StemCell Therapy

Introduction

[Note: Many of the medical and scientific terms used in this summary are found in the NCI Dictionary of Genetics Terms. When a linked term is clicked, the definition will appear in a separate window.]

[Note: Many of the genes described in this summary are found in the Online Mendelian Inheritance in Man (OMIM) database. When OMIM appears after a gene name or the name of a condition, click on OMIM for a link to more information.]

Colorectal cancer (CRC) is the third most commonly diagnosed cancer in both men and women.

Estimated new cases and deaths from CRC in 2015:[1]

About 75% of patients with CRC have sporadic disease with no apparent evidence of having inherited the disorder. The remaining 25% of patients have a family history of CRC that suggests a hereditary contribution, common exposures among family members, or a combination of both. Genetic mutations have been identified as the cause of inherited cancer risk in some colon cancerprone families; these mutations are estimated to account for only 5% to 6% of CRC cases overall. It is likely that other undiscovered genes and background genetic factors contribute to the development of familial CRC in conjunction with nongenetic risk factors.

(Refer to the PDQ summaries on Colorectal Cancer Screening; Colorectal Cancer Prevention; Colon Cancer Treatment; and Rectal Cancer Treatment for more information about sporadic CRC.)

Colorectal tumors present with a broad spectrum of neoplasms, ranging from benign growths to invasive cancer and are predominantly epithelial-derived tumors (i.e., adenomas or adenocarcinomas).

Pathologists have classified the lesions into the following three groups:

Research, however, suggests increased CRC risk in some families who have multiple members affected with juvenile polyposis, Peutz-Jeghers syndrome, and hyperplastic polyposis.[2-4]

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Genetics of Colorectal Cancer - National Cancer Institute

DNA, or deoxyribonucleic acid, is the hereditary material in humans and almost all other organisms. Nearly every cell in a persons body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

The information in DNA is stored as a code made up of four chemical bases: adenine (A), guanine (G), cytosine (C), and thymine (T). Human DNA consists of about 3 billion bases, and more than 99 percent of those bases are the same in all people. The order, or sequence, of these bases determines the information available for building and maintaining an organism, similar to the way in which letters of the alphabet appear in a certain order to form words and sentences.

DNA bases pair up with each other, A with T and C with G, to form units called base pairs. Each base is also attached to a sugar molecule and a phosphate molecule. Together, a base, sugar, and phosphate are called a nucleotide. Nucleotides are arranged in two long strands that form a spiral called a double helix. The structure of the double helix is somewhat like a ladder, with the base pairs forming the ladders rungs and the sugar and phosphate molecules forming the vertical sidepieces of the ladder.

An important property of DNA is that it can replicate, or make copies of itself. Each strand of DNA in the double helix can serve as a pattern for duplicating the sequence of bases. This is critical when cells divide because each new cell needs to have an exact copy of the DNA present in the old cell.

DNA is a double helix formed by base pairs attached to a sugar-phosphate backbone.

The National Human Genome Research Institute fact sheet Deoxyribonucleic Acid (DNA) provides an introduction to this molecule.

Information about the genetic code and the structure of the DNA double helix is available from GeneEd.

The New Genetics, a publication of the National Institute of General Medical Sciences, discusses the structure of DNA and how it was discovered.

Nature Educations Scitable offers a thorough description of DNA, including its components and organization. It also includes a short animated video.

A basic explanation and illustration of DNA can be found on Arizona State Universitys Ask a Biologist website.

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What is DNA? - Genetics Home Reference

genetics,study of heredity in general and of genes in particular. Genetics forms one of the central pillars of biology and overlaps with many other areas such as agriculture, medicine, and biotechnology.

Since the dawn of civilization, humankind has recognized the influence of heredity and has applied its principles to the improvement of cultivated crops and domestic animals. A Babylonian tablet more than 6,000 years old, for example, shows pedigrees of horses and indicates possible inherited characteristics. Other old carvings show cross-pollination of date palm trees. Most of the mechanisms of heredity, however, remained a mystery until the 19th century, when genetics as a systematic science began.

Genetics arose out of the identification of genes, the fundamental units responsible for heredity. Genetics may be defined as the study of genes at all levels, including the ways in which they act in the cell and the ways in which they are transmitted from parents to offspring. Modern genetics focuses on the chemical substance that genes are made of, called deoxyribonucleic acid, or DNA, and the ways in which it affects the chemical reactions that constitute the living processes within the cell. Gene action depends on interaction with the environment. Green plants, for example, have genes containing the information necessary to synthesize the photosynthetic pigment chlorophyll that gives them their green colour. Chlorophyll is synthesized in an environment containing light because the gene for chlorophyll is expressed only when it interacts with light. If a plant is placed in a dark environment, chlorophyll synthesis stops because the gene is no longer expressed.

Genetics as a scientific discipline stemmed from the work of Gregor Mendel in the middle of the 19th century. Mendel suspected that traits were inherited as discrete units, and, although he knew nothing of the physical or chemical nature of genes at the time, his units became the basis for the development of the present understanding of heredity. All present research in genetics can be traced back to Mendels discovery of the laws governing the inheritance of traits. The word genetics was introduced in 1905 by English biologist William Bateson, who was one of the discoverers of Mendels work and who became a champion of Mendels principles of inheritance.

Although scientific evidence for patterns of genetic inheritance did not appear until Mendels work, history shows that humankind must have been interested in heredity long before the dawn of civilization. Curiosity must first have been based on human family resemblances, such as similarity in body structure, voice, gait, and gestures. Such notions were instrumental in the establishment of family and royal dynasties. Early nomadic tribes were interested in the qualities of the animals that they herded and domesticated and, undoubtedly, bred selectively. The first human settlements that practiced farming appear to have selected crop plants with favourable qualities. Ancient tomb paintings show racehorse breeding pedigrees containing clear depictions of the inheritance of several distinct physical traits in the horses. Despite this interest, the first recorded speculations on heredity did not exist until the time of the ancient Greeks; some aspects of their ideas are still considered relevant today.

Hippocrates (c. 460c. 375 bce), known as the father of medicine, believed in the inheritance of acquired characteristics, and, to account for this, he devised the hypothesis known as pangenesis. He postulated that all organs of the body of a parent gave off invisible seeds, which were like miniaturized building components and were transmitted during sexual intercourse, reassembling themselves in the mothers womb to form a baby.

