Twenty-five per cent of Australian adults are estimated to be clinically obese. The common view is that obesity is a self-inflicted condition. But one Melbourne clinic is challenging that perception.

Austin Health Obesity Physician, Professor Joe Proietto says he treats obesity as a chronic genetic disease.

"The view that obesity is genetic is controversial, however the evidence is very strong that there is a genetic predisposition to obesity," said Professor Proietto.

In a new SBS documentary Obesity Myth, doctors are trying to treat patients through a combination of diet, medication and surgery, tailored specifically for their genetic make-up.

Professor Proietto believes the environment has far less bearing on weight than genetics.

But Sydney University Obesity Research Director, Dr Nick Fuller says blaming genetics is only going to make the obesity crisis worse.

"We are finding more and more genes that contribute to obesity but genetics are not the reason for the increase in prevalence of obesity," said Dr Fuller.

Dr Fuller believes dieting is not the most effective solution.He believes weight loss should happen slowly, to trick the body into believing it is at a new set weight point.

"They need to lose a small amount of weight before the usual response to weight loss kicks in and maintain that weight so they can reprogram their set weight before going on to lose weight," said Dr Fuller.

Helene Jagdon has been trying to lose weight for 30 years. She has tried every fad diet and training regime in the book.

Only in the last few years under Dr Fuller's strategy has she been able to lose 14 kilograms and keep it off.

"He didn't make us feel like we were on a diet, he was just guiding us to what foods we can eat and not really saying what foods we can't eat.

"He was just saying if you feel like having a laksa, have a laksa, but maybe limit it to one takeaway treat in a week," said Ms Jagdon.

Now sitting at a comfortable 68 kilograms, Helene has maintained her passion for cooking and is inspiring people half her age to lose weight without dramatically changing their lives.

Preview: The Obesity Myth

The three-part documentary series The Obesity Myth starts September 4 on SBS at 7.30pm.

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Could genetics be the reason behind obesity? - SBS

Rush Neurologist Gian Pal, MD, MS, the primary investigator for the National Institute of Health-funded clinical study Parkinson disease and DBS: cognitive effects in GBA mutation carriers. Credit: Rush Photo Group

In the first ever clinical investigation involving genetic screening for Parkinson's disease, researchers are testing whether the presence of a specific genetic mutation identifies which patients are the best candidates for deep brain stimulation surgery, and whether neurologists should perform that procedure differently based on that genetic information.

"We are at a very promising time in Parkinson's disease (PD) research. Finding the connections between the vast amounts of genetic data and cognitive data we are gathering will allow us to tailor future therapies based on genetic biomarkers," said Rush neurologist Gian Pal, MD, MS, the primary investigator for the National Institute of Health-funded clinical study "Parkinson disease and DBS: cognitive effects in GBA mutation carriers"

Deep brain stimulation (DBS) is a surgical procedure in which a battery-operated medical device implanted in the brain delivers electrical stimulation to specific areas in the brain that control movement, thus altering the abnormal signals that cause many PD motor symptoms.

DBS is typically used for individuals whose symptoms cannot be adequately controlled with medication and has proven to dramatically improve motor function and potentially reduce medication burden for many PD patients.

Research suggests that patients who carry a mutation in the glucocerebrosidase (GBA) gene may respond differently to DBS than those who do not carry the mutation. These GBA mutation carriers compose 10-17 percent of subjects undergoing DBS, and typically have higher deposits of alpha-synuclein protein in the brain. Abnormal accumulation of alpha-synuclein is thought to be a key reason for the development and progress ion of PD. These higher levels of alpha-synuclein in patients with the GBA mutation carriers may translate to even more problems with thinking, movement, behavior, and mood than expected in typical PD. Dr. Pal and colleagues are hoping to understand how DBS affects motor function and cognition in these GBA mutation carriers over time.

"If we can determine how GBA mutation carriers respond to DBS, we can better counsel patients on expectations from the surgery, and potentially target a different region of the brain to maximize the benefit and minimize side effects from the surgery. This would be the first time that genetics would inform a clinical decision in the field of PD"

"Deep brain stimulation is a tremendous option for many Parkinson's disease patients, but not all," said Pal, who is developing a programmatic line of research involving genetics and surgical treatments for PD at the Rush Parkinson's Disease and Movement Disorders Program.

