Category Archives: Genetics

Caring Connections Hosts Talk About Genetics and Cancer and When to Consider Testing – Bangor Daily News

Thursday, May 25, 2017 6 p.m. to 7:30 p.m.

Location: Bangor YMCA, 17 Second Street, Bangor, Maine

For more information: 207-941-2808; bangory.org

On Thursday May 25th, at 6 pm, Caring Connections, a cooperative program of the Bangor YMCA and Eastern Maine Medical Center, will host a talk on genetic testing with Margaret Rieley, MD, ABMG. Dr. Rieley is a physician specializing in the role inherited genetic changes have in our health. She has been working with EMMC Cancer Care since 2014.

About 5 to 10 percent of cancers have an association with an inherited risk. At the present time testing is most commonly available for risks associated with breast, colon, melanoma, ovarian, pancreatic, prostate and uterine cancers. It is now possible to evaluate a large number of genes simultaneously through a blood sample.

When a change associated with an increased risk is identified in someone who has been diagnosed with cancer, it can help them make decisions about their care. Family members can be tested and if they carry the same gene change, screening plans can identify potential cancers at the earliest possible stage.

This presentation is open to anyone interested in learning more about this topic. For more information or to register, call Caring Connections at 941-2808 x 338.

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Caring Connections Hosts Talk About Genetics and Cancer and When to Consider Testing - Bangor Daily News

NIMH awards CMU team $7 mil for autism genetics research – CMU The Tartan Online

A team of researchers from various institutions, including some from Carnegie Mellon, working on the Autism Sequencing Consortium (ASC) project has been awarded funding from the National Institute of Mental Health (NIMH) to continue their work through 2022. The grant totals seven million dollars and will allow ASC to expand their work even further in its search for genetic markers of autism. Autism is a spectrum of mental disorders ranging from mild forms that have little to no impact on peoples lives to severe forms that prevent patients from communicating properly, getting regular jobs, or going to regular schools.

ASC was established in 2010 in order to collect, share, and analyze genetic markers from autistic patients, with the ultimate goal of finding genetic signatures correlated with autism.

In our latest project we analyze the entire genomes of 500 autism families. Thats a tremendous amount of data 3 billion base pairs per genome, says Kathryn Roeder, a professor of statistics and computational biology at Carnegie Mellon and a principal investigator of the ASC project, in a university press release.

The grant from NIMH will allow ASC to expand the sample a hundred times larger, to over 50,000 families. So far, around 29,000 individual genomes have been sequenced as part of the project, which is the largest autism sequencing study to date.

According to Bernie Devlin, another principal investigator on the project and a professor of psychiatry and genetics at the University of Pittsburghs School of Medicine, increasing the sample size is necessary to make important discoveries about autism in the long term. Another professor on the team of collaborators, Joseph D. Buxbaum, who is the G. Harold and Leila Y. Mathers Research Professor of Psychiatry, Neuroscience and Genetics and Genomic Sciences at Mount Sinai, summed up the importance of being able to increase the sample size: Historically, the number of risk genes found has steadily increased with the number of patients studied, so its important that we continue to add patients to the data set. He described the team as being thrilled to receive this grant, which he said would accelerate crucial research work.

The research work by the ASC has already produced tangible results on the path to ASCs ultimate goal of determining genetic associations for autism. It has, among other things, developed statistical tools that identified 65 different genes associated with autism risk and predicted the existence of several hundred more such markers, provided information about the possible genetic makeup of autism, and found that although some rare genetic markers can dramatically heighten the risk for autism, most genetic risks for the disorder are carried in common gene variants.

The awarding of this grant means that these findings may well be the roadmap toward finding a more comprehensive set of genetic data for autism and paving the way toward novel methods for helping autistic patients.

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NIMH awards CMU team $7 mil for autism genetics research - CMU The Tartan Online

Recommended Reading: The genetics of better beer – Engadget

You Want Better Beer? Good. Here's a Better Barley Genome Adam Rogers, Wired

The beer industry certainly isn't hurting for money these days, but a group of scientists are trying to figure out how to make the beverage even better. They're doing so by breaking down the genome of barley, a key ingredient in the brewing process that that turns starch into sugar for yeast to transform into alcohol during fermentation. Wired has the story of how the geneticists could be on the way to improving suds for all of us to enjoy.