Aristotle (384322 bce) emphasized the importance of blood in heredity. He thought that the blood supplied generative material for building all parts of the adult body, and he reasoned that blood was the basis for passing on this generative power to the next generation. In fact, he believed that the males semen was purified blood and that a womans menstrual blood was her equivalent of semen. These male and female contributions united in the womb to produce a baby. The blood contained some type of hereditary essences, but he believed that the baby would develop under the influence of these essences, rather than being built from the essences themselves.

Aristotles ideas about the role of blood in procreation were probably the origin of the still prevalent notion that somehow the blood is involved in heredity. Today people still speak of certain traits as being in the blood and of blood lines and blood ties. The Greek model of inheritance, in which a teeming multitude of substances was invoked, differed from that of the Mendelian model. Mendels idea was that distinct differences between individuals are determined by differences in single yet powerful hereditary factors. These single hereditary factors were identified as genes. Copies of genes are transmitted through sperm and egg and guide the development of the offspring. Genes are also responsible for reproducing the distinct features of both parents that are visible in their children.

In the two millennia between the lives of Aristotle and Mendel, few new ideas were recorded on the nature of heredity. In the 17th and 18th centuries the idea of preformation was introduced. Scientists using the newly developed microscopes imagined that they could see miniature replicas of human beings inside sperm heads. French biologist Jean-Baptiste Lamarck invoked the idea of the inheritance of acquired characters, not as an explanation for heredity but as a model for evolution. He lived at a time when the fixity of species was taken for granted, yet he maintained that this fixity was only found in a constant environment. He enunciated the law of use and disuse, which states that when certain organs become specially developed as a result of some environmental need, then that state of development is hereditary and can be passed on to progeny. He believed that in this way, over many generations, giraffes could arise from deerlike animals that had to keep stretching their necks to reach high leaves on trees.

British naturalist Alfred Russel Wallace originally postulated the theory of evolution by natural selection. However, Charles Darwins observations during his circumnavigation of the globe aboard the HMS Beagle (183136) provided evidence for natural selection and his suggestion that humans and animals shared a common ancestry. Many scientists at the time believed in a hereditary mechanism that was a version of the ancient Greek idea of pangenesis, and Darwins ideas did not appear to fit with the theory of heredity that sprang from the experiments of Mendel.

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genetics | Britannica.com

"Inbred" redirects here. For the 2011 British film, see Inbred (film).

Inbreeding is the production of offspring from the mating or breeding of individuals or organisms that are closely related genetically, in contrast to outcrossing, which refers to mating unrelated individuals.[1] By analogy, the term is used in human reproduction, but more commonly refers to the genetic disorders and other consequences that may arise from incestuous sexual relationships and consanguinity.

Inbreeding results in homozygosity, which can increase the chances of offspring being affected by recessive or deleterious traits.[2] This generally leads to a decreased biological fitness of a population[3][4] (called inbreeding depression), which is its ability to survive and reproduce. An individual who inherits such deleterious traits is referred to as inbred. The avoidance of such deleterious recessive alleles caused by inbreeding, via inbreeding avoidance mechanisms, is the main selective reason for outcrossing.[5][6] Crossbreeding between populations also often has positive effects on fitness-related traits.[7]

Inbreeding is a technique used in selective breeding. In livestock breeding, breeders may use inbreeding when, for example, trying to establish a new and desirable trait in the stock, but will need to watch for undesirable characteristics in offspring, which can then be eliminated through further selective breeding or culling. Inbreeding is used to reveal deleterious recessive alleles, which can then be eliminated through assortative breeding or through culling. In plant breeding, inbred lines are used as stocks for the creation of hybrid lines to make use of the effects of heterosis. Inbreeding in plants also occurs naturally in the form of self-pollination.

Offspring of biologically related persons are subject to the possible impact of inbreeding, such as congenital birth defects. The chances of such disorders is increased the closer the relationship of the biological parents. (See coefficient of inbreeding.) This is because such pairings increase the proportion of homozygous zygotes in the offspring, in particular deleterious recessive alleles, which produce such disorders.[8] (See inbreeding depression.) Because most recessive alleles are rare in populations, it is unlikely that two unrelated marriage partners will both be carriers of the alleles. However, because close relatives share a large fraction of their alleles, the probability that any such deleterious allele is inherited from the common ancestor through both parents is increased dramatically. Contrary to common belief, inbreeding does not in itself alter allele frequencies, but rather increases the relative proportion of homozygotes to heterozygotes. However, because the increased proportion of deleterious homozygotes exposes the allele to natural selection, in the long run its frequency decreases more rapidly in inbred population. In the short term, incestuous reproduction is expected to produce increases in spontaneous abortions of zygotes, perinatal deaths, and postnatal offspring with birth defects.[9] The advantages of inbreeding may be the result of a tendency to preserve the structures of alleles interacting at different loci that have been adapted together by a common selective history.[10]

Malformations or harmful traits can stay within a population due to a high homozygosity rate and it will cause a population to become fixed for certain traits, like having too many bones in an area, like the vertebral column in wolves on Isle Royale or having cranial abnormalities in Northern elephant seals, where their cranial bone length in the lower mandibular tooth row has changed. Having a high homozygosity rate is bad for a population because it will unmask recessive deleterious alleles generated by mutations, reduce heterozygote advantage, and it is detrimental to the survival of small, endangered animal populations.[11] When there are deleterious recessive alleles in a population it can cause inbreeding depression. The authors think that it is possible that the severity of inbreeding depression can be diminished if natural selection can purge such alleles from populations during inbreeding.[12] If inbreeding depression can be diminished by natural selection than some traits, harmful or not, can be reduced and change the future outlook on a small, endangered populations.