The Rush Parkinson's Disease and Movement Disorders Program is one of the largest and oldest such centers in the country, treating more than 2,000 patients annually. Rush has been a longstanding Parkinson's Disease Foundation Center of Excellence, based on decades of clinical and research excellence, and is now also recognized as a National Parkinson Foundation Center of Excellence as well.

Explore further: Drug discovery: Alzheimer's and Parkinson's spurred by same enzyme

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Rush testing if genetic clues identify best candidates for Parkinson's surgery - Medical Xpress

Brian J. O'Roak, Ph.D., assistant professor of molecular and medical genetics, OHSU, January 4, 2017. Credit: OHSU/John Valls

Autism spectrum disorder affects approximately one out of every 68 children in the United States. Despite expansive study, the origin and risk factors of the complex condition are not fully understood.

To better understand the root causes, an international team led by researchers at OHSU in Portland, Oregon has applied a new systematic analysis to a cohort of 2,300 families who have a single child affected with autism. The study focused on identifying and characterizing low-lying genetic mutations that may have been missed in previous research, given these mutations are only present in a fraction of the bulk DNA of an individual.

Known as postzygotic mosaic mutations, or PMMs, these genetic changes occur after the conception of the human zygote during the development cycle of a fetus. An individual will contain a mosaicor assortmentof mutated and non-mutated cells with the level of mosaicism depending on the time and location of the mutation's occurrence. This emerging class of genetic risk factors has recently been implicated in various neurologic conditions, however, their role in more complex disorders, such as autism, has been unclear.

Autism risk due to unexpected mosaic mutations

By comparing genetic sequencing data of these familiespart of the Simons Simplex Collection, a permanent repository of precisely characterized genetic samplesthe research team determined that approximately 11 percent of previously reported new mutations affecting a single DNA base, which were thought to have be present at the time of human conception, actually show evidence of the mutation occurring during the development process.

"This initial finding told us that, generally, these mosaic mutations are much more common than previously believed. We thought this might be the tip of a genetic iceberg waiting to be explored," said the study's principal investigator Brian O'Roak, Ph.D., an assistant professor of molecular and medical genetics in the OHSU School of Medicine.

To investigate this possibility, a custom approachleveraging next generation sequencing and molecular barcodes - was developed to both identify these low-level mutations, and also validate that they are, in fact, real and not technological artifacts. With this more sensitive method, the rate of potentially PMMs increased to 22 percent of the new mutations present in children.

The researchers then compared the rates of PMMs that result in different predicted effects on the genome in affected children and their unaffected siblings. This lead to an unexpected finding that so-called "silent" mosaic mutations were enriched in the affected children, contributing risk to approximately 2 percent of the individuals with autism in this cohort. These types of mutations are generally believed to be neutral, as they don't alter the genetic coding of proteins. However, the team found evidence that these mutations might actually be altering how genetic messages are stitched together.

The study also found preliminary evidence that mosaic mutations that alter the protein code of genes essential for development, or genes that resist mutations, are also enriched in individuals with autism. This contributes risk to an additional 1 to 2 percent of individuals with autism. Many of the PMMs occurred in some of the most highly validated autism risk genes identified to date, further suggesting that these mutations are contributing to autism genetic risk. Due to this, the research team believes that overall, mosaic mutations may contribute to autism risk in 3 to 4 percent of this cohort.

Understanding the timeline and location of mosaic mutations

Determining exactly when and where these mutations are occurring during development is challenging. The PMMs identified were present in 10 to 75 percent of the cells examined from the children's blood, suggesting that they likely occurred early in development. However, the exact timeline was not known.

By leveraging the unique family design of the Simons Simplex Collection cohort, O'Roak's team analyzed the parents' genomes and discovered that 6.8 percent of the supposedly "new" mutations present in children at conception could actually be traced back to a PMM that occurred early in the development of their parent. These mutations were generally present in 20 to 75 percent of the parents' blood cells, providing indirect evidence that many of the PMMs occurring in children did in fact happen very early during development and that they likely contribute mosaicism across the body, including in the brain.

