/or longer median overall survival. This improved clinical response was most evident in patients from East Asia, in women, and in cases with the adenocarcinoma cell type.

Thus, lung cancer in smokers and that occurring in never smokers, particularly in East Asian women, appear to present two contrasting facets of lung cancer. In the first case, a potent carcinogen has been identified, but the precise way in which it causes cancer is unclear. In the second instance, a driver mutation which leads to cancer has been identified in a large proportion of cases, but evidence for environmental triggers is either weak or lacking. (A driver mutation is a genetic alteration that is responsible for both the initiation and progression of cancer).

Other research has identified a number of striking differences in genomic signatures and driver mutations between lung cancers occurring in smokers versus in those who have never smoked. For example, mutations in the tumor suppressor gene TP53 are more common in lung cancers in smokers than in LCINS. In addition, mutations in the KRAS oncogene are also common in lung cancers occurring in smokers but are rare in LCINS (43% vs. 0%). Conversely, EGFR mutations are common in LCINS but rare in lung cancer occurring in smokers (in one large study: 54% vs. 16%).

In addition, next generation sequencing studies indicate that the total number of mutations involving genes in protein coding regions was significantly higher in smokers than in never smokers (median 209 vs. 18). This represents a 90 percent lower incidence of mutations in never smokers.

The smaller number of genetic alterations identified in lung cancer in never smokers suggests that the majority, if not all, may play a role in the carcinogenic process. For this reason, it has been suggested that lung cancer in never smokers may provide a relatively enriched and easily identified set of oncogenic drivers for lung cancer.

The more frequent occurrence of EGFR mutations in LCINS has been found in different populations and geographic regions. The discovery of activating EGFR-TK mutations led to a number of randomized clinical trials comparing EGFR-TK inhibitors to chemotherapy in the front-line treatment of patients with EGFR-TK mutations. These trials have now established EGFR-TK inhibitors as the standard front-line treatment for patients with advanced-stage NSCLC that is positive for EGFR-TK mutation. Patients who harbor an EGFR-TK mutation have a 60% response rate to erlotinib (Tarceva).

Two researchers involved the treatment of LCINS concluded their review as follows, With the advances in sequencing technology and decreasing costs it is possible that, in the near future, advanced-stage LCINS may be primarily treated with molecularly targeted therapy, and it would be possible to achieve prolonged periods of disease control similar to the treatment of chronic myeloid leukemia (CML) and gastrointestinal stromal tumor (GIST).

In spite of these advances, it must be emphasized that the landscape of mutations in lung cancer is complex, and there is a tendency for these cancers to develop resistance to the first-line targeted therapy. For this reason, intensive work is focused on new targeted treatments, combinations of several agents, and use of immunotherapies in addition.

First, epidemiologic studies investigating low-level, hard-to-measure, or subtle exposures, such as environmental tobacco smoke, radon exposure, and asbestos should focus on validated lifetime non-smokers, since smoking is such a powerful risk factor for lung cancer. (The risk of lung cancer posed by smoking is much stronger than that posed by asbestos).

Because so little is known about the causes of LCINS, there may be a tendency to overstate the importance of associations with potential risk factors that have been studied, rather than acknowledge that the findings of these studies are unlikely to account for a large proportion of LCINS.

In regard to passive smoking, a French study that examined major mutations associated with lung cancer in never smokers and smokers found no clear association between passive smoke exposure and a smoker-like mutation profile in lifelong, never-smokers with lung cancer. They concluded that, Passive smoking alone appeared to be insufficient to determine a somatic profile in lung cancer.

Second, characterizing the common and divergent mechanisms of malignant transformation in lung cancer occurring among smokers and that in never smokers could contribute to a better understanding of the genomic changes underlying malignant transformation and progression. As one group of researchers wrote, The mutually exclusive nature of certain mutations is a strong argument in favor of separate genetic paths to cancer for ever smokers and never smokers.

Third, the difficulty of identifying major causal factors in LCINS reminds us, that for many cancers, in spite of fifty years of epidemiologic research, we still have not identified major causal factors (exposures) for many common cancers, which might lend themselves to prevention. This is true for colorectal cancer, breast cancer, pancreatic cancer, prostate cancer, brain cancer, leukemia, and others.

This, in turn, underscores how difficult it is to pinpoint external causes of cancers that in most cases take decades to develop. Smoking as a cause of lung cancer and human papillomavirus as a cause of cervical cancer are exceptions to be noted and appreciated.

That said, we are seeing that identifying driver mutations that give rise to a particular cancer can lead to the development of effective targeted therapies that can greatly extend survival. These therapies represent long-sought, dramatic progress in treating serious cancers. This progress is independent of identifying the causal factor responsible for the cancer.

Geoffrey Kabat is a cancer epidemiologist and the author of Hyping Health Risks: Environmental Hazards in Daily Life and the Science of Epidemiology and Getting Risk Right: Understanding Science of Elusive Health Risks. He has a long-standing interest in lung cancer and, particularly, lung cancer occurring in never smokers, and has published on risk factors associated with that condition, including passive smoking, hormonal factors, and body weight.

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Unraveling the mystery of who gets lung cancer and why - Genetic Literacy Project

image:Jordan Kharofa, MD. view more

Credit: Photo/University of Cincinnati

While recommended screenings beginning at age 45 have helped decrease colorectal cancer cases in older adults, cancer rates are continuing to increase in younger populations.

Since 2009, the rate of new colorectal cancer diagnoses in patients under age 50 has increased by 2% each year.

"When I started practice and residency around 2010, Id uncommonly see patients who were less than 50 years old," said Jordan Kharofa, MD, associate professor in the Department of Radiation Oncology in the University of Cincinnatis College of Medicine, a University of Cincinnati Cancer Center member and a UC Health physician. "But more and more were seeing these patients in our clinics now to the point where it doesnt strike us as an exception to the rule."

The research is still unclear exactly what is causing increased cancer rates in young people, but Kharofa said one hypothesis is that patients diets and the bacteria in their gut are contributing factors. This led he and his colleagues to research the relationship between bacteria in the fecal microorganisms, or microbiome, and rates of colorectal cancer in younger populations.

Kharofa delivered a poster presentation on his findings at the recent American Society of Clinical Oncology annual meeting in Chicago.

The microbiome is a term used for the collection of microbes, including microorganisms like bacteria, that live on or in the human body. Kharofa said advances in DNA sequencing have allowed researchers to better characterize what species of bacteria are present in the microbiome, leading to a boom in research over the past 10 years.

In the past, wed have to culture specific bacteria and isolate them, and thats really complicated, he said. But now with the genetics and the cost of sequencing going down, we can quickly characterize what species are where and try to understand if they have implications for normal health and disease.

Kharofa said previous studies have shown that certain bacteria species present in the gut are associated with colorectal cancer. The research team then asked the question if these cancer-causing bacteria were elevated specifically in younger colorectal cancer patients compared to older patients and to healthy patients.