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Recommended Reading: The genetics of better beer - Engadget

The genetics of photosensitive sneezing, explained / Boing Boing – Boing Boing

If you're among the one in four people who sneeze when you move from a dark place into the sunlight, this nifty little explainer from a fellow traveler gives a great overview of causation theories over the millennia. Turns out it is just one transposed letter in the second chromosome that causes the effect.

The dominant photic sneeze reflex trait gets passed on if one of your parents gives it to you. He clarifies his "sneeze gene" video title:

The Sun Sneeze Gene (YouTube / Veritasium)

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Flashlight fish, also called lanterneye fish and scientifically photoblepharon (light-eye), are strange and wondrous creatures best viewed during a night dive in the Pacific.

Nuno Dias shot this absolutely insane surfing footage that looks more like a snowboarder out in front of an avalanche than a surfer on a wave.

Poliahu, the Hawaiian snow goddess who lives atop Mauna Kea, is the namesake for this stunning and inspiring footage from Sunchaser Pictures.

Bamboo has lots of uses beyond just being panda food. Things like bikes, roads, scaffolding, and musical instruments are made from the fast-growing grass. But unless you are participating in a tropical-themed LARP, you probably wouldnt want a shirt made from bamboo stalks. So why dobamboo bed sheets make any sense? Because yarn extracted from []

If you want to work in tech, but dont have any desire to code web apps to help businesses sell things to other business, you might want to consider a career in cybersecurity. Judging from the apparent complete infiltration of Russian hackers in American cyberspace,it seems fair to speculate that theres a major shortage of []

All moms are different. But all moms like getting flowers on Mothers Day, and thats a fact (not, however a fact we can document in any fashion.) Instead of getting chewed out for forgetting to call her on the second Sunday of May, you can take care of it ahead of time with Telefloras flower []

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The genetics of photosensitive sneezing, explained / Boing Boing - Boing Boing

Seattle Genetics (SGEN) Q1 Loss Widens, Sales Top Estimates – Yahoo Finance

Seattle Genetics, Inc.SGEN reported a loss of 42 cents per share for the first quarter of 2017, wider than the Zacks Consensus Estimate of a loss of 41 cents and the year-ago loss of 15 cents per share.

Revenues came in at $109.1 million, down 1.8% year over year, primarily due to lower royalty revenues from the sales of Adcetris. Revenues, however, beat the Zacks Consensus Estimate of $103.3 million.

Seattle Genetics share price has gained 29.1% year to date compared with the Zacks classified Medical - Biomedical and Genetics industrys rise of 4.8% in the same period.

Quarter in Detail

Seattle Genetics top line comprises product revenues, collaboration and license agreement revenues and royalties.

The companys only marketed product, Adcetris, generated revenues of $70.3 million, up 20% year over year.

Collaboration and license agreement revenues increased 8.2% to almost $21.8 million. Collaboration revenues included fees earned from the companys agreement with Takeda Pharmaceutical Company Ltd. for Adcetris and other ADC collaborations.

Royalty revenues declined 47.5% year over year to $16.98 million. The decline was due to unfavorable year-over-year comparisons. The company had received a milestone payment of $20 million from Takeda in the first quarter of 2016 on international sales of Adcetris.

Research and development (R&D) expenses were $118.2 million, up 27.3% year over year. Also, selling, general and administrative (SG&A) expenses increased 29.1% to $38.4 million. Costs were high primarily due to investment in vadastuximabtalirine, Adcetris collaboration activities for product supply to Takeda and pipeline development.

In its call, the company asserted that there was no erosion of its share in the relapsed HL business despite the FDA approval for Merck & Co., Inc.s MRK Keytruda as the second PD-1 inhibitor for the treatment of relapsed Hodgkin lymphoma in Mar 2017.

2017 Outlook Update

The company reiterated its outlook for net sales of Adectris to be in the range of $280 million to $300 million. Although the company expects royalty revenues to decrease in the second quarter, it continues to expect it in the range of $50 million to $55 million for the full year.