There may also be other deleterious effects besides those caused by recessive diseases. Thus, similar immune systems may be more vulnerable to infectious diseases (see Major histocompatibility complex and sexual selection).[13]

Inbreeding history of the population should also be considered when discussing the variation in the severity of inbreeding depression between and within species. With persistent inbreeding, there is evidence that shows inbreeding depression becoming less severe. This is associated with the unmasking and eliminating of severely deleterious recessive alleles. It is not likely, though, that eliminating can be so complete that inbreeding depression is only a temporary phenomenon. Eliminating slightly deleterious mutations through inbreeding under moderate selection is not as effective. Fixation of alleles most likely occurs through Mullers Ratchet, when an asexual populations genomes accumulate deleterious mutations that are irreversible.[14]

Autosomal recessive disorders occur in individuals who have two copies of the gene for a particular recessive genetic mutation.[15] Except in certain rare circumstances, such as new mutations or uniparental disomy, both parents of an individual with such a disorder will be carriers of the gene. These carriers do not display any signs of the mutation and may be unaware that they carry the mutated gene. Since relatives share a higher proportion of their genes than do unrelated people, it is more likely that related parents will both be carriers of the same recessive gene, and therefore their children are at a higher risk of a genetic disorder. The extent to which the risk increases depends on the degree of genetic relationship between the parents: The risk is greater when the parents are close relatives and lower for relationships between more distant relatives, such as second cousins, though still greater than for the general population.[16] A study has provided the evidence for inbreeding depression on cognitive abilities among children, with high frequency of mental retardation among offspring in proportion to their increasing inbreeding coefficients.[17]

Children of parent-child or sibling-sibling unions are at increased risk compared to cousin-cousin unions.[18]

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Inbreeding - Wikipedia, the free encyclopedia

A chimera (also spelled chimaera) (from the creature Chimera in Greek mythology) is a single organism composed of genetically distinct cells. This can result in male and female organs, two different blood types, or subtle variations in form.[1] Animal chimeras are produced by the merger of multiple fertilized eggs. In plant chimeras, however, the distinct types of tissue may originate from the same zygote, and the difference is often due to mutation during ordinary cell division. Normally, chimerism is not visible on casual inspection; however, it has been detected in the course of proving parentage.[2]

Another way that chimerism can occur in animals is by organ transplantation, giving one individual tissues that developed from two different genomes. For example, a bone marrow transplant can change someone's blood type.

An animal chimera is a single organism that is composed of two or more different populations of genetically distinct cells that originated from different zygotes involved in sexual reproduction. If the different cells have emerged from the same zygote, the organism is called a mosaic. Chimeras are formed from at least four parent cells (two fertilized eggs or early embryos fused together). Each population of cells keeps its own character and the resulting organism is a mixture of tissues. There are some reports of human chimerism.[1]

This condition is either inherited or it is acquired through the infusion of allogeneic hematopoietic cells during transplantation or transfusion. In nonidentical twins, chimerism occurs by means of blood-vessel anastomoses. The likelihood of offspring being a chimera is increased if it is created via in vitro fertilization[citation needed].[3] Chimeras can often breed, but the fertility and type of offspring depends on which cell line gave rise to the ovaries or testes; varying degrees of intersex differences may result if one set of cells is genetically female and another genetically male.

Tetragametic chimerism is a form of congenital chimerism. This condition occurs through the fertilization of two separate ova by two sperm, followed by aggregation of the two at the blastocyst or zygote stages. This results in the development of an organism with intermingled cell lines. Put another way, the chimera is formed from the merging of two nonidentical twins (although a similar merging presumably occurs with identical twins, but as their DNA is almost identical, the presence would not be immediately detectable in a very early (zygote or blastocyst) phase). As such, they can be male, female, or have mixed intersex characteristics.

As the organism develops, it can come to possess organs that have different sets of chromosomes. For example, the chimera may have a liver composed of cells with one set of chromosomes and have a kidney composed of cells with a second set of chromosomes. This has occurred in humans, and at one time was thought to be extremely rare, though more recent evidence suggests that it is not as rare as previously believed.[1][4]

This is particularly true for the marmoset. Recent research shows most marmosets are chimeras, sharing DNA with their fraternal twins.[5] 95% of Marmoset fraternal twins trade blood through chorionic fusions, making them hematopoietic chimeras.[6][7]

Most chimeras will go through life without realizing they are chimeras. The difference in phenotypes may be subtle (e.g., having a hitchhiker's thumb and a straight thumb, eyes of slightly different colors, differential hair growth on opposite sides of the body, etc.) or completely undetectable. Chimeras may also show, under a certain spectrum of UV light, distinctive marks on the back resembling that of arrow points pointing downwards from the shoulders down to the lower back; this is one expression of pigment unevenness called Blaschko's lines.[8]

Affected persons may be identified by the finding of two populations of red cells or, if the zygotes are of opposite sex, ambiguous genitalia and intersex alone or in combination; such persons sometimes also have patchy skin, hair, or eye pigmentation (heterochromia). If the blastocysts are of opposite sex, genitals of both sexes may be formed: either ovary and testis, or combined ovotestes, in one rare form of intersex, a condition previously known as true hermaphroditism.

Note that the frequency of this condition does not indicate the true prevalence of chimerism. Most chimeras composed of both male and female cells probably do not have an intersex condition, as might be expected if the two cell populations were evenly blended throughout the body. Often, most or all of the cells of a single cell type will be composed of a single cell line, i.e. the blood may be composed predominantly of one cell line, and the internal organs of the other cell line. Genitalia produce the hormones responsible for other sex characteristics. If the sex organs are homogeneous, the individual will not be expected to exhibit any intersex traits.

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Chimera (genetics) - Wikipedia, the free encyclopedia

DNA from the Beginning is organized around key concepts. The science behind each concept is explained by: animation, image gallery, video interviews, problem, biographies, and links. DNAftb blog: It's the season of hibernation, something I've always wished I could do. Oh, to wrap up in a ball, sleep away the winter, and wake to a beautiful spring day like Bambi! Although the thought has always intrigued me, it never really occurred to me what a feat hibernation actually is. It turns out that all of the bears, squirrels, rabbits ... that I thought were just sleeping, are breaking biological laws!! If I was to stay dormant for 5 months, without food or drink and little to no movement in freezing temperatures [...] Feature: We have relaunched the Weed to Wonder site as a flexible "e-book" that can be viewed as a website, an app, or a printable PDF. Mailing List Gene News - Scientists stumble across unknown stem-cell type Find the DNALC on: Language options:

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DNA from the Beginning - An animated primer of 75 ...