"In addition to a need for broader research focused on the role that mosaicism plays in autism and related disorders, our data argue that physicians should be requiring more sensitive testing of both children and parents, when a new disorder-related genetic mutation is identified," O'Roak said. "These mutation can go from being in a few percent of the cells of a parent to 100 percent of the cells of a child. If present, at even low levels in the parents, the risk of additional children receiving this mutation is dramatically increased."

"Exonic mosaic mutations contribute risk for Autism Spectrum Disorder" published today in The American Journal of Human Genetics.

Explore further: Late-breaking mutations may play an important role in autism

More information: Deidre R. Krupp et al. Exonic Mosaic Mutations Contribute Risk for Autism Spectrum Disorder, The American Journal of Human Genetics (2017). DOI: 10.1016/j.ajhg.2017.07.016

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Study identifies new genetic risk factor for developing autism spectrum disorder - Medical Xpress

Nanoparticles (orange) deliver temporary gene therapy to immune cells (blue) to give them disease-fighting tools. (Fred Hutch Illustration / Kimberly Carney)

CAR T immunotherapies are all the rage in the medical community, reprogramming a patients immune system to fight cancer. For some patients, theyve produced near-miraculous recoveries, and they could be a huge breakthrough in cancer treatment.

The business community is taking note as well: Kite Pharma, a biotech company developing these therapies, announced a deal to be acquired for $11.9 billion on Monday, sending stock prices of Seattle immunotherapy developer Juno Therapeuticsskyrocketing.

But there are still giant pitfalls to using the therapies on a large scale because they are incredibly complex and expensive to produce. Researchers from Seattles Fred Hutchinson Cancer Research Center are taking the problem head-on with new hit-and-run gene editing technology.

In a study published Wednesday in the journal Nature Communications, researchers led by Dr.Matthias Stephan reported they have developed a nanoparticle delivery system that can temporarily alter cells so they are able to fight cancer and other diseases.

The best part? The treatment is a powder that just needs to be mixed with water to activate and even better, it could be an essential breakthrough in making cutting-edge medical technology affordable for patients.

Stephan told GeekWire in a previous piece on the technology that his goal is to make immunotherapy so easy to access that it replaces chemotherapy as the front-line treatment for cancer.

What I envision is like the Walgreens flu shot scenario, or you go to your doctor and you get hepatitis B shot, he said at the time. You go there every Friday, and thats it.

We realized in order to outcompete chemotherapy, we have to design something that is at least as affordable and can be manufactured at large scale by one biotech company and shipped out to local infusion centers, Stephan said. At the moment, CAR T cell therapies must be made individually for each patient in specialized labs.

Heres how the new tech works: The nanoparticles designed by Stephan and his team act like shipping containers for bundles of mRNA, the molecules that tell cells how to build disease-fighting proteins. The nanoparticles also have molecules attached to the outside to help them find the right kind of cells, like a shipping label on a package.

When the mRNA is delivered to the cell, it prompts the cell to grow disease-fighting features, like the chimeric antigen receptor in CAR T cells that help them identify and kill cancer.Researchers said the technology could potentially be used to develop treatments for HIV, diabetes and other immune-related diseases.

In the short run, the tech could help researchers discover new treatments and therapies in the lab. It could one day be used in hospitals and clinics around the world, but will first need to undergo extensive clinical trials to ensure the tech is effective and safe to use in humans.

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New 'hit-and-run' gene editing tool temporarily rewrites genetics to treat cancer and HIV - GeekWire

Clay Siegall

Seven years after Copenhagen-based Genmab inked a collaboration deal with Seattle Genetics, the US biotech has decided to opt-in on a development partnership.

The pact struck in 2010 gave Genmab rights to Seattle Genetics antibody-drug conjugate tech so it could work on a new approach for its HuMax-TF antibody targeting the tissue factor antigen. A year later they struck a deal giving Seattle Genetics an opt-in on tisotumab vedotin, now in several Phase I/II studies for solid tumors, including recurrent cervical cancer.

Whatever data that early program has produced was good enough to persuade Seattle Genetics to agree to share the development costs and any profits 50/50.