Pipeline Update

Seattle Genetics continues to work on expanding Adcetris label further through 3 phase III trials. We note that the company reported positive data from ALCANZA phase III study recently and is planning to submit a supplemental Biologics License Application (BLA) by mid-2017.

The company expects top-line data from the phase III ECHELON-1 study (frontline classical Hodgkin lymphoma) during 2017 while top-line data from the ECHELON-2 study (frontline CD30-expressing mature T-cell lymphoma) should be out in 2018 (previously expected in the 2017 to 2018 timeframe).

In addition, the company continues to enroll patients in the phase III study on vadastuximabtalirine in combination with hypomethylating agents in older patients with newly diagnosed acute myeloid leukemia. Also, the company plans to start a phase II study in younger patients with newly diagnosed AML in the second half of 2017.

Our Take

While the company missed bottom line expectations, sales came in ahead of estimates in the first quarter of 2017. With the approval of Keytruda, investors should focus on Adcetris sales in the upcoming quarters. However, the FDA has lifted the clinical hold on two phase I trials of its candidate, vadastuximabtalirine in acute myeloid leukemia (AML) in March.

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Seattle Genetics, Inc. Price, Consensus and EPS Surprise | Seattle Genetics, Inc. Quote

Zacks Rank & Stocks to Consider

Seattle Genetics carries a Zacks Rank #4 (Sell).

A couple of better-ranked stocks in the health care sector include Heska Corporation HSKA and Regeneron Pharmaceuticals, Inc. REGN. While Heska sports a Zacks Rank#1 (Strong Buy), Regeneron carries a Zacks Rank #2 (Buy). You can see the complete list of todays Zacks #1 Rank stocks here.

Heskas earnings estimates increased from $1.53 to $1.65 for 2017 and from $1.80 to $2.01 for 2018 over the last 60 days. The company posted positive earnings surprises in eachof the four trailing quarters with an average beat of 291.54%.

Regenerons earnings estimates remained almost stable for 2017 and 2018, respectively, over the past 30 days. The company recorded positive earnings surprises in three of the last four quarters, with the average being 8.08%.

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Want the latest recommendations from Zacks Investment Research? Today, you can download 7 Best Stocks for the Next 30 Days. Click to get this free report Merck & Company, Inc. (MRK): Free Stock Analysis Report Regeneron Pharmaceuticals, Inc. (REGN): Free Stock Analysis Report Seattle Genetics, Inc. (SGEN): Free Stock Analysis Report Heska Corporation (HSKA): Free Stock Analysis Report To read this article on Zacks.com click here. Zacks Investment Research

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Seattle Genetics (SGEN) Q1 Loss Widens, Sales Top Estimates - Yahoo Finance

Genetics Reveal How Tibetans Evolved To Deal With High Altitude – IFLScience

Living at altitude really puts a strain on the human body. From slowing digestion to the extreme cold, there is a lot to contend with the higher up you go. Yet people living on the Tibetan Plateau have managed to survive at an altitude of around 4,500 meters (15,000 feet) for thousands of years.

A team of geneticists have nowuncovered exactly how they manage this, including the genes they may have gainedfrom an extinct species of human. After sequencing the entire genomes of 27 Tibetans, they managed to find five different genes that help them live at such lofty heights. The results highlight the influencethe extreme environment faced by these people, who have been living there for at least 3,000 years, has hadontheir evolution.

The five gene variants discovered are all related to helping the body cope with the low levels of oxygen, high altitude, and poor diet. Theyalso show how the ancestors to Tibetans at some point had shenanigans with an extinct human species. Some of these have already been identified before, as the researchers found the genes EPAS1 and EGLN1 both present in the population. These induce the body to produce more hemoglobin, which transports oxygen around the body when at altitude.

But they also uncovered a few genes we didnt know about. Related to low oxygen levels, PTGIS and KCTD12 were also found in the genome of the Tibetans, as well as a variant of VDR, which has been linked to vitamin D metabolism. The researchers suspect that this may help the people deal with vitamin D deficiency, which is a common problem on the plateau due to the poor growing conditions, and thus diet.