Stem Cells: Tools for Human Genetics and Heart Regeneration
Department of Medicine Grand Rounds presentation by Dr. Charles Murry, professor, Department of Pathology, Bioengineering and Medicine/Cardiology; Director, Center for Cardiovascular Biology;...

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Stem Cells: Tools for Human Genetics and Heart Regeneration - Video

Genetics Policy Institute (GPI) and the Regenerative Medicine Foundation (RMF) Announce Merger Plan
The Genetics Policy Institute (GPI), producer of the annual World Stem Cell Summit, and the Regenerative Medicine Foundation (RMF) have agreed to merge in order to leverage their resources...

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Genetics Policy Institute (GPI) and the Regenerative Medicine Foundation (RMF) Announce Merger Plan - Video

Genetics Video Pluripotent Stem Cells

By: Emerson Pk

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Genetics Video Pluripotent Stem Cells - Video

Catherine Malabou. Epigenetics and Plasticity. 2012
#8234;www.egs.edu Catherine Malabou, philosopher and author, talking about the relationship between genetics and the philosophical concept of life. In this lecture Catherine Malabou discusses the mechanization of life, Derrida #39;s concept of the trace as bare life, epigenetics as the transformation of genetic code and the development of the brain in relationship to Michel Foucault, Girogio Agamben, Jacques Derrida, Martin Heidegger, François Jacob, Daniel Dennet and Thomas Jenuwein focusing on determinism, fragility, zoe, bios, dasein, stem cells, the passage from genotype to phenotype, interfering RNA, neural plasticity, symbolic life and biology. Public open lecture for the students and faculty of the European Graduate School EGS Media and Communication Studies department program Saas-Fee Switzerland Europe. 2012. Catherine Malabou. Catherine Malabou, Ph.D., born in 1959, was a student at the École normal supérieure (ENS) and Sorbonne University in France. She wrote her dissertation on Georg Wilhelm Friedrich Hegel under the direction of the French philosopher Jacques Derrida, completing it in 1994. The thesis was published in 1996 under the title L #39;Avenir de Hegel, plasticité, temporalité, dialectique (The Future of Hegel: Plasticity, Temporality, and Dialectic). Catherine Malabou has taught at Nanterre University in Paris, the University of California at Berkeley, the New School for Social Research in New York City and currently is a full-time professor at the Centre for ...From:egsvideoViews:1 0ratingsTime:01:36:54More inEducation

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Catherine Malabou. Epigenetics and Plasticity. 2012 - Video

Bernard Siegel - Aging: The Disease, The Cure, The Implications
Bernard Siegel is the full-time Executive Director of the nonprofit Genetics Policy Institute (GPI) based in Palm Beach Gardens, Florida. He received his undergraduate and law degrees from the University of Miami (BA 1972, JD 1975). He is a member of the Florida Bar since 1975. In 2002, Mr. Siegel filed the landmark case seeking a guardian for the alleged clone, "Baby Eve." The case was widely credited for exposing Clonaid , the so-called "human cloning company" as a sham. In 2003, he traded his 30-year courtroom career to found GPI, which leads the global cause in support of stem cell research. He is a recognized policy expert relating to stem cell research, regenerative medicine and cloning. Working with the world #39;s leading stem cell researchers, Mr. Siegel played a pivotal role in protecting the research in the United Nations, which was under the threat of being banned by world treaty. He also works with grassroots activists throughout the United States, educating lawmakers and formulating effective strategies supporting research for cures. Mr. Siegel serves on the board of directors of Americans for Cures and on the advisory boards of the Sabrina Cohen Foundation for Stem Cell Research, The Brooke Ellison Project and Genomics Education Institute. He is a member of the American Society for Bioethics + Humanities. He is a member of the International Society for Stem Cell Research and serves as the co-chair of the ISSCR Governmental Affairs Committee. Mr. Siegel has been ...From:Jeriaska JeriaskaViews:0 0ratingsTime:18:57More inEducation

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Bernard Siegel - Aging: The Disease, The Cure, The Implications - Video

CAMBRIDGE, Mass. & BOTHELL, Wash.--(BUSINESS WIRE)--

Millennium: The Takeda Oncology Company, a wholly owned subsidiary of Takeda Pharmaceutical Company Limited (TSE:4502), and Seattle Genetics, Inc. (SGEN) today announced the initiation of an international phase 3 clinical trial evaluating ADCETRIS (brentuximab vedotin) as part of a frontline combination chemotherapy regimen in patients with previously untreated advanced Hodgkin lymphoma (HL). The trial is being conducted under a Special Protocol Assessment (SPA) agreement from the U.S. Food and Drug Administration (FDA) and the trial also received scientific advice from the European Medicines Agency (EMA). ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30, a defining marker of classical HL.

Millennium is pleased to announce the initiation of the phase 3 trial of ADCETRIS in patients with previously untreated advanced Hodgkin lymphoma. This is a key step in our efforts to explore the potential of this targeted therapy as part of a frontline treatment regimen, said Karen Ferrante, MD, Chief Medical Officer, Millennium.The trial is part of our ongoing development program to explore patient populations that may benefit from treatment with ADCETRIS in earlier lines of therapy and in other CD30-expressing malignancies.

There have been no new therapies approved for patients with newly diagnosed HL in many decades, representing a significant need to identify additional treatment options in this setting, said Thomas C. Reynolds, M.D., Ph.D., Chief Medical Officer, Seattle Genetics. We believe through this novel ADCETRIS-containing regimen we have the potential to redefine the treatment of frontline HL. This trial is also an important part of our development plan for ADCETRIS, and may serve as confirmatory to our U.S. accelerated approval in relapsed HL and systemic anaplastic large cell lymphoma.

Study Design

The randomized, open-label, phase 3 trial will investigate ADCETRIS+AVD1 versus ABVD2 as frontline therapy in patients with advanced classical HL. The primary endpoint is modified progression free survival (mPFS) per independent review facility assessment using the Revised Response Criteria for malignant lymphoma. Secondary endpoints include overall survival (OS), complete remission (CR) and safety. The multi-center trial will be conducted in North America, Europe, Latin America and Asia. The study will enroll approximately 1,040 eligible patients (approximately 520 patients per treatment arm) who have histologically-confirmed diagnosis of Stage III or IV classical HL who have not been previously treated with systemic chemotherapy or radiotherapy.