Seattle Genetics has run into a series of late-stage mishaps over the past year. The biotech was forced to scrap a Phase III study of vadastuximab and halt a slate of other trials as researchers puzzled out what caused an imbalance of deaths between the drug and control arms. Just a few weeks before the June imbroglio, Seattle Genetics was also forced to throw the towel in on a $2 billion deal to collaborate with Immunomedics, further limiting its late-stage effort. Seattle Genetics mainstay franchise drug did score a win on frontline Hodgkin lymphoma at the end of H1, but the gain was so marginal that some analysts fretted it looked like the kind of small advantage that may not be worth much commercially.

Our ADC partnership with Genmab has generated promising Phase I/II data for tisotumab vedotin in patients with recurrent cervical cancer. As Seattle Genetics opts into co-development of this clinical program, we add another potential product to our strong pipeline, said Seattle Genetics CEO Clay Siegall.

Full-text daily reports for those who discover, develop, and market drugs. Join 17,000+ biopharma pros who read Endpoints News by email every day.

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Seven years in the making, Seattle Genetics picks up early option on Genmab's ADC effort - Endpoints News

August 30, 2017

Scientists have discovered a network of genes and genetic regulatory elements in the lining of the intestines that has stayed remarkably the same from fishes to humans. Many of these genes are linked to human illnesses, such as inflammatory bowel diseases, diabetes, and obesity.

The findings, which appear in the journal PLOS Biology, establish the fish as an experimental platform for studying how this ancient genetic information -- distilled over 420 million years of evolution -- controls the development and dysfunction of the intestine.

"Our research has uncovered aspects of intestinal biology that have been well-conserved during vertebrate evolution, suggesting they are of central importance to intestinal health," said John F. Rawls, Ph.D., senior author of the study and associate professor of molecular genetics and microbiology at Duke University School of Medicine. "By doing so, we have built a foundation for mechanistic studies of intestinal biology in non-human model systems like fish and mice that would be impossible to perform in humans alone."

The intestine serves a variety of important functions that are common to all vertebrates. It takes up nutrients, stimulates the immune system, processes toxins and drugs, and provides a critical barrier to microorganisms. Defects in the intestinal epithelial cells lining the intestine have been implicated in a growing number of ailments, including inflammatory bowel diseases, colorectal cancer, food allergy, diabetes, obesity, malnutrition and infectious diarrheas.

For decades, scientists have relied on animal models to gather information on intestinal epithelial cells that could help combat human diseases. But it wasn't clear just how alike these cells were across multiple species.

In this study, Rawls and his team used a comparative biology approach to tackle that question. Research associate Colin R. Lickwar, Ph.D., and colleagues generated genome-wide data from intestinal epithelial cells in four evolutionarily distant species: zebrafish, stickleback fish, mouse and human. Lickwar then created maps for each of the species depicting not only the activity level of all of the genes, but also the location of specific genetic sequences or regulatory elements that flipped those genes on and off.

Lickwar was surprised to find a striking amount of similarity between the different vertebrate species. He identified a common set of genes -- an intestinal epithelial cell signature -- some of which had shared patterns of activity in specific regions along the length of the intestine. What's more, many of the genes included in this conserved signature had previously been implicated in a variety of human diseases. Lickwar and Rawls wondered if this conserved genetic signature was controlled by regulatory elements that might also be shared between species.

To test if this was the case, they took various regulatory elements from fish, mice, and humans and stuck them into the zebrafish. Because zebrafish are transparent organisms, the researchers could look under the microscope for patterns of color to tell whether a green fluorescent protein or red fluorescent protein, which they had inserted along with the regulatory element, had been flipped on in the intestine. They found that the regulatory switches transplanted from the other species worked in zebrafish, indicating a remarkable level of conservation.

"Our findings suggest that intestinal epithelial cells use an ancient core program to do their job in the body of most vertebrates," said Lickwar, who is lead author of the study. "Now that we have identified this core program, we can more easily translate results back and forth between humans and zebrafish."

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Genetics of digestion stayed remarkably the same from fishes to humans, research shows - News-Medical.net

August 29, 2017

Studies have shown that an early age of drinking initiation (ADI) increases the chance of developing an alcohol use disorder (AUD). There is limited evidence that ADI differs across ethnic groups. This study examined whether the pathway from ADI to AUD symptoms by early adulthood is influenced by two factors: ethnicity and having the alcohol metabolizing gene variant allele, ALDH2*2. This allele produces an inactive enzyme that leads to higher levels of acetaldehyde during alcohol metabolism, which are associated with unpleasant effects after drinking alcohol and a decreased risk for an AUD.