The comprehensive analysis of whole-genome sequence data from Tibetans provides valuable insights into the genetic factors underlying this population's unique history and adaptive physiology at high altitude, explains Tatum Simonson, who co-authored the study published in PLOS Genetics, in astatement.

Simonson continues: This study provides further context for analyses of other permanent high-altitude populations, who exhibit characteristics distinct from Tibetans despite similar chronic stresses, as well as lowland populations, in whom hypoxia-related challenges, such those inherent to cardiopulmonary disease or sleep apnea, elicit a wide-range of unique physiological responses.

But what is really interesting is how the genetics of the Tibetan people can provide insight into how an extinct species of human, the Denisovans, lived. Known only from a few hand bones found in a cave in Siberia, it is thought that the EPAS1 gene is derived from these mysterious people, suggesting that as a species, they too may have been adapted to high altitudes.

Link:
Genetics Reveal How Tibetans Evolved To Deal With High Altitude - IFLScience

Can’t hack it in high altitudes? It’s all about genetics – CBC.ca

Try to walk a mile in a Tibetan person's shoes and you will fail miserably.That's because they have evolved to live at high altitudes better than anyone else on the planet.

Just in time for the climbing season to open on Mount Everest, anew study from the University of Texas, Houston, tells us about the genes behind this incredible ability.

It's estimatedthat humans have been continually living on the Tibetan plateau for almost 60,000 years. That gives a lot of time for adaptations to develop and populations to evolve in order to live better in these extreme conditions.

When you are up there high on the Tibetan plateau, life is tough.When I was in Tibet in 2010 and again in 2011, it was amazing how hard it was just to walk around.There are a lotof high-altitude places in the world, but Lhasa, at an altitude of 3,600 metres, is one of the highest places where humans have lived for thousands of years.

I spoke with Chad Huff, the senior author of the study.

"Tibetan high-altitude adaptation is perhaps the most extreme example we have of human adaptation where most individuals from low altitude have a very difficult time at 15,00 feet," he said. "Tibetans survive and thrive there, so it's really fascinating as to the genetics behind those adaptations."

And that's what this new paper, published in the Open Access Journal PLOS, investigated; they looked at the genetic changes in Tibetans that make them such great mountaineers.

After sequencing the complete genomes of 27 Tibetans, they identified five possible genes that relate to the Tibetans' ability to thrive at such high altitudes.Two of them, EGL1andEPAS1,have been previously found,and both seem to be related to how much hemoglobin is in the blood.

Hemoglobin is what carries oxygen in the blood. When you acclimate to higher altitudes,your body adjusts to the low oxygen concentrations by making more hemoglobin to suck up more of that hard-to-get oxygen.

The two genes, EGL1andEPAS1,found in Tibetan populations seem to be doing the opposite: they seem to be decreasing the hemoglobin concentrations.

This makes no sense, until you realize that having blood thick with hemoglobin makes your heart pump harder and your vessels strain more. Having a heart that works harder all the time, coupled with vessels that are strained, doesn't add up to a healthy individual.This is one problem observed with the ethnic Han population, the dominant population of lowland Chinawho are trying to live in the Tibetan plateau to take advantage of some of the resource extraction that is happening.The non-Tibetansshow significant negative health effects, while the Tibetans show no such problems.

There's no exact number yet, but it looks like some of these genetic changes are as recent as 10,000 years old.The most common adaptation, and the one with the most variability in the population, is 45,000 years old. But still, that's pretty quick in evolutionary time, especially in humans who reproduce relatively slowly.

Chad Huff offers more insight.

"It is quite fast for humans. There are a few examples of somewhat faster evolution in humans, the lactase persistence in Europeans is one example; it's a few thousand years younger, butEPAS1andEGL1are among the strongest signals and fastest sweeps in human evolution."

You have to remember, the selective pressures the forces that pick the strongest individuals to survive are strong up there on the plateau. I can speak from experience.When I was hiking to Everest base camp it was one step breathe, two steps, breathe.I couldn't believe how hard it was,and there was my Tibetan guide, sprintingby, seemingly unfazed.

Researchers were interested in how Sherpa's work at such high altitudes. (Craig Steinback)

Yes, the study showed that Tibetans are literally genetically superior to anyone else trying to summit.