For more information, please visit http://www.clinicaltrials.gov.

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

ADCETRIS received accelerated approval from the U.S. Food and Drug Administration (FDA) in August 2011 for two indications: (1) the treatment of patients with Hodgkin lymphoma after failure of autologous stem cell transplant (ASCT) or after failure of at least two prior multi-agent chemotherapy regimens in patients who are not ASCT candidates, and (2) the treatment of patients with systemic anaplastic large cell lymphoma (sALCL) after failure of at least one prior multi-agent chemotherapy regimen. The indications for ADCETRIS are based on response rate. There are no data available demonstrating improvement in patient-reported outcomes or survival with ADCETRIS.

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Millennium and Seattle Genetics Initiate Global Phase 3 Clinical Trial of ADCETRIS® in Previously Untreated Advanced ...

BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) today announced that its collaborator, Millennium: The Takeda Oncology Company, a wholly owned subsidiary of Takeda Pharmaceutical Company Limited, announced that the European Commission has granted conditional marketing authorization for ADCETRIS (brentuximab vedotin). ADCETRIS was approved for two indications: (1) the treatment of adult patients with relapsed or refractory CD30-positive Hodgkin lymphoma (HL) following autologous stem cell transplant (ASCT) or following at least two prior therapies when ASCT or multi-agent chemotherapy is not a treatment option, and (2) for the treatment of adult patients with relapsed or refractory systemic anaplastic large cell lymphoma (sALCL). As a result, under the collaboration Seattle Genetics will receive two milestone payments from Millennium, one for each indication, totaling $25 million. ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30.

The approval of ADCETRIS by the European Commission marks a significant milestone for the product and for the many relapsed or refractory HL and systemic ALCL patients in need of effective new treatment options in Europe, said Clay B. Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. In addition to the U.S. and EU approvals of ADCETRIS, we are making regulatory progress for approval in Canada while Millennium and Takeda are pursuing regulatory approvals in other countries. Complementing these regulatory activities is a robust ADCETRIS clinical development program to support our goal of establishing it as the foundation of therapy for CD30-positive malignancies.

The conditional marketing authorization for ADCETRIS is valid in the 27 member states of the European Union (EU) as well as Norway, Liechtenstein and Iceland. Similar to accelerated approval regulations inthe United States, conditional marketing authorizations are granted in the EU to medicinal products that fulfill an unmet medical need with a positive benefit/risk assessmentand whose immediate availability would result in a significant public health benefit. Conditional marketing authorization by the European Commission includes obligations to provide additional clinical data at a later stage to confirm the positive benefit-risk assessment. The ADCETRIS Marketing Authorization Application was filed by Takeda Global Research & Development Centre (Europe) to the European Medicines Agency.

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

ADCETRIS received accelerated approval from the U.S. Food and Drug Administration (FDA) in August 2011 for relapsed HL and sALCL.

Seattle Genetics and Millennium are jointly developing ADCETRIS. Under the terms of the collaboration agreement, Seattle Genetics has U.S. and Canadian commercialization rights and the Takeda Group has rights to commercialize ADCETRIS in the rest of the world. Seattle Genetics and the Takeda Group are funding joint development costs for ADCETRIS on a 50:50 basis, except in Japan where the Takeda Group will be solely responsible for development costs. Seattle Genetics is entitled to royalties based on a percentage of Millennium's net sales in its territory at rates that range from the mid-teens to the mid-twenties based on sales volume, subject to offsets for royalties paid by Millennium to third parties.

About Seattle Genetics

Seattle Genetics is a biotechnology company focused on the development and commercialization of monoclonal antibody-based therapies for the treatment of cancer. The FDA granted accelerated approval of ADCETRIS in August 2011 for two indications. ADCETRIS is being developed in collaboration with Millennium: The Takeda Oncology Company. In addition, Seattle Genetics has three other clinical-stage ADC programs: SGN-75, ASG-5ME and ASG-22ME. Seattle Genetics has collaborations for its ADC technology with a number of leading biotechnology and pharmaceutical companies, including Abbott, Bayer, Celldex Therapeutics, Daiichi Sankyo, Genentech, GlaxoSmithKline, Millennium, Pfizer and Progenics, as well as ADC co-development agreements with Agensys, an affiliate of Astellas, and Genmab. More information can be found at http://www.seattlegenetics.com.

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Seattle Genetics Announces ADCETRIS® Receives European Commission Conditional Marketing Authorization

CAMBRIDGE, Mass. & BOTHELL, Wash.--(BUSINESS WIRE)--

Millennium: The Takeda Oncology Company, a wholly owned subsidiary of Takeda Pharmaceutical Company Limited (TSE:4502), and Seattle Genetics, Inc. (SGEN) today announced the initiation of an international phase 3 clinical trial evaluating ADCETRIS (brentuximab vedotin) as part of a frontline combination chemotherapy regimen in patients with previously untreated advanced Hodgkin lymphoma (HL). The trial is being conducted under a Special Protocol Assessment (SPA) agreement from the U.S. Food and Drug Administration (FDA) and the trial also received scientific advice from the European Medicines Agency (EMA). ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30, a defining marker of classical HL.

Millennium is pleased to announce the initiation of the phase 3 trial of ADCETRIS in patients with previously untreated advanced Hodgkin lymphoma. This is a key step in our efforts to explore the potential of this targeted therapy as part of a frontline treatment regimen, said Karen Ferrante, MD, Chief Medical Officer, Millennium.The trial is part of our ongoing development program to explore patient populations that may benefit from treatment with ADCETRIS in earlier lines of therapy and in other CD30-expressing malignancies.

There have been no new therapies approved for patients with newly diagnosed HL in many decades, representing a significant need to identify additional treatment options in this setting, said Thomas C. Reynolds, M.D., Ph.D., Chief Medical Officer, Seattle Genetics. We believe through this novel ADCETRIS-containing regimen we have the potential to redefine the treatment of frontline HL. This trial is also an important part of our development plan for ADCETRIS, and may serve as confirmatory to our U.S. accelerated approval in relapsed HL and systemic anaplastic large cell lymphoma.