Researchers examined 604 college students recruited from the University of California, San Diego: 214 of Korean ancestry (107 men, 107 women), 200 of European ancestry (106 men, 94 women), and 190 of Chinese ancestry (99 women, 91 men), each with both biological parents having the same heritage. Participants were genotyped for the ALDH2*2 variant allele and completed a self-report assessment.

The effect of ADI as a risk factor for developing AUD symptoms varied with both ethnicity and ALDH2*2 status. ADI was not associated with AUD symptoms in Korean-Americans with an ALDH2*2 allele or in Chinese-Americans regardless of ALDH2*2 status. This indicates that being Korean (and having the protective ALDH2*2 allele) or Chinese buffered the risk for developing AUD symptoms associated with an early ADI. Although an earlier ADI places some individuals at risk to develop AUD symptoms, the path from ADI to AUD symptoms is complex and can be modified by other factors.

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Pathway from ADI to AUD symptoms influenced by ethnicity and genetics - News-Medical.net

Liverpool Womens Hospital is to expand its ability to genetically test newborn babies 12-fold.

The NHS Foundation Trust will be able to screen all infants for inherited conditions or illnesses and plan for early treatment as part of a major new IT project.

IT firm Novosco will introduce the computing system which also contribute to a major population health programme in Liverpool - analysing genetic information by location, identifying and enabling work to prevent localised health issues.

The role of genetics in healthcare is one of the most rapidly expanding areas of development for Liverpool Womens.

It provides a regional clinical genetics service covering a population of around 2.8 million people from across Merseyside, Cheshire and the Isle of Man.

Chief executive Kathryn Thomson posted on the trusts website: To discover that you or any child you have or plan to have may be at risk of a genetic disorder which could cause disability or a rare condition is traumatic.

People are sometimes shocked and anxious and wonder what the future might hold.

They need as much information and support as possible to help them cope.

That is why the often unsung work of our clinical genetics team is so important, providing diagnosis and supporting families when they need it most.

Novosco managing director Patrick McAliskey said: We are delighted to secure this contract which will enable the trust to take genetic testing to the next level and play an important role in the identification and prevention of conditions and illnesses in new-born babies and the wider population.

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Liverpool Women's Hospital to increase genetic testing of babies - Liverpool Echo

Thirty million American women and men will struggle with eating disorders in their lifetime, and these life-threatening conditions have a higher mortality rate than any other psychiatric illness. For example, someone struggling with anorexia for five years has a 5 per cent, or one in20 chance, of dying.

While more and more people have come to understand that eating disorders are diseases of the brain, there's still awidespreadbeliefthat people with these devastating conditionsare vain, attention-seeking, or lacking in will power. But apaperjust published in Plos One makes it clear that this isn't true. The studyevaluated the genomes of95 individuals with diagnosed eating disorders andidentified 430 genes, clustered into two large groups, that are more likely to be damaged than in people without those disorders.

This adds to a growing body of research shows that eating disorders are powerful, biologically-driven illnesses. The new studysupports previous findings that the risk of developing an eating disorder is 50-80 per cent geneticthatpatientshave inherited damaged copies of genes that increase their risk of developing disordered eating. And understanding which genes are damaged can practitioners create better treatment treatment protocols.

In the PlosOne study, patients with eating disorders were clustered into two main groups. In the first, the damaged genes fell into a class of gut neuropeptides affecting that control appetite,food intakeand digestion/absorption of nutrients, making patients more likely to binge. Roughly half of this group struggled with restricted eating patterns, and the other half were binge eaters. The research confirms reports by our patients who believe their behavior is biologically driven.

The second group of patients had a cluster of genes involved in the function of the immune system and inflammation, which has long been known to suppress appetite. Patients with damaging mutations in the inflammation cluster are much more likely to have restricted-eating patterns. More research is needed to test a possible connection between eating disorders and auto-immune conditions like irritable bowel disease.

The new findings are consistent with known environmental eating disorder triggers. Faddieting, excessive exercise, or medical illness, are examples of negative energy states that have long been seen as possible eating disorder triggers. Negative energy states can set up behavioral changes like food binges or restricted food intake, triggering preexisting genetic drivers for eating disorders. Based on these findings, we argue that eating disorders are biologically driven illnesses that alter mood and behavior, similar to how the lack of thyroid hormone can result in depression in a patient with hypothyroidism.