Kharofa collaborated with a team including Nicholas J. Ollberding, PhD, a Cincinnati Childrens Hospital Medical Center bioinformatician and associate professor in the UC Department of Pediatrics. Using genetic data from 11 previous studies, the team analyzed microbiome data from 609 patients who were healthy and 692 patients with colorectal cancer.

The research found two species of bacteria most closely associated with causing colorectal cancer were not found in higher levels among young patients, meaning these bacteria are unlikely to be responsible for increased cancer rates in young people.

Five other bacteria were found in higher levels in young people, including one species that is associated with a sulfur microbial diet, or a diet that is both high in processed meats, low-calorie drinks and liquor and low in raw fruits, vegetables and legumes.

Other epidemiologic studies without access to stool have revealed connections between a sulfur microbial diet and a higher increased risk of cancer in younger people, and Kharofa said this study is consistent with these previous findings.

Although these patients arent obese, there may be dietary patterns that happen early in life that enrich for certain bacteria such as this one, Kharofa said. Its not that what youre eating has carcinogens in them, but the byproducts produced during bacteria metabolism may lead to carcinogenic chemicals. Its possible that interactions between diet and the microbiome may mediate the formation of colorectal cancer cells and heightened risk in younger populations over the last several decades.

While more research is needed, Kharofa said a tangible takeaway from the study is for young people to eat more raw fruits and vegetables and legumes and less processed meats in their diets.

Theres still a lot we dont understand about how the diet influences the microbiome and how that might influence cancer, but this is a small sneak peek at something that might be going on, he said. Theres a lot of reasons to eat less processed foods and diets rich in raw fruits, vegetables and legumes, and this might be one more.

Kharofa said further research will look to learn more about the bacteria species that were found in higher levels in younger patients and how these species contribute both to the development of cancer and to the cancers response to treatment.

As the role of bacteria becomes clearer, there is also the potential for more advanced and tailored screening for younger patients.

Its really difficult to just screen everybody because the rates are pretty low in the entire population of individuals less than 45 years old, he said. But if you are able to profile the microbiome and maybe do targeted screening in some patients who had higher risk based on their stool, that might be a worthwhile investigation.

Even if a person is younger, Kharofa said anyone with symptoms should be evaluated by a doctor. Signs and symptoms of colorectal cancer include rectal bleeding or blood in the stool; persistent abdominal discomfort, including gas, bloating, fullness or cramps; diarrhea, constipation or feeling that the bowel does not fully empty; unknown weight loss; fatigue and vomiting.

Screening is for asymptomatic people, and anyone with symptoms needs to be evaluated, Kharofa said. We unfortunately see these patients presenting later at diagnosis because their symptoms were ignored. If youre young and you have symptoms, you need to be evaluated.

Other contributing authors to the research were Senu Apewokin, MD, associate professor in the UC College of Medicine, and Theresa Alenghat, PhD, member of Cincinnati Childrens Hospital Medical Centers Division of Immunobiology and an associate professor in the UC Department of Pediatrics.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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How diet and the microbiome affect colorectal cancer - EurekAlert

Researchers have recently successfully treated Type 1 diabetes by transplanting insulin-producing pancreas cells into the patient.

University of Missouri scientists are partnering with Harvard and Georgia Tech to create a new diabetes treatment that involves transplanting insulin-producing pancreatic cells

Type 1 diabetes is estimated to affect around 1.8 million Americans. Although type 1 diabetes often develops in childhood or adolescence, it can occur in adulthood.

Despite active research, type 1 diabetes has no cure. Treatment methods include taking insulin, monitoring your diet, managing blood sugar levels, and exercising regularly. Scientists have also recently discovered a new treatment method that holds promise.

A group of researchers from the University of Missouri, Georgia Institute of Technology, and Harvard University has proved the successful use of a novel Type 1 diabetes treatment in a large animal model in a new study published in Science Advances on May 13th. Their method includes transferring insulin-producing pancreas cells, known as pancreatic islets, from a donor to a recipient without the need for long-term immunosuppressive medicines.

According to Haval Shirwan, a professor of child health and molecular microbiology and immunology at the MU School of Medicine and one of the studys primary authors, people with Type 1 diabetes immune system may malfunction, leading it to target itself.

The immune system is a tightly controlled defense mechanism that ensures the well-being of individuals in an environment full of infections, Shirwan said. Type 1 diabetes develops when the immune system misidentifies the insulin-producing cells in the pancreas as infections and destroys them. Normally, once a perceived danger or threat is eliminated, the immune systems command-and-control mechanism kicks in to eliminate any rogue cells. However, if this mechanism fails, diseases such as Type 1 diabetes can manifest.

Diabetes impairs the bodys ability to produce or utilize insulin, a hormone that aids in the regulation of blood sugar metabolism. People with Type 1 diabetes are unable to manage their blood sugar levels because they do not produce insulin. This lack of control may result in life-threatening problems including heart disease, kidney damage, and vision loss.

Shirwan and Esma Yolcu, a professor of child health and molecular microbiology and immunology at the MU School of Medicine, have spent the last two decades targeting an apoptosis mechanism that prevents rogue immune cells from causing diabetes or rejection of transplanted pancreatic islets by attaching a molecule called FasL to the islets surface.

A type of apoptosis occurs when a molecule called FasL interacts with another molecule called Fas on rogue immune cells, and it causes them to die, said Yolcu, one of the studys first authors. Therefore, our team pioneered a technology that enabled the production of a novel form of FasL and its presentation on transplanted pancreatic islet cells or microgels to prevent being rejected by rogue cells. Following insulin-producing pancreatic islet cell transplantation, rogue cells mobilize to the graft for destruction but are eliminated by FasL engaging Fas on their surface.

Haval Shirwan and Esma Yolcu work in their lab at the Roy Blunt NextGen Precision Health building. Credit: University of Missouri

One advantage of this new method is the opportunity to potentially forgo a lifetime of taking immunosuppressive drugs, which counteract the immune systems ability to seek and destroy a foreign object when introduced into the body, such as an organ, or in this case, cell, transplant.

The major problem with immunosuppressive drugs is that they are not specific, so they can have a lot of adverse effects, such as high instances of developing cancer, Shirwan said. So, using our technology, we found a way that we can modulate or train the immune system to accept, and not reject, these transplanted cells.

Their method utilizes technology included in a U.S. patent filed by the University of Louisville and Georgia Tech and has since been licensed by a commercial company with plans to pursue FDA approval for human testing. To develop the commercial product, the MU researchers collaborated with Andres Garca and the team at Georgia Tech to attach FasL to the surface of microgels with proof of efficacy in a small animal model. Then, they joined with Jim Markmann and Ji Lei from Harvard to assess the efficacy of the FasL-microgel technology in a large animal model, which is published in this study.