When I was there my guide had been to camp 4, the last one before the summit, more than a handful of times. That would be considered a huge success for most people attempting to climb Everest, and yetit was largely uncelebrated.

There is no doubt that in mountaineering, the earlier lack of credit for the Sherpas has been a huge controversy. Maybe because it is so much easier for them, it's almost as if the rest of the world hasn't been acknowledging the incredible risksthey take because it's so natural.

And yet, more Sherpas have been killed on Everest in the last three climbing seasons than ever before.And now we embark on another Everest climbing season, poised to the busiest ever.

The Sherpas are the lifeline to the mountain;no one can climb it without them.They set the routes, fix the ropes,carry a lot of the gearand do it better than anyone else on the planet.

Summitting Everest is an absolutely monumental achievement, and what the Tibetan people have survived and how they've adapted to the life in the mountains is equally monumental.

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Can't hack it in high altitudes? It's all about genetics - CBC.ca

Seattle Genetics (SGEN) Q1 2017 Results – Earnings Call Transcript – Seeking Alpha

Seattle Genetics, Inc. (NASDAQ:SGEN)

Q1 2017 Earnings Call

April 27, 2017 4:30 pm ET

Executives

Peggy Pinkston - Seattle Genetics, Inc.

Clay B. Siegall - Seattle Genetics, Inc.

Darren S. Cline - Seattle Genetics, Inc.

Todd E. Simpson - Seattle Genetics, Inc.

Jonathan Drachman, M.D. - Seattle Genetics, Inc.

Analysts

Michael Schmidt - Leerink Partners LLC

Paul Choi - Barclays Capital, Inc.

Shawn Fu - JPMorgan Securities LLC

Salveen Richter - Goldman Sachs & Co.

Yatin Suneja - SunTrust Robinson Humphrey, Inc.

Operator

Please stand by. We're about to begin. Good day and welcome to the Seattle Genetics First Quarter Financial Results Conference Call. Today's conference is being recorded. At this time, I'd like to turn the call over to Peggy Pinkston Vice President, Investor Relations. Please go ahead.

Peggy Pinkston - Seattle Genetics, Inc.

Thank you operator and good afternoon everyone. I'd like to welcome all of you to Seattle Genetics First quarter 2017 conference call.

With me today are Clay Siegall, President and Chief Executive Officer; Todd Simpson, Chief Financial Officer; Eric Dobmeier, Chief Operating Officer; Jonathan Drachman, Chief Medical Officer and Executive Vice President, Research and Development and Darren Cline, Executive Vice President, Commercial.

Following our prepared remarks today, we will open the line for questions. If we are unable to get to all of your questions, we will be available after the conclusion of the call.

Today's conference call will include forward-looking statements regarding future events or the future financial and operating performance of the company. Such forward-looking statements are only predictions based on current expectations, and actual results may vary materially from those projected.

Please refer to the documents that we file from time to time with the SEC, including the company's Form 10-K for the year ended December 31, 2016 for information concerning the risk factors that could cause actual results to differ materially from those contained in any forward-looking statements.

Now I'll turn the call over to Clay.

Clay B. Siegall - Seattle Genetics, Inc.

Thanks, Peg, and good afternoon, everyone. Thank you for joining us. Today, we'll discuss upcoming activities and review recent progress towards our goal of becoming a multi-product oncology company.

I'll start with the summary of our three main areas of focus. First, building ADCETRIS into a major global brand. Second, advancing our late stage clinical programs, notably vadastuximab talirine or 33A and enfortumab vedotin or 22ME. And third, investing in a robust pipeline of earlier stage programs, including SGN-LIV1A and others across both hematologic malignancies and solid tumors.

Our first quarter sales of ADCETRIS in the U.S. and Canada were $70.3 million, a 20% increase over the first quarter of 2016. We remain on track with our 2017 guidance for ADCETRIS product sales in our territory of $280 million to $300 million. We are executing well commercially with our current labels. We are also preparing for several significant clinical and regulatory milestones intended to drive future growth of the ADCETRIS franchise. These are based on three phase 3 trials, ALCANZA, ECHELON-1 and ECHELON-2.