Failure to understand the underlying causes of eating disorders creates stigma, making it less likely for those who struggle to get treatment. People with any medical condition deserve support and access to the best treatment. Someone with cancer wouldnt be denied treatment for their illness. Likewise, patients with eating disorders shouldnt feel guilty about their illness and they should have access to safe, effective treatment.

Biology isnt destiny. Eating disorders treatment is most effective if its accompanied by a general understanding that eating illnesses are biologically driven.

Lasting recovery from an eating disorder is possibleand those who struggle deserve understanding and support without guilt or judgment.

Read this article:
The Genetics of Eating Disorders - Scientific American (blog)

COPENHAGEN, Denmark & BOTHELL, Wash.--(BUSINESS WIRE)--Genmab A/S (Nasdaq Copenhagen: GEN) and Seattle Genetics, Inc. (Nasdaq: SGEN) announced today that Seattle Genetics, Inc. has exercised its option to co-develop tisotumab vedotin. The companies originally entered into a commercial license and collaboration agreement in October 2011 under which Seattle Genetics had the right to exercise a co-development option for tisotumab vedotin at the end of Phase I clinical development. Tisotumab vedotin, an antibody-drug conjugate (ADC) targeting tissue factor, is currently being evaluated in Phase I/II clinical studies in solid tumors. Going forward, Genmab and Seattle Genetics will co-develop and share all future costs and profits for tisotumab vedotin on a 50:50 basis.

The combination of Genmabs differentiated HuMax-TF antibody and Seattle Genetics clinically-validated antibody-drug conjugate (ADC) technology has resulted in encouraging preliminary data for tisotumab vedotin in selected solid tumors. We very much look forward to working with Seattle Genetics to further develop this exciting first-in-class ADC product, said Jan van de Winkel, Ph.D., Chief Executive Officer of Genmab.

Our ADC partnership with Genmab has generated promising Phase I/II data for tisotumab vedotin in patients with recurrent cervical cancer. As Seattle Genetics opts into co-development of this clinical program, we add another potential product to our strong pipeline, said Clay Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. Together with Genmab, we look forward to advancing tisotumab vedotin for the treatment of solid tumors.

Preliminary data from the ongoing Phase I/II study of tisotumab vedotin in solid tumors (GEN701) were announced in June 2017, demonstrating antitumor activity and manageable safety in recurrent cervical cancer patients. This announcement can be found here. Updated preliminary data from the Phase I/II study will be presented in an oral presentation at the European Society for Medical Oncology (ESMO) 2017 Congress in Madrid (Spain), September 8-12, 2017.

Todays news does not impact the 2017 financial guidance issued by Genmab on May 10, 2017.

About the collaboration

In October 2011, Genmab and Seattle Genetics, Inc. entered into a commercial license and collaboration agreement for ADCs. Under the agreement, Genmab was granted rights to utilize Seattle Genetics ADC technology with its HuMax-TF antibody. Seattle Genetics was granted rights to exercise a co-development and co-commercialization option at the end of Phase I clinical development for tisotumab vedotin. With todays news Seattle Genetics exercises its option to co-develop tisotumab vedotin and the companies will share all future costs and profits for the product on a 50:50 basis. Seattle Genetics will be responsible for commercialization activities in the US, Canada, and Mexico, while Genmab will be responsible for commercialization activities in all other territories. Each party has the option to co-promote by employing up to 40 percent of the sales effort in the other partys territories.

About tisotumab vedotin

Tisotumab vedotin is an antibody-drug conjugate (ADC) composed of a human antibody that binds to tissue factor (TF) and Seattle Genetics ADC technology that utilizes a cleavable linker and the cytotoxic drug monomethyl auristatin E (MMAE). TF is a protein involved in tumor signaling and angiogenesis. Based on its high expression on many solid tumors and its rapid internalization, TF was selected as a target for an ADC approach. Tisotumab vedotin is in Phase I/II clinical studies for solid tumors.