Haval Shirwan looks at a sample through a microscope in his lab at the Roy Blunt NextGen Precision Health building. Credit: University of Missouri

This study represents a significant milestone in the process of bench-to-bedside research, or how laboratory results are directly incorporated into use by patients in order to help treat different diseases and disorders, a hallmark of MUs most ambitious research initiative, the NextGen Precision Health initiative.

Highlighting the promise of personalized health care and the impact of large-scale interdisciplinary collaboration, the NextGen Precision Health initiative is bringing together innovators like Shirwan and Yolcu from across MU and the UM Systems three other research universities in pursuit of life-changing precision health advancements. Its a collaborative effort to leverage the research strengths of MU toward a better future for the health of Missourians and beyond. The Roy Blunt NextGen Precision Health building at MU anchors the overall initiative and expands collaboration between researchers, clinicians, and industry partners in the state-of-the-art research facility.

I think by being at the right institution with access to a great facility like the Roy Blunt NextGen Precision Health building, will allow us to build on our existing findings and take the necessary steps to further our research, and make the necessary improvements, faster, Yolcu said.

Haval Shirwan and Esma Yolcu. Credit: University of Missouri

Shirwan and Yolcu, who joined the faculty at MU in the spring of 2020, are part of the first group of researchers to begin working in the NextGen Precision Health building, and after working at MU for nearly two years they are now among the first researchers from NextGen to have a research paper accepted and published in a high-impact, peer-reviewed academic journal.

Reference: FasL microgels induce immune acceptance of islet allografts in nonhuman primates by Ji Lei, Mara M. Coronel, Esma S. Yolcu, Hongping Deng, Orlando Grimany-Nuno, Michael D. Hunckler, Vahap Ulker, Zhihong Yang, Kang M. Lee, Alexander Zhang, Hao Luo, Cole W. Peters, Zhongliang Zou, Tao Chen, Zhenjuan Wang, Colleen S. McCoy, Ivy A. Rosales, James F. Markmann, Haval Shirwan and Andrs J. Garca, 13 May 2022, Science Advances.DOI: 10.1126/sciadv.abm9881

Funding was provided by grants from the Juvenile Diabetes Research Foundation (2-SRA-2016-271-S-B) and the National Institutes of Health (U01 AI132817) as well as a Juvenile Diabetes Research Foundation Post-Doctoral Fellowship and a National Science Foundation Graduate Research Fellowship. The content is solely the responsibility of the authors and does not necessarily represent the official views of the funding agencies.

The studys authors would also like to acknowledge Jessica Weaver, Lisa Kojima, Haley Tector, Kevin Deng, Rudy Matheson, and Nikolaos Serifis for their technical contributions.

Potential conflicts of interest are also noted. Three of the studys authors, Garca, Shirwan, and Yolcu, are inventors on a U.S. patent application filed by the University of Louisville and the Georgia Tech Research Corporation (16/492441, filed Feb. 13, 2020). In addition, Garca and Shirwan are co-founders of iTolerance, and Garca, Shirwan, and Markmann serve on the scientific advisory board for iTolerance.

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Harvard Scientists Have Developed a Revolutionary New Treatment for Diabetes - SciTechDaily

Upon receiving a diagnosis of type 1 diabetes (T1D), many people have the same reaction: But why me?

Some people have T1D that runs in their family, while others have no idea how or why they received a diagnosis. Often, to their frustration, those questions go unanswered.

But some people can seemingly link their T1D diagnosis to a previous virus they had endured directly before their onset of T1D.

This makes sense, as T1D is an autoimmune disease. This means your bodys own immune system mistakenly attacks its own insulin-producing beta cells. Although scientists dont know the exact causes or reasons why T1D develops, some researchers believe this haywire immune system reaction is the result of a virus triggering your bodys defense system to go into overdrive.

Viruses are now one main hypothesis of the cause of T1D. In particular, coxsackievirus is on the rise in those with newly diagnosed T1D. That has led some to wonder if theres a direct correlation between this virus, or any virus for that matter.

Read on for more about coxsackievirus, how it materializes in people, and what research has to say about its potential for causing T1D.

Coxsackievirus is a virus thats part of the enterovirus family, which lives in the human digestive tract. This enterovirus family also includes polioviruses, hand, foot, and mouth disease (HFMD), and hepatitis A virus.

This virus spreads easily from person to person, usually through human touch or on surfaces contaminated with feces. The virus can live for several days without a host, making it extremely easy to spread.

When theres a coxsackievirus outbreak, its most likely to affect babies and children younger than 5 years old, as its easily spreadable in places such as daycare centers, schools, and summer camps. Youre most contagious the first week that youre sick, and the best preventive mechanism is hand washing.

Usually, infection with this virus results in these mild flu-like symptoms initially:

Many people have no symptoms at all, and most people recover without treatment. But sometimes the virus can trigger more serious conditions or reactions, such as with HFMD, where a blister-like rash may appear on your hands or feet or in your mouth.

Theres no specific treatment for this virus, and antibiotics dont help with viral infections.

When a virus invades your body, your immune system produces antibodies to fight off that infection. T cells are in charge of developing antibodies as well as fighting off the virus.

But if the virus has some of the same antigens (or substances that cause your immune system to produce antibodies against them) as your bodys own pancreatic beta cells (in the case of T1D), the T cells sometimes start attacking your bodys own beta cells.

This miscommunication is common and results in autoimmune diseases like T1D. Once all the beta cells have been destroyed, T1D is developed and diagnosed. This is why people sometimes receive a diagnosis of T1D a few months after recovering from a bad virus.

But it can sometimes take more than a year for your bodys T cells to destroy the majority of your beta cells (sometimes people experience the honeymoon phase of diabetes, where their pancreas is still producing a minimal amount of insulin), but that original viral infection is hypothesized to be a trigger in the development of T1D.

Not every virus can trigger this reaction ending in T1D. The virus must have antigens that are similar enough to the antigens in pancreatic beta cells. Those viruses include:

Theres mounting evidence that the coronavirus disease 19 (severe acute respiratory syndrome coronavirus 2) pandemic is causing a tidal wave of new T1D diagnoses to be received by both children and adults. But the full repercussions of the pandemic are yet to be seen.

A 2018 study showed that kids exposed to enteroviruses are more likely to develop T1D.

The Environmental Determinants of Diabetes in the Young study found, through nearly 8,000 stool samples of children in the United States and Europe, an association between an exposure and infection with coxsackievirus. This study followed participants for 30 days or longer and focused on the development of an autoimmune reaction that can lead to a T1D diagnosis.

In a Finland-based study, researchers tested more than 1,600 stool samples from 129 children who had recently developed T1D. They also tested 282 children without diabetes for enterovirus RNA, a marker of previous exposure to infection.

Researchers also found 60 percent of the control group showed signs of prior infection (without diabetes), compared with 75 percent of the group with T1D.

They also found that children who developed T1D were exposed to the virus more than a year before their diabetes was diagnosed. Taking this lag time of viral infection to T1D diagnosis into account, the researchers believed that children with diabetes are exposed to three times more enteroviruses than children without diabetes.