Starting with ALCANZA. We plan to submit a supplemental BLA to the FDA in mid 2017. As a reminder, our phase 3 ALCANZA trial was conducted in CD30-expressing cutaneous T-cell lymphoma. The results showed a highly statistically significant benefit in favor of ADCETRIS across the primary and all secondary endpoints.

We received Breakthrough Therapy Designation for ADCETRIS in CD30-expressing mycosis fungoides and primary cutaneous anaplastic large cell lymphoma, the most common subtypes of CTCL. We plan to submit the ALCANZA data to the FDA along with data from two investigator-sponsored trials in other subtypes of CTCL with the goal of obtaining a broad label in CTCL. The submission is on track for mid-year.

Another significant upcoming activity for the ADCETRIS program is the release of top line data this year from our phase 3 ECHELON-1 trial in frontline Hodgkin lymphoma. The ECHELON-1 trial is assessing modified progression-free survival in newly diagnosed advanced Hodgkin lymphoma patients. Patients were randomized to receive either an ADCETRIS-containing regimen called A+AVD or the standard of care known as ABVD. This trial represents a substantial opportunity for ADCETRIS to redefine and improve the treatment paradigm for newly diagnosed Hodgkin lymphoma patients, which has not changed in decades.

Looking ahead to 2018, we expect to report data from ECHELON-2, our phase 3 trial of ADCETRIS in frontline mature T-cell lymphoma, often referred to by clinicians as peripheral T-cell lymphoma. We are evaluating progression-free survival of ADCETRIS plus CHP compared to standard of care CHOP, or CHOP chemotherapy, in newly diagnosed patients. This is a second opportunity to redefine and improve outcomes in a frontline non-Hodgkin lymphoma patient setting that has not changed in many years.

I'll now turn to vadastuximab talirine, or SGN-CD33A. We are conducting trials of 33A in AML and myelodysplastic syndrome, both of which broadly express CD33. Our first registration pathway with 33A is the ongoing CASCADE phase 3 trial in older patients with AML. CASCADE is a global randomized study comparing 33A plus decitabine or azacitidine to either of these hypomethylating agents alone. The primary endpoint is overall survival. Enrollment has been strong towards our target of over 500 patients.

We are also advancing 33A in frontline younger patients with AML. We plan to initiate a randomized phase 2 trial later this year, adding 33A to the standard regimen of cytarabine and daunorubicin or 7+3. This trial is designed to assess whether adding 33A to the standard frontline regimen can improve MRD-negative TR rate and event-free survival in frontline fit AML patient.

Our rationale for advancing 33A into two late stage AML trials is based on data from separate phase 1 trials. One of 33A plus HMAs in older AML patients and another of 33A plus 7+3 in younger AML patients. As reported at ASH in December, in both trials, the composite complete remission rate was more than 70%. And notably, in both studies, we observed a high percent of responders who were negative for minimal residual disease.

In these single-arm trials, interim survival measures were superior among responding patients who achieved MRD-negative remissions compared to responding patients who are not MRD-negative. Based on these data, we believe that adding 33A to standard regimens for AML could potentially be well-tolerated and yield superior outcomes to standard treatment alone.

In addition to AML, we are evaluating 33A in myelodysplastic syndrome through an ongoing phase 1/2 trial. In this trial, we are pursuing a similar strategy, combining 33A with azacitidine in newly diagnosed patients with high risk MDS and comparing tolerability and activity with azacitidine alone.

Next, I'll provide an update on enfortumab vedotin, or 22ME, our lead ADC for solid tumors. 22ME is in clinical development for metastatic urothelial cancer under our co-development collaboration with Astellas. Based on positive feedback from the FDA, we intend to initiate a pivotal monotherapy phase 2 trial in patients previously treated with a checkpoint inhibitor, with the intent of providing the data for potential registration under the FDA's accelerated approval regulations. We plan to initiate this study in the second half of 2017.

We believe that 22ME could play an important role in this setting. This is an unmet medical need, given that the majority of patients treated with checkpoint inhibitors fail to respond and require further treatment options. We are also planning to combine 22ME with checkpoint inhibitors in a trial that we expect to begin late this year as part of our broad clinical development program.