About Genmab

Genmab is a publicly traded, international biotechnology company specializing in the creation and development of differentiated antibody therapeutics for the treatment of cancer. Founded in 1999, the company has two approved antibodies, DARZALEX (daratumumab) for the treatment of certain multiple myeloma indications, and Arzerra (ofatumumab) for the treatment of certain chronic lymphocytic leukemia indications. Daratumumab is in clinical development for additional multiple myeloma indications, other blood cancers, and solid tumors. A subcutaneous formulation of ofatumumab is in development for relapsing multiple sclerosis. Genmab also has a broad clinical and pre-clinical product pipeline. Genmab's technology base consists of validated and proprietary next generation antibody technologies - the DuoBody platform for generation of bispecific antibodies, and the HexaBody platform which creates effector function enhanced antibodies. The company intends to leverage these technologies to create opportunities for full or co-ownership of future products. Genmab has alliances with top tier pharmaceutical and biotechnology companies. For more information visit http://www.genmab.com.

About Seattle Genetics

Seattle Genetics is an innovative biotechnology company that develops and commercializes novel antibody-based therapies for the treatment of cancer. The companys industry-leading antibody-drug conjugate (ADC) technology harnesses the targeting ability of antibodies to deliver cell-killing agents directly to cancer cells. ADCETRIS (brentuximab vedotin), the companys lead product, in collaboration with Takeda Pharmaceutical Company Limited, is the first in a new class of ADCs commercially available globally in 67 countries for relapsed classical Hodgkin lymphoma and relapsed systemic anaplastic large cell lymphoma (sALCL). Seattle Genetics is also advancing enfortumab vedotin, an ADC for metastatic urothelial cancer, in a planned pivotal trial in collaboration with Astellas. Headquartered in Bothell, Washington, Seattle Genetics has a strong pipeline of innovative therapies for blood-related cancers and solid tumors designed to address significant unmet medical needs and improve treatment outcomes for patients. The company has collaborations for its proprietary ADC technology with a number of companies including AbbVie, Astellas, Bayer, Celldex, Genentech, GlaxoSmithKline and Pfizer. More information can be found at http://www.seattlegenetics.com

Forward Looking Statement for Genmab

This Company Announcement contains forward looking statements. The words believe, expect, anticipate, intend and plan and similar expressions identify forward looking statements. Actual results or performance may differ materially from any future results or performance expressed or implied by such statements. The important factors that could cause our actual results or performance to differ materially include, among others, risks associated with pre-clinical and clinical development of products, uncertainties related to the outcome and conduct of clinical trials including unforeseen safety issues, uncertainties related to product manufacturing, the lack of market acceptance of our products, our inability to manage growth, the competitive environment in relation to our business area and markets, our inability to attract and retain suitably qualified personnel, the unenforceability or lack of protection of our patents and proprietary rights, our relationships with affiliated entities, changes and developments in technology which may render our products obsolete, and other factors. For a further discussion of these risks, please refer to the risk management sections in Genmabs most recent financial reports, which are available on http://www.genmab.com. Genmab does not undertake any obligation to update or revise forward looking statements in this Company Announcement nor to confirm such statements in relation to actual results, unless required by law.

Genmab A/S and its subsidiaries own the following trademarks: Genmab; the Y-shaped Genmab logo; Genmab in combination with the Y-shaped Genmab logo; the DuoBody logo; the HexaBody logo; HuMax; HuMax-CD20; DuoBody; HexaBody and UniBody. Arzerra is a trademark of Novartis AG or its affiliates. DARZALEX is a trademark of Janssen Biotech, Inc.

Forward Looking Statement for Seattle Genetics

Certain of the statements made in this press release are forward looking, such as those, among others, relating to the therapeutic potential of tisotumab vedotin and its possible benefits and uses, and planned development activities including future clinical trials. Actual results or developments may differ materially from those projected or implied in these forward-looking statements. Factors that may cause such a difference include the inability to show sufficient activity and the risk of adverse events as tisotumab vedotin advances in clinical trials and regulatory actions. More information about the risks and uncertainties faced by Seattle Genetics is contained under the caption Risk Factors included in the companys Quarterly Report on Form 10-Q for the quarter ended June 30, 2017 filed with the Securities and Exchange Commission.Seattle Genetics disclaims any intention or obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise.

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Genmab and Seattle Genetics to Co-develop Tisotumab Vedotin for Solid Tumors - Business Wire (press release)