Viral infections arent the only hypothesized cause of T1D, but research is homing in on viruses as a common trigger. Studies have shown that even if pregnant people are exposed to enteroviruses, such as coxsackievirus, theyre more likely to give birth to children who eventually develop T1D.

Researchers arent exactly sure what the precise cause of T1D is, and the virus hypothesis is just one theory. Many people believe that T1D is caused by a mix of genetic and environmental factors and that the disease may just be finally triggered by catching a virus such as coxsackievirus or another enterovirus.

While preventing viral spread is always important, even if all enteroviruses were prevented, T1D wouldnt be prevented in everyone, but it would probably make a big difference.

Researchers are hopeful with new trials showing vaccines against enteroviruses could potentially prevent many new diagnoses of T1D, but they wont prevent all people from receiving diagnoses of course.

While theres no vaccine to prevent T1D, Dr. Denise Faustman, Director of the Massachusetts General Hospital Immunobiology Laboratory, is working on that research front. Her work focuses on the bacillus Calmette-Gurin (BCG) vaccine, traditionally used to prevent tuberculosis, and how it can help people with T1D. Specifically, this century-old BCG vaccine may boost a substance called tumor necrosis factor, which eliminates T cells and helps develop more beneficial cells called regulatory T cells.

If you have diabetes, this could help improve your blood sugar and A1C levels while lowering your insulin requirements even years after your initial vaccination. That research is expected to continue for at least several more years beyond 2022.

The exact causes of T1D arent known. But research shows enteroviruses, and in particular coxsackievirus, may play a part in the development of this autoimmune condition. Most researchers believe it to be a mix of both environmental and genetic factors, with perhaps a viral infection trigger. Research remains ongoing, and the development of a coxsackievirus vaccine could go a long way in preventing people worldwide from receiving diagnoses of T1D in the future.

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Do Viruses and Coxsackievirus Cause Type 1 Diabetes? - Healthline

While managing diabetes can be challenging, you can still do the things you enjoy in life. (Getty Images)

This diabetes week, and every week, it's important that just because diabetes is a hidden condition, it doesn't get ignored.

One in 14 of us live with the condition, while even more care for a loved one who does, according to Diabetes UK.

So, whether you might suspect you have diabetes, support someone else with it, are recently diagnosed, or just want to learn more about the condition, here are the basics of what there is to know.

Read more: Kate Moss' daughter Lila proudly sports blood glucose monitor in Fendace campaign

If you're diagnosed with diabetes, a medical professional will explain all you need to know about managing it. (Getty Images)

Diabetes is a lifelong condition that causes a person's blood glucose levels (also called blood sugar) to become too high, according to the NHS. There are two main types, Type 1 and Type 2, though some can also get Gestational diabetes.

Pre-diabetes is when people have blood glucose levels above the normal range, but are not high enough to be diagnosed with the condition itself. But it's important to keep in mind that if your levels are higher than most, your risk of developing full-scale diabetes is increased.

Getting diabetes diagnosed early is key to prevent it from getting progressively worse, which can happen if left untreated.

The finger-prick test has long been used to manage diabetes, though there are now more advanced methods. (Getty Images)

Type 1 diabetes is where the body's immune system attacks and destroys the cells that produce insulin. You need to take insulin every day to keep your blood glucose levels under control. Type 1 is not linked with age, being overweight or lifestyle factors, whereas Type 2 is.

The NHS website says you should see a GP if you have symptoms of type 1, which include:

feeling very thirsty

peeing more than usual, particularly at night

feeling very tired

losing weight without trying

thrush that keeps coming back

blurred vision

cuts and grazes that are not healing

fruity-smelling breath

Type 1 signs and symptoms can come on quickly, particularly in children.

To get tested, your GP will do a urine test and might also check your blood glucose level. If they suspect you have diabetes, you'll be advised to go to hospital immediately for further assessments, where you will stay until you get results (usually the same day).

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If you are diagnosed, then a specialist diabetes nurse will explain everything you need to know about the condition, including how to manage it, test your own blood glucose and how to inject insulin.

Finger-prick tests have long been used to manage diabetes, though you can now check your glucose levels at any time with a continuous glucose monitor (CGM) or flash monitor.

This involves using a sensor, a small device you attach to your arm or tummy that senses how much glucose is in the 'interstitial' fluid under your skin, and a reader or receiver, which shows the results (you can also read them on your smartphone). Some types have optional alarms to alert you if your levels go too low or high.

Read more: What types of dementia are there? Signs and symptoms to see your GP about

While interstitial fluid readings have made many people living with diabetes' lives much easier, it's important to remember they're a few minutes behind your blood glucose levels. This means you'll still need to do finger-prick checks every now and then, particularly when you drive or have a hypoglycaemia (when your blood glucose level is too low), as this tells you what your level is at that moment.

Although being diagnosed with and managing diabetes can be difficult at times, you can still do the things you enjoy. This useful NHS guide on being newly diagnosed provides information to help, including how to recognise and treat a hypo, useful websites, online courses and more.

Do you have the symptoms of diabetes? (Getty Images)

Type 2 diabetes is where the body does not produce enough insulin, or the body's cells do not react to insulin. It is far more common than type 1, with around 90% of all adults in the UK with diabetes living with it.

It can be linked to being overweight or inactive, or having a family history of type 2 diabetes. You're also more at risk of this type of diabetes if you're over 40 (or 25 for south Asian people), have a close relative with diabetes, are overweight or obese, are of Asian, African-Caribbean or black African heritage.

Many people can have type 2 diabetes without realising, because symptoms don't always make you feel unwell.

The NHS website says you should see a GP if you have symptoms of type 2 (similar to type 1), which include:

peeing more than usual, particularly at night

feeling thirsty all the time

feeling very tired

losing weight without trying to

itching around your penis or vagina, or repeatedly getting thrush

cuts or wounds taking longer to heal

blurred vision

You should also see a GP if you're worried you may have a higher risk of getting type 2. You check your risk here.

Some people find checking blood glucose levels with a continuous glucose monitor (CGM) or flash monitor easier. (Getty Images)

Gestational diabetes can also occur during pregnancy, when some women have such high levels of blood glucose that their body is unable to produce enough insulin to absorb it all.

While it can happen at any stage of pregnancy, it is more common in the second or third trimester. It usually disappears after giving birth.

That said, it can cause problems for you and your baby during pregnancy and after birth, but the risks can be reduced if the condition is detected early and well managed.

Read more: How to stay safe in hot weather: Top tips to avoid heatstroke this summer

With the causes of Type 1 and Type 2 different, a doctor will explain how management differs. (Getty Images)

Elaborating on the above, the amount of sugar in the blood is controlled by a hormone called insulin, which is produced by the pancreas (a gland behind the stomach), the NHS explains.

Normally, when food is digested and enters your bloodstream, insulin moves glucose out of the blood and into cells, where it's broken down to produce energy.

However, if you have diabetes, your body is unable to break down glucose into energy because there's either not enough insulin to move it, or the insulin produced doesn't work properly.

While there are no lifestyle changes you can make to lower your risk of of type 1 diabetes, you can help manage type 2 diabetes through healthy eating, regular exercise and achieving a healthy body weight.

There's nothing you can't eat if you have type 2 diabetes, but the NHS suggests limiting certain foods. You should eat a wide range of food (fruit, veg and some starchy foods like pasta), keep sugar, fat and salt to a minimum, and make sure you eat breakfast, lunch and dinner every day do not skip meals.

If you need to change your diet, it might be easier to make small changes every week, it adds.

Altering your lifestyle in small ways can go a long way to reduce your risk of type 2 diabetes. (Getty Images)

Diet, exercise and a healthy lifestyle can also help to reduce the likelihood of getting type 2 diabetes, with more than 13.6 million people in the UK at an increased risk.

"Fortunately even in people with a strong family history of diabetes making positive lifestyle choices can help avoid diabetes altogether," says Dr Sundhya Raman, Medical Doctor and Lifestyle Medicine Physician, Plant Based Health Professionals.

In terms of diet, Ruman says we should try to avoid "processed foods, sugar-sweetened foods and drinks, saturated fats (found in animal source foods and tropical oils), and red and processed meats".

On exercise, she explains it is never too late to start, and build up gradually. "Most people think they need to be quite fit before they get a benefit from exercising, but in fact going from doing nothing to doing something is when the biggest gains are achieved."

It seems sleep is very important too. "We should all be aiming for 7-8 hours of sleep a night, and people who chronically sleep less than this amount raise their risk of diabetes by about 30%," she says.

"When we dont get enough sleep we also have dysregulated levels of our hunger and satiety hormones so are more likely to eat more, particularly foods that are not good for us and make us put on weight, so sleep should also be a priority."

Of all lifestyle factors, Raman says poor diet is the biggest risk. "In studies, the dietary group who have the lowest rates of diabetes are whole-food plant based. They are also the group that tend to have the lowest BMI compared with any other dietary group such as pescatarians or omnivores, and we know that a high BMI is one of the most significant risk factors [for having diabetes].

Some believe food is medicine when it comes to reducing your risk of diabetes, or even reversing it. (Getty Images)

Plant-based diets can reduce the risk of type 2 diabetes by up to 60%, according to Plant Based Health Professionals. But how does this work?

Soluble fibre, she explains helps us to feel full and maintain a healthy weight, release the carbohydrate from our food into our bloodstream slowly, and is the superfood for bugs that live in our colon, of which a healthy balance of can lower the risk of diabetes.

"Plant foods are also full of antioxidants that help reduce the damage that happens to our cells from everyday activities, as well as some of the more damaging things we do such as eating the wrong kinds of foods or sitting for prolonged periods," Ruman adds. "We also know that some of the compounds in plant foods switch on genes that optimise our metabolism.

She also says wholegrains are the food type that have been shown in studies to be particularly important in reducing diabetes and cardiovascular risk. However, in the UK we don't have specific guidelines on how many portions to eat, or any legislation on what can be termed a wholegrain, so people can eat processed foods with few wholegrains, thinking they are improving their health, or think they're bad for people with diabetes, as are often grouped under carbs.

Read more: Earth Day 2022: 7 ways to reduce your carbon 'foodprint' to save the planet

"I would recommend 3 portions of wholegrains per day, ideally as unprocessed as possible." She also reccomends a variety of fruit and vegetables, as well as variety in your nuts, seeds, wholegrains, lentils, legumes, herbs and spices, while prioritising plant sources of proteins over those from animal sources.

In some cases, plant-based are also effective at reversing Type 2 diabetes, effective at reversing insulin resistance, which is thought to happen fat gets stored in our muscle and liver, and damages cells."One of the ways in which a whole-food plant-based diet is incredibly beneficial is that people tend to lose weight when they follow this dietary pattern, and we know that weight loss can reverse diabetes."

Make sure you consult a doctor before making any big dietary changes.

For more information, visit the NHS' website on diabetes, or seek support from Diabetes UK on 0345123 2399.

Watch: Diabetes drug leads to significant weight loss in those with obesity, study finds

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Diabetes Week: Types 1 and 2 symptoms, causes and prevention - Yahoo Entertainment

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Great sex, anecdotally, is uninhibited and free of worry. Its a time to put aside the usual responsibilities that plague you and just enjoy the moment. But diabetes and sex have a slightly complicated relationship. For people with type 1 diabetes, fully detaching from responsibilities isnt an option in fact, it can be dangerous. Its no surprise then that a study conducted by Oxford University professors found that 62 percent of people with diabetes say their condition has negatively impacted their relationships with their partners.

Having to think about your type 1 diabetes during intimacy can be agitating and even disheartening. But its important to remember that many adults have to do some planning before sex. Some men have to take pills for erectile dysfunction. Tons of women need lubricant due to a hormonal imbalance. And lets not forget about all of the people who need a lumbar support pillow for missionary. Everyone deserves to enjoy sex. Heres what you need to know about having safe and enjoyable sex, when you have type 1 diabetes.

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There are several reasons that those with type 1 diabetes cant explore the Kama Sutra without some planning. First off, a lot of sex depending on how you go about it counts as a workout. It gets your blood pumping, it gets you sweating and, like any exercise, it impacts blood sugar levels. While people who dont have diabetes can handle these blood sugar fluctuations fairly well, people with diabetes need to be careful.

Next, theres the added factor of booze. Its common for people to enjoy a drink (or a few) before having sex. Alcohol helps loosen those inhibitions and make you feel relaxed. But, if you drink too much or dont stick to diabetic-friendly cocktails, your blood sugar levels can go on a roller coaster.

The ways sex plays on blood sugar levels dont stop there. Even if you stay sober for sex, the mere excitement of being with a partner can impact blood sugar levels. So, while its frustrating, the fact that sex affects blood sugar levels cannot be ignored.

Source: kali9 / Getty

If you know that your night will likely end in sex, take steps to put your blood sugar levels in a healthy range by the time intimacy occurs. This means being careful about what you eat, using insulin when necessary and even monitoring other physical activity throughout the day. If your sessions in the sack are particularly active, then you might need to skip your afternoon workout. You dont want to put yourself at risk of low blood sugar mid-coitus due to over-exertion.

Source: NurPhoto / Getty

Even if you eat right and monitor your blood sugar levels, things can still go awry after a few rounds with your partner. Be sure to keep snacks on the nightstand so you can reach for them if you feel your blood sugar levels dropping. Better yet, incorporate sexy foods like strawberries or chocolate sauce (sugar-free if necessary) into sex so it doesnt feel like snack time is putting a pause on the fun.