Study Design

The randomized, open-label, phase 3 trial will investigate ADCETRIS+AVD1 versus ABVD2 as frontline therapy in patients with advanced classical HL. The primary endpoint is modified progression free survival (mPFS) per independent review facility assessment using the Revised Response Criteria for malignant lymphoma. Secondary endpoints include overall survival (OS), complete remission (CR) and safety. The multi-center trial will be conducted in North America, Europe, Latin America and Asia. The study will enroll approximately 1,040 eligible patients (approximately 520 patients per treatment arm) who have histologically-confirmed diagnosis of Stage III or IV classical HL who have not been previously treated with systemic chemotherapy or radiotherapy.

For more information, please visit http://www.clinicaltrials.gov.

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

ADCETRIS received accelerated approval from the U.S. Food and Drug Administration (FDA) in August 2011 for two indications: (1) the treatment of patients with Hodgkin lymphoma after failure of autologous stem cell transplant (ASCT) or after failure of at least two prior multi-agent chemotherapy regimens in patients who are not ASCT candidates, and (2) the treatment of patients with systemic anaplastic large cell lymphoma (sALCL) after failure of at least one prior multi-agent chemotherapy regimen. The indications for ADCETRIS are based on response rate. There are no data available demonstrating improvement in patient-reported outcomes or survival with ADCETRIS.

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Millennium and Seattle Genetics Initiate Global Phase 3 Clinical Trial of ADCETRIS® in Previously Untreated Advanced ...

Seattle Genetics (Nasdaq: SGEN) is a biotech company focused on the development of monoclonal antibody-based treatments for cancer. The company's antibody-drug conjugate, or ADC, technology treats cancer by sending in an antibody and an attached drug, which bind with cancer cells and stops cell division from the inside. The company currently has one drug, Adcertis, available for sale.

The company has a small field of competitors in the ADC realm. Leading that pack is ImmunoGen (Nasdaq: IMGN) with a targeted antibody payload, or TAP, technology that works similarly to ADC technology, and has led to the company striking several large partnerships to license it. Pfizer (NYSE: PFE) is in the early stages of developing its own ADC technology, even as it works on other drugs created with Seattle Genetics' technology that could become competitors for Adcertis. Medarex, a subsidiary of Bristol-Myers Squibb (NYSE: BMY) , has ADC technology and is developing monoclonal antibody drugs that could compete with Adcertis.

Here are three ways Seattle Genetics is working to expand its revenues past the currently narrow definitions of its sole drug on the market.

Geographic expansionAdcetris is a treatment that's been approved by the Food and Drug Administration for resistant forms of Hodgkin lymphoma and systemic anaplastic large cell lymphoma. The drug was approved last summer, but revenues have failed to ramp up sharply due in part to the domestic limitation of the drug.

Geographic expansion could be just around the corner. A European Commission decision is expected any day now, following a July committee recommendation, which would make the treatment available in 27 countries. Canadian approval is following right behind. Health Canada accepted the New Drug Submissionfor Adcetris back in May, and a decision is expected in early 2013.

Adcetris is a partnership between Seattle Genetics and Millennium, an oncology subsidiary of Takeda. The partnership grants Seattle Genetics the drug rights in the U.S. and Canada, and requires Millennium to pay up to $230 million in milestone payments plus a double-digit percentage of net sales from its global markets.

Expanded useExpanding the approved indications for Adcetris would also boost its revenues. Seattle Genetics' pipeline is half full of trials for new indications. There are two phase 3 trials that deserve closer attention.

The AETHERA trialtests Adcetris versus a placebo in patients at risk for residual Hodgkin lymphoma after an autologous stem-cell transplant. The study has a primary endpoint of progression-free survival, and secondary endpoints include overall survivability and safety. Data is expected in late 2013 or early 2014.

The ALCANZA trialcompares Adcetris to methotrexate or bexarotene in patients with specific mature type of t-cell lymphoma. This trial is still enrolling, so its data will come in behind ATHERA, which finished enrollment in late September.

There are also Adcetris trials in earlier stages. The potential indications include front-line HL when used in conjunction with chemotherapy, front-line HL in elderly populations, and non-lymphoma malignancies.

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3 Things to Watch With Seattle Genetics

BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) today announced that its collaborator, Millennium: The Takeda Oncology Company, a wholly owned subsidiary of Takeda Pharmaceutical Company Limited, announced that the European Commission has granted conditional marketing authorization for ADCETRIS (brentuximab vedotin). ADCETRIS was approved for two indications: (1) the treatment of adult patients with relapsed or refractory CD30-positive Hodgkin lymphoma (HL) following autologous stem cell transplant (ASCT) or following at least two prior therapies when ASCT or multi-agent chemotherapy is not a treatment option, and (2) for the treatment of adult patients with relapsed or refractory systemic anaplastic large cell lymphoma (sALCL). As a result, under the collaboration Seattle Genetics will receive two milestone payments from Millennium, one for each indication, totaling $25 million. ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30.

The approval of ADCETRIS by the European Commission marks a significant milestone for the product and for the many relapsed or refractory HL and systemic ALCL patients in need of effective new treatment options in Europe, said Clay B. Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. In addition to the U.S. and EU approvals of ADCETRIS, we are making regulatory progress for approval in Canada while Millennium and Takeda are pursuing regulatory approvals in other countries. Complementing these regulatory activities is a robust ADCETRIS clinical development program to support our goal of establishing it as the foundation of therapy for CD30-positive malignancies.

The conditional marketing authorization for ADCETRIS is valid in the 27 member states of the European Union (EU) as well as Norway, Liechtenstein and Iceland. Similar to accelerated approval regulations inthe United States, conditional marketing authorizations are granted in the EU to medicinal products that fulfill an unmet medical need with a positive benefit/risk assessmentand whose immediate availability would result in a significant public health benefit. Conditional marketing authorization by the European Commission includes obligations to provide additional clinical data at a later stage to confirm the positive benefit-risk assessment. The ADCETRIS Marketing Authorization Application was filed by Takeda Global Research & Development Centre (Europe) to the European Medicines Agency.

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

ADCETRIS received accelerated approval from the U.S. Food and Drug Administration (FDA) in August 2011 for relapsed HL and sALCL.