We are positioned for several key milestones in 2017 that have the potential to significantly advance Seattle Genetics towards our goal of improving the lives of people with cancer and further establish the company as a leader in the field of oncology. We are expanding globally and are in a strong financial position to continue executing on our priorities.

Now, I will turn the call over to Darren to discuss our commercial activities. After that, Todd will discuss our first quarter financial results, and then Jonathan will highlight our research and development progress. Darren?

Darren S. Cline - Seattle Genetics, Inc.

Thanks, Clay. In the first quarter, ADCETRIS sales were $70.3 million, an increase of 20% over the first quarter of last year. ADCETRIS continues to be the standard of care in its original approved indications of relapsed HL and relapsed ALCL.

As the brand approaches its 6th year on the market strong long-term follow-up data from our initial pivotal trials have further enhanced the clinical value proposition in these settings today. Despite the recent FDA approval of a second PD-1 inhibitor in relapsed Hodgkin lymphoma setting, we have seen no erosion in share in our existing relapsed HL business. Most prescribers have indicated they view the checkpoint inhibitor agents as interchangeable and would use both in post ADCETRIS later lines of therapy or palliative setting if necessary.

Beyond our current business, we're continuing to prepare ADCETRIS to become a major global brand. Our commercial resources are focused on launch preparedness for upcoming CTCL indication and most importantly our frontline Hodgkin lymphoma indication. In the near term, the CTCL approval will represent another important commercial milestone for ADCETRIS. Physicians and market research have been impressed with the strength of the ALCANZA data, and we believe it supports our goal for ADCETRIS to be the foundation of treatment for CD30-expressing lymphomas.

Leading up to ECHELON-1 results, we've invested resources to better understand how ADCETRIS plus AVD will be integrated into current practice in both community and academic setting, and how we can ensure rapid adoption of this novel regimen in the event of FDA approval. In parallel, we are also continuing education efforts to raise awareness and highlight the unmet need that exist specifically for advanced stage Hodgkin lymphoma patients, who currently receive ABVD.

Lastly, our ECHELON-2 trial will potentially provide patients and providers a new targeted therapy option beyond traditional chemotherapy that will address the high unmet need in newly diagnosed T-cell lymphoma. Although, we are in the early stages of commercial planning for the E-2 launch, we have been ensuring our education efforts in CTCL and ALCL will be complementary to our frontline MTCL approval education efforts in the future. I look forward to updating you on our progress in preparing for these important growth opportunities for ADCETRIS.

Now I'd like to turn the call over to Todd to discuss our financial results.

Todd E. Simpson - Seattle Genetics, Inc.

Great. Thanks, Darren, and thanks to everyone for joining us on the call this afternoon. We ended the first quarter with $536 million in cash and investments. This along with our strong ADCETRIS sales and our collaborations enables us to continue executing on our strategy of expanding the ADCETRIS label advancing our 33A and 22ME programs and investing in the rest of our oncology pipeline.

Today, I'll summarize our financial results for the first quarter of 2017. Total revenues in the first quarter were $109 million, including ADCETRIS net sales of $70 million. As Clay mentioned, we continue to expect that total ADCETRIS sales for 2017 will be in the range of $280 million to $300 million.

Royalty revenues in the first quarter were $17 million compared to $32 million in the first quarter of 2016. Recall that in the first quarter of last year; royalties included a one-time $20 million sales milestone from Takeda. Excluding that milestone, first quarter 2017 royalties increased 38% compared to last year. This was driven by higher Takeda sales and by those sales reaching a higher royalty rates here in the fourth quarter of last year.

As a reminder, the royalty rate paid by Takeda begins in the mid-teens increases to the high-teens at $100 million in sales into the low 20%s at $200 million and ultimately to the mid 20%s. Since the rates reset annually and because we report royalties one quarter in arrears, royalty revenues will decrease in the second quarter, although we continue to expect them to be in the range of $50 million to $55 million for the full year. Collaboration revenues were $22 million in the first quarter, driven by amounts earned under our ADCETRIS collaboration with Takeda and our ADC deals.

R&D expenses were $118 million in the first quarter; ADCETRIS continues to be