Source: FG Trade / Getty

Sex is always better when you can communicate with your partner. That is true about every topic, from what positions work for you to managing your blood sugar levels. Notify your partner in advance that sex can impact your blood sugar, and that you might need to pause during the activities to have a snack or take insulin. Additionally, if you can tell tonight is just not a good night to do the deed, speak up. Pushing yourself through sex when your blood sugar levels are off can be dangerous.

Source: Andriy Onufriyenko / Getty

If you wear an insulin pump or a blood glucose monitor, you might be tempted to remove this during sex. Some diabetics struggle to feel sexy when wearing these devices (and nothing else) in front of a partner. First off, theres no shame in wearing a device that keeps you alive and enables you to live the way that you enjoy. However, there are some practicalities to consider, like the fact that these devices can get tangled or fall off during sex.

If you want to remove your device during sex, make sure to get your blood sugar levels in a healthy range right before the activities. And then put the device back on immediately after sex. If your blood sugar levels arent stable enough for device removal, get creative and choose positions that let you keep the device on. Again, communication is key here.

Source: Andreas Stamm / Getty

It is important to know that type 1 diabetes can impact sexual function in many ways. For women, high blood sugar can lead to vaginal dryness, according to the Journal of Natural Science, Biology and Medicine. For men, blood sugar issues can cause erectile dysfunction. And people of all genders can experience mood swings and a low libido in connection to type 1 diabetes.

While there are practical fixes for vaginal dryness like finding a lubricant you love the other symptoms can be more complicated to treat. If you are struggling with any of these issues, first off, know that its common for people with type 1 diabetes and is nothing to be embarrassed about. Then talk to your doctor about the best way to treat the problem.

Having type 1 diabetes doesnt have to mean the end of a fun, playful and even erotic sex life. It simply means you have to do a little extra planning. But when you have a partner with whom you can communicate openly, that planning wont feel like a burden. And when you know your body will be safe and taken care of, then you can let go and be in the moment.

RELATED CONTENT:7 Things Doctors Wish Black Women Knew About Diabetes

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Diabetes And Sex: Have Safe Sex While Managing Diabetes - MadameNoire

Wilmington, Delaware, United States: According to Transparency Market Researchs latest report on the global diabetes devices market for the historical period 20172018 and forecast period 20192027, increase in prevalence of diabetes, and increase in adoption of insulin pumps among type 1 diabetes patients are projected to drive the global diabetes devices market during the forecast period.

According to the report, the global diabetes devices market was valued at US$ 41.8 Bn in 2018 and is anticipated to expand at a CAGR of 6.4% from 2019 to 2027.

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Increase in Prevalence of Diabetes Expected to Drive Global Diabetes Devices Market: Key Drivers

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Increase in Adoption of Insulin Pump among Type 1 Diabetes Patients Boost Market Growth

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Threat of Alternative Therapies for Diabetes to Hamper Market

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Global Diabetes Devices Market: Competitive Landscape

This report profiles major players in the global diabetes devices market based on various attributes such as company overview, financial overview, product portfolio, business strategies, and recent developments

The global diabetes devices market is highly fragmented, with the presence of a number of international as well as regional players

Leading players operating in the global diabetes devices market are

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Diabetes Devices Market to Expand at the CAGR of 6.4% from 2019 to 2027, Increase in Prevalence of Diabetes Expected to Drive Global Market - BioSpace

If you live with diabetes, you may be aware that having the condition and its complications may put you at greater risk of developing anemia. But how are the two conditions related and what does this mean for you?

This article will investigate the relationship between diabetes and anemia, and what you should know if you have diabetes-related complications impacting your life.

According to the National Heart, Lung, and Blood Institute, Anemia is a condition in which the blood doesnt have enough healthy red blood cells to function properly. This leads to reduced oxygen flow to the bodys organs.

There are more than 3 million cases of anemia diagnosed in the United States every year, making this a very common condition.

You may experience the following symptoms:

Its important to note that some anemia symptoms are similar to symptoms of high blood sugar, including dizziness, lightheadedness, extreme fatigue, rapid heart rate, and headache.

Check your blood sugar often to make sure youre not confusing high blood sugar for suspected anemia. If your symptoms continue for a few days or weeks without high blood sugar numbers or ketones, call a healthcare professional to get checked for anemia.

Diabetes doesnt cause anemia and anemia doesnt cause diabetes. The two conditions are related, though.

Up to 25 percent of Americans with type 2 diabetes also have anemia. So its relatively common for people with diabetes, and especially diabetes-related complications, to also develop anemia.

However, if you have one condition or the other, you wont automatically develop the other condition.

As seen in this 2004 study, Anemia is a common complication of people with diabetes who develop chronic kidney disease because damaged or failing kidneys dont produce a hormone called erythropoietin (EPO), which signals to the bone marrow that the body needs more red blood cells to function.

Early stages of kidney disease (nephropathy) may be asymptomatic, but if youre diagnosed with anemia and you have diabetes, it might be a sign that your kidneys arent working properly.

People with diabetes are also more likely to have inflamed blood vessels. This prevents the bone marrow from even receiving the EPO signal to create more red blood cells to begin with. That makes anemia a more likely result.

Additionally, if you have existing anemia and are then diagnosed with diabetes, it may make you more likely to develop diabetes-related complications, such as retinopathy and neuropathy (eye and nerve damage).

A lack of healthy red blood cells can additionally worsen kidney, heart, and artery health, systems that are already taxed with a life lived with diabetes.

Certain diabetes medications can decrease your levels of the protein hemoglobin, which is needed to carry oxygen through the blood. These diabetes medications can increase your risk of developing anemia:

Since blood loss is also a significant contributor to the development of anemia, if you have diabetes and are on kidney dialysis, you may want to talk with your healthcare team about your increased risk of anemia as well.

Anemia can affect blood sugar levels in several ways.

One 2010 study found that anemia produced false high blood sugar levels on glucose meters, leading to dangerous hypoglycemia events after people overtreat that false high blood sugar.

As shown in a 2014 study, theres a direct link between anemia caused by iron deficiency and higher amounts of glucose in the blood. A 2017 review of several studies found that in people both with and without diabetes, iron-deficiency anemia was correlated with increased A1C numbers.

This resulted from more glucose molecules sticking to fewer red blood cells. After iron-replacement therapy, HbA1c levels in the studies participants decreased.

If you receive an anemia diagnosis and you live with diabetes, there are many excellent treatment options.

Treatment will depend on the underlying cause of the condition, but may include supplementation with iron and/or vitamin B.

If your anemia is caused by blood loss, a blood transfusion may be necessary. If your bodys blood production is reduced, medications to improve blood formation may be prescribed.

Diabetes and anemia are closely related, though neither directly causes the other condition.

Diabetes-related complications such as kidney disease or failure and inflamed blood vessels may contribute to anemia. Certain diabetes medications can also increase the likelihood of developing anemia. Anemia may also make diabetes management more challenging, with higher A1C results, false high blood sugars, and a potential risk of worsening organ health leading to future diabetes complications.

Still, anemia is very treatable with supplementation, dietary or medication changes.

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Anemia and Diabetes: What You Should Know - Healthline

Patient education is a component of prevention of progression of kidney disease. Paul Flynn and colleagues at SUNY Downstate Health Science University, Brooklyn, New York, interviewed patients with end-stage kidney disease (ESKD) secondary to diabetic kidney disease to determine their knowledge of their disease and how it relates to chronic kidney disease (CKD).

Results of the interviews were reported during a poster session at the NKF 2022 Spring Clinical Meetings. The poster was titled Knowledge Gaps Regarding Chronic Kidney Disease and Diabetes in a Population of Inner-City Dialysis Patients.

The survey was administered to 15 randomly selected dialysis patients with diabetes. The survey included questions about patient knowledge about diabetes and kidney disease at the time of diagnosis. The researchers also collected demographic information.

Mean age of the respondents was 64.3 years, 53% (n=8) were male, 47% (n=7) had less than a college education, 89% (n=8/9) made less than $40,000 per year. Mean time with diabetes was 29.0 years. Eight of 13 patients saw an endocrinologist, and four reported most recent hemoglobin A1c (HbA1c) >10%. Twelve of 13 respondents reported they had no knowledge of what CKD was and 10 of 13 did not know at the time of their diabetes diagnosis that diabetes could cause kidney disease.

There was no correlation between knowledge and age, education, length of time with diabetes, income, or sex. Patients who were older were lesse likely to see an endocrinologist (r=0.64; P=.019), checked their glucose less frequently (r=0.71; P=.006), and did not check after eating (r=0.62; P=.023). Thirteen of 14 patients said they did know what HbA1c was, 11 of 14 knew that insulin decreases blood glucose levels, 12 of 14 knew that a person with type 2 diabetes had increased blood glucose, and ten of 14 patients knew that HbA1c should be checked every 3 months. Six of 13 patients did not know what a nephrologist is and nine of 13 did not know how kidney function is measured.

In summary, the authors said, In our population of inner-city dialysis patients with diabetes mellitus: (1) The majority were knowledgeable about diabetes, although older patients were less likely to see an endocrinologist and check their blood sugar frequently or after eating. (2) The majority of patients had no knowledge of kidney disease and did not know that diabetes could cause kidney disease at the time of their diagnosis. (3) Almost half of patients currently did not know what a nephrologist was and did not know how kidney function is measured. (4) An early education program for our underserved population regarding the relationship between kidney disease and diabetes should be designed in the hopes of delaying progression to ESKD.

Source: Flynn P, Sherman B, Wei L, et al. Knowledge gaps regarding chronic kidney disease and diabetes in a population of inner-city dialysis patients. Abstract of a poster presented at the National Kidney Foundation 2022 Spring Clinical Meetings (Abstract 273), Boston, Massachusetts, April 6-10, 2022.

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Patient Knowledge of Diabetes and CKD in an Inner-City Population - DocWire News

BASEL, Switzerland, June 16, 2022 /PRNewswire/ --Ascensia Diabetes Care, a global diabetes care company,maker of CONTOURblood glucose monitoring (BGM) system portfolio and distributor of Eversense Continuous Glucose Monitoring (CGM) Systems, announces that its partner Senseonics Holdings, Inc. has received CE Mark approval for the Eversense E3 Continuous Glucose Monitoring (CGM) System, clearing the way for its use in European Union (EU) member countries. Ascensia plans to make the next-generation system, which can be used for up to 6 months, available to patients in certain European markets from the third quarter of 2022.

The fully implantable, long-term Eversense E3 CGM System has been designed to deliver key improvements on the currently available Eversense XL CGM System, whilst building on the unique benefits that European users already experience. The next-generation system offers exceptional accuracy and long-term sensor wear, alongside reduced frequency of calibration and significantly enhanced sensor survivability. Unlike the XL System, the new E3 System has also been approved for non-adjunctive use, meaning that it can inform insulin treatment decisions without confirmation of glucose levels from fingerstick testing. Both Eversense XL and Eversense E3 are approved for use up to 6 months, making them the longest lasting CGM sensors available. This gives people with diabetes freedom from the burdens associated with other available CGM systems, such as weekly or bi-weekly self-insertions.

Eversense E3 is already available in the U.S. following FDA approval and launch earlier this year. Following the CE Mark approval in Europe the Eversense E3 System will be distributed in Germany, Italy, Spain (including Andorra), the Netherlands, Poland, Switzerland, Norway and Sweden.

Robert Schumm, President at Ascensia Diabetes Care, said, "This approval is an exciting milestone for us as we look forward to bringing Eversense E3 to people with diabetes across Europe. From this next-generation system you can expect the excellent features and benefits that European users currently experience with Eversense XL, but with design improvements that address requests we repeatedly hear from patients and healthcare providers. Our role is to make sure that as many people have access to this innovative product as possible, and efforts are already under way to launch this system in certain European countries in the coming months."

Developed by Senseonics and brought to people with diabetes by Ascensia, the newly approved Eversense E3 CGM System offers patients:

"The features and benefits of this improved system offer people with diabetes unparalleled flexibility, convenience and accuracy," said Elaine Anderson, Head of Eversense CGM Business Unit at Ascensia Diabetes Care. "Choice is key in managing diabetes and we are proud to work alongside our partner Senseonics to bring an outstanding and unique CGM option to patients and healthcare providers across Europe and in the U.S."

People in these markets who are interested in getting started with Eversense XL now can visit http://www.ascensia.com/eversense for more information, and will be among the first to know when Eversense E3 is commercially available.

* There is no glucose data generated when the transmitter is removed.

1 Garg S. et al. Evaluation of Accuracy and Safety of the Next-Generation Up to 180-Day Long-Term Implantable Eversense Continuous Glucose Monitoring System: The PROMISE Study. Diabetes Technology & Therapeutics 2021; 24(2): 1-9.DOI: 10.1089/dia.2021.0182

SOURCE Ascensia Diabetes Care

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ASCENSIA DIABETES CARE ANNOUNCES EUROPEAN APPROVAL OF THE NEXT-GENERATION EVERSENSE E3 CONTINUOUS GLUCOSE MONITORING SYSTEM - PR Newswire

What should diabetes health care professionals consider when treating patients who have sickle cell trait or disease?

World Sickle Cell Day is observed annually on June 19th to raise awareness of sickle cell disease, a group of inherited red blood cell disorders that affect more than 100,000 people in the United States and 20 million people worldwide. For people with sickle cell disease, red blood cells are crescent or sickle shaped and do not bend or move easily, which can block blood flow to the rest of the body and cause repeated infections and episodes of pain.

Hemoglobinopathies (also called hemoglobin variants) are inherited red blood cell conditions that affect hemoglobin, the protein that carries oxygen through the body. One of the most common hemoglobinopathies is hemoglobin S, the sickle cell gene. In a severe form of sickle cell disease, sickle cell anemia, a patient inherits two genes for hemoglobin S.