Seattle Genetics and Millennium are jointly developing ADCETRIS. Under the terms of the collaboration agreement, Seattle Genetics has U.S. and Canadian commercialization rights and the Takeda Group has rights to commercialize ADCETRIS in the rest of the world. Seattle Genetics and the Takeda Group are funding joint development costs for ADCETRIS on a 50:50 basis, except in Japan where the Takeda Group will be solely responsible for development costs. Seattle Genetics is entitled to royalties based on a percentage of Millennium's net sales in its territory at rates that range from the mid-teens to the mid-twenties based on sales volume, subject to offsets for royalties paid by Millennium to third parties.

About Seattle Genetics

Seattle Genetics is a biotechnology company focused on the development and commercialization of monoclonal antibody-based therapies for the treatment of cancer. The FDA granted accelerated approval of ADCETRIS in August 2011 for two indications. ADCETRIS is being developed in collaboration with Millennium: The Takeda Oncology Company. In addition, Seattle Genetics has three other clinical-stage ADC programs: SGN-75, ASG-5ME and ASG-22ME. Seattle Genetics has collaborations for its ADC technology with a number of leading biotechnology and pharmaceutical companies, including Abbott, Bayer, Celldex Therapeutics, Daiichi Sankyo, Genentech, GlaxoSmithKline, Millennium, Pfizer and Progenics, as well as ADC co-development agreements with Agensys, an affiliate of Astellas, and Genmab. More information can be found at http://www.seattlegenetics.com.

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Seattle Genetics Announces ADCETRIS® Receives European Commission Conditional Marketing Authorization

PALM BEACH, Fla.--(BUSINESS WIRE)--

Genetics Policy Institute (GPI) announced today that Bernard Siegel, Executive Director of GPI, will make two keynote presentations this month at regional conferences: Midwest Conference on Stem Cell Biology and Therapy October 5-7 in Rochester, Michigan and BioFlorida Conference 2012 October 7-9 in Miami, Florida.

Siegel will present a keynote address titled The Power of Advocacy at the Midwest Conference on Stem Cell Biology and Therapy. The Genetics Policy Institute joined with the Oakland University William Beaumont Institute for Stem Cell and Regenerative Medicine (ISCRM) as a collaborating partner for the event. Researchers from hospitals, medical organizations, academic institutions and the business community throughout the Midwest will discuss not only the latest advances in this rapidly expanding field of medical science, but the ethical and moral issues that surround it.

"I am pleased to participate in these important conferences, which showcase the latest scientific developments in their respective regions and beyond. ISCRM and the World Stem Cell Summit have a strong connection, as the Institute was officially launched at our 2010 Summit in Detroit, said Bernard Siegel, GPI's Executive Director and founder of the annual World Stem Cell Summit.

BioFloridas 15th annual Conference is the premier event for Floridas bioscience community. This years meeting will bring together more than 500 professionals from across Florida, the Southeast and the nation to discuss major trends and issues, including topics related to product development, scientific research, business development, financing and public policy.

Siegels keynote address at BioFlorida is titled: The Mandate to Deliver Cures: Aligning Patient Advocacy, Industry and Science. Former Governor Jeb Bush will deliver the second keynote at BioFloridas annual Conference.

The 2012 World Stem Cell Summit is in West Palm Beach, Florida this December, so we have been working closely with the biotechnology community here. I am delighted to partner with BioFlorida as they advance Floridas bioscience industry," said Siegel, who also serves on the Executive Committee of the Alliance for Regenerative Medicine and Board of the Coalition for Advancement of Medical Research. He serves as spokesperson for the Stem Cell Action Coalition.

ABOUT GPI:The Genetics Policy Institute (GPI) supports stem cell research to develop therapeutics and cures. GPI pursues its mission by honoring leadership through the Stem Cell Action Awards, producing the World Stem Cell Summit, publishing theWorld Stem Cell Report, organizing educational initiatives and fostering strategic collaborations. For more information, visitwww.genpol.org.

ABOUT THE WORLD STEM CELL SUMMIT:The 2012 World Stem Cell Summit is presented by GPI and is co-organized by the Interdisciplinary Stem Cell Institute (ISCI) at the University of Miami Miller School of Medicine, Diabetes Research Institute, Beckman Research Institute at City of Hope, Karolinska Institute (home of the Nobel Prize in Physiology and Medicine), International Translational Regenerative Medicine Center (ITRC) and the Institute for Integrated Cell-Material Sciences (iCeMS) at Kyoto University. The Summit is the flagship meeting of the world stem cell community. The 2012 Summit will be held at the Palm Beach County Convention Center in West Palm Beach, Florida, December 3-5, 2012. For more information, visit http://www.worldstemcellsummit.com.

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Bernard Siegel to Deliver Keynote Addresses at Midwest Conference on Stem Cell Biology and Therapy and BioFlorida ...

CAMBRIDGE, Mass. & BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) and Millennium: The Takeda Oncology Company, a wholly owned subsidiary of Takeda Pharmaceutical Company Limited (TSE:4502), today announced the completion of patient enrollment in a phase III clinical trial of ADCETRIS (brentuximab vedotin) for post-transplant Hodgkin lymphoma (HL) patients. The phase III trial, also known as the AETHERA trial, is evaluating ADCETRIS versus placebo for the treatment of patients at high risk of residual Hodgkin lymphoma following autologous stem cell transplant (ASCT). ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30, a defining marker of classical HL.

We are pleased to complete the enrollment of this important phase III trial, evaluating the use of ADCETRIS for Hodgkin lymphoma patients who are at high risk of residual disease following an ASCT, said Thomas C. Reynolds, M.D., Ph.D., Chief Medical Officer of Seattle Genetics. The AETHERA trial is designed to provide the medical community with valuable insight into the potential for ADCETRIS to consolidate responses in Hodgkin lymphoma patients following a transplant, and will be the first data on the use of ADCETRIS in a maintenance-type setting. We anticipate data from this trial will be available in late 2013 or early 2014.

Completing enrollment of the AETHERA trial in the post-transplant Hodgkin lymphoma patient population at high risk for residual disease is a significant milestone for our ADCETRIS clinical development program, said Karen Ferrante, M.D., Chief Medical Officer, Millennium. We look forward to continuing to work with our partner Seattle Genetics to determine the potential benefit of this targeted treatment in other CD30-expressing tumors.