Patients can also inherit one sickle cell gene and have sickle cell trait, often with no signs or symptoms. This means that many patients are unaware they have sickle cell trait. It is also worth noting that certain populations are more likely to inherit sickle cell traitabout 1 in 13 African Americans and about 1 in 100 Hispanics/Latinos have sickle cell trait.

Sickle Cell Hemoglobinopathies and the A1C Test

For patients who have the sickle cell gene or other hemoglobinopathies, some A1C testing methods for blood glucose may produce unreliable results. An A1C test with falsely high outcomes could lead to the prescription of more aggressive treatments, resulting in increased episodes of hypoglycemia. Conversely, falsely low outcomes could lead to the undertreatment of diabetes.

Laboratories use many different assay methods to measure A1C. Health care professionals should suspect the presence of a hemoglobinopathy when

For more information about hemoglobinopathies and alternative tests to measure blood glucose levels, view NIDDKs health information on Sickle Cell Trait & Other Hemoglobinopathies & Diabetes.

And to learn more about NIDDK Director Dr. Griffin P. Rodgers career researching blood conditions, including sickle cell, watch the videos below.

Link:
Understanding the Link between Diabetes Care and Sickle Cell Disease | NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases...

The number of children being treated at paediatric diabetes units (PDUs) in England and Wales has increased by more than 50% amid a perfect storm of rising obesity levels and the cost of living crisis, health leaders have said.

Diabetes UK said alarming obesity levels among children had led to a concerning climb in the number diagnosed with type 2 diabetes, and predicted that the cost of living crisis could lead to further problems in the years to come.

Data from NHS Digital shows that almost one in seven children start primary school obese a rise of almost 50% in just a year. More than a quarter are obese by the time they finish primary school.

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The high levels of obesity combined with the squeeze on personal finances are creating a perfect storm which risks irreversible harm to the health of young people, Diabetes UK said. It accused the government of letting our children down as it called for concerted action to tackle obesity.

It comes after the governments decision to delay measures to reduce unhealthy eating, weakening its anti-obesity strategy by postponing for a year a ban on buy one, get one free deals for foods high in fat, salt and sugar.

Demand for care for children with type 2 diabetes at paediatric diabetes units across England and Wales has increased by more than 50% in the last five years, according to the Diabetes UK analysis. A total of 973 children with type 2 diabetes were treated in PDUs in 2020-21, up from 621 in 2015-16.

PDUs employ a team of specialists to care for children with type 2 diabetes that can include consultants, nurses and dieticians. The team usually work in a hospital setting, where a child may attend appointments as an outpatient rather than being seen at their GPs surgery. Previous statistics have shown that in England alone, about 1,600 children have been diagnosed with type 2 diabetes.

Diabetes UK said children in the most deprived parts of England and Wales were disproportionately affected by the disease, with four in 10 children and young people with type 2 diabetes living in the poorest areas, compared with only one in 19 from the richest. This is similar to data for childhood obesity prevalence, it said.

The charity said that in light of the additional burden of the cost of living crisis, the poorest children would bear the brunt for decades to come.

Chris Askew, the chief executive of Diabetes UK, said: We are very concerned that this spike in childhood obesity will translate into an even greater increase in children with type 2 diabetes in the coming years, a crisis fuelled by longstanding health inequalities and made worse still by impacts of the cost of living crisis.

Government needs to entirely rethink its commitment to child health. This must start with urgently reversing the decision to backtrack on their obesity strategy commitments and go further still, with bold steps to address childhood obesity and poorer outcomes for children living in poverty in the forthcoming health disparities white paper.

The UK government is letting our children down. With soaring numbers of children now living with obesity, and numbers diagnosed with type 2 diabetes on a very concerning climb, we are facing a perfect storm, which risks irreversible harm to the health of young people.

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Child type 2 diabetes referrals in England and Wales jump 50% amid obesity crisis - The Guardian

LUBBOCK, Texas (PRESS RELEASE) The following is a press release from Covenant Health:

Covenant Childrens will host a free Diabetes Camp called New Beginnings for children ages 5-14 who have diabetes. The camp will be July 13-16, 2022, from 9 a.m. to 4 p.m., with each day at a different location in Lubbock. Locations will include the Science Spectrum, Main Event, YWCA and Spirit Ranch.

Due to the recent loss of the local American Diabetes Association chapter in the area, Covenant Childrens and Covenant Health Foundation recognized the need to replace the annual diabetes camp that used to be held by the organization.

We recognize the value and impact that a camp for children with diabetes holds. Kids with diabetes, and their families, need to know and see they are not alone, said Brittny Ayola, Covenant Childrens PICU nurse manager and diabetes education program coordinator.

The camp is free and open to all children in Lubbock and the surrounding area. Lunches, snacks, t-shirt and activities are covered; however, housing is not provided for attendees from out of town. Children will need to bring their own diabetes supplies.

As a diabetic herself, Ayola said when she was growing up, there were no camps in Lubbock, so she had to go out of town for similar experiences. Ayola said it can feel very isolating to have a chronic condition that takes daily management and being able to do normal activities with other children who also have diabetes can have a vast impact.

There will be medical professionals who have had diabetes training to oversee safety and give parents peace of mind while their child builds friendships and enjoys the camp. Through the day campers will do carb counts, take insulin and check blood sugar together.

On the last day of camp, there will be vendor booths for parents and families to learn more about diabetes technology, products and medications.

There are still spots available. The deadline to register is July 1, or when spots are full. Parents can sign up their child through the form at the following link: https://bit.ly/39tVGH5

If children with diabetes over the age of 15 are interested in participating, there are opportunities to help as a junior counselor or counselor. Contact Brittny Ayola at AYOLABS2@covhs.org or (806) 786-2968 for more information.

About Covenant Health:

Covenant Childrens is the only independently licensed, freestanding, childrens hospital in West Texas and eastern New Mexico and is one of only eight members of the Childrens Hospital Association of Texas and is the only one in our region.

As a faith-based health care system, it is Covenant Healths vision to create Health for a Better World. As the Best Hospital in the Panhandle Plains region as voted by U.S. News and World Report, Covenant Health has consistently provided exceptional health care to West Texas, and eastern New Mexico for more than 100 years. Our clinically integrated health network of eight hospitals, and more than 6,000 caregivers allows us to provide our patients with better access to care using more innovative technology and procedures, while focusing on new age approaches to health care like education and preventative medicine. To learn more about Covenant Health, please visit covenanthealth.org or our Facebook, LinkedIn, or Twitter, pages.

(Press release from Covenant Health)

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Covenant Childrens to host diabetes camp in July - KLBK | KAMC | EverythingLubbock.com

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Originally posted here:
Pattern of contraceptive use among reproductive-aged women with diabetes and/or hypertension: findings from Bangladesh Demographic and Health Survey -...