The AETHERA trial is a randomized, double-blind, placebo-controlled phase III study, comparing progression-free survival in 329 post-ASCT patients receiving ADCETRIS to those receiving placebo. Patients must be at high risk for residual HL, defined as those with a history of refractory HL, those who relapse or progress within one year from receiving front-line chemotherapy and/or those who have disease outside of the lymph nodes at the time of pre-ASCT relapse. Secondary endpoints of the trial include overall survival, safety and tolerability. Patients receive ADCETRIS every three weeks for up to approximately one year. This international multi-center trial is being conducted in the United States, Europe and Russia.

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

ADCETRIS received accelerated approval from the U.S. Food and Drug Administration (FDA) for two indications: (1) the treatment of patients with Hodgkin lymphoma after failure of autologous stem cell transplant (ASCT) or after failure of at least two prior multi-agent chemotherapy regimens in patients who are not ASCT candidates, and (2) the treatment of patients with systemic anaplastic large cell lymphoma (sALCL) after failure of at least one prior multi-agent chemotherapy regimen. The indications for ADCETRIS are based on response rate. There are no data available demonstrating improvement in patient-reported outcomes or survival with ADCETRIS.

ADCETRIS is not approved for use outside the United States. The marketing authorization application for ADCETRIS in relapsed or refractory Hodgkin lymphoma and sALCL, filed by Takeda Global Research & Development Centre (Europe), was accepted for review by the European Medicines Agency (EMA) in June 2011. In July 2012, the Committee for Medicinal Products for Human Use (CHMP) of the EMA issued a positive opinion for the conditional approval of ADCETRIS, supporting an approval decision in the European Union.

Seattle Genetics and Millennium are jointly developing ADCETRIS. Under the terms of the collaboration agreement, Seattle Genetics has U.S. and Canadian commercialization rights and the Takeda Group has rights to commercialize ADCETRIS in the rest of the world. Seattle Genetics and the Takeda Group are funding joint development costs for ADCETRIS on a 50:50 basis, except in Japan where the Takeda Group will be solely responsible for development costs.

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Seattle Genetics and Millennium Complete Enrollment in Phase III AETHERA Trial of ADCETRIS® for Post-Transplant ...

While $34.7 million is a touch more than $34.5 million, that's not exactly huge quarter-over-quarter growth from Seattle Genetics' (Nasdaq: SGEN) Adcetris.

Still, investors seem to be shaking off the lackluster growth, and for good reason: Sales of Adcetris -- a drug for treating relapsed Hodgkin lymphoma and anaplastic large-cell lymphoma -- are a very small part of the long-term success of Seattle Genetics.

The light growth seems to be the result of declining business at academic centers, where sales dropped off as patients stopped treatment because they finished their therapy cycles or had a strong enough response to undergo a stem-cell transplant.

The number of community doctors using the drug increased in the second quarter, which is good news for the sales trajectory, as most of the lymphoma patients for whom Adcetris is appropriate are seen in the community setting.

Don't expect much growth in the second half, though; management is guiding for sales of $140 million to $150 million in 2012 -- either flat or a 17% increase from the first half of the year to the second half.

Seattle Genetics lost $12.3 million on a GAAP basis in the quarter but didn't actually burn any cash. In fact, the cash, cash equivalents, and investments increased by $21.5 million during the quarter. I don't know how long investors can expect that to continue, as the biotech is still using product manufactured prior to approval.

Of course, aside from Adcetris, Seattle Genetics can bring in cash by licensing out its antibody-drug conjugate technology, which has attracted some big names, including Roche, GlaxoSmithKline (NYSE: GSK) , Pfizer (NYSE: PFE) , and Abbott Labs (NYSE: ABT) .

Internally, Seattle Genetics' future depends on expanding the use of Adcetris into frontline setting for the two lymphomas it's currently approved to treat, as well as other types of cancer. The potential there towers over the $150 million Seattle Genetics will bring in this year.

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A Growth-Free Quarter -- and That's OK

BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) today announced that its collaborator, Millennium: The Takeda Oncology Company, a wholly owned subsidiary of Takeda Pharmaceutical Company Limited, has received a positive recommendation from the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) for the conditional marketing authorization of ADCETRIS (brentuximab vedotin) for two indications: (1) the treatment of adult patients with relapsed or refractory CD30-positive Hodgkin lymphoma (HL) following autologous stem cell transplant (ASCT) or following at least two prior therapies when ASCT or multi-agent chemotherapy is not a treatment option, and (2) for the treatment of adult patients with relapsed or refractory systemic anaplastic large cell lymphoma (sALCL). ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30.

The positive opinion from CHMP and broad label recommendation is a key step in the European regulatory process for ADCETRIS and brings us closer to our goal of making this important new therapy globally available to patients with relapsed Hodgkin lymphoma or systemic ALCL, said Clay B. Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. If approved in the European Union, ADCETRIS will represent the first new therapeutic advance for relapsed Hodgkin lymphoma patients in several decades and further validates the potential of ADCs in the treatment of cancer.

The European Commission, which has the authority to approve medicines for use in the European Union, generally follows the recommendations of the CHMP and typically renders a final decision within three months of the CHMP opinion. If the CHMP recommendation is formally adopted by the European Commission, ADCETRIS would be approved for marketing in all 27 member states of the European Union.

European Commission approval will trigger two milestone payments, one for each indication, totaling $25 million to Seattle Genetics under the collaboration agreement between Seattle Genetics and Millennium: The Takeda Oncology Company. Seattle Genetics is also entitled to tiered double-digit royalties with percentages starting in the mid-teens and escalating to the mid-twenties based on net sales of ADCETRIS within Millenniums territories, subject to offsets for royalties paid by Millennium to third parties.

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

ADCETRIS received accelerated approval from the U.S. Food and Drug Administration (FDA) in August 2011 for relapsed HL and sALCL.

Seattle Genetics and Millennium are jointly developing ADCETRIS. Under the terms of the collaboration agreement, Seattle Genetics has U.S. and Canadian commercialization rights and the Takeda Group has rights to commercialize ADCETRIS in the rest of the world. Seattle Genetics and the Takeda Group are funding joint development costs for ADCETRIS on a 50:50 basis, except in Japan where the Takeda Group will be solely responsible for development costs.

About Seattle Genetics

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Seattle Genetics Announces ADCETRIS® Receives Positive CHMP Opinion for Conditional Approval in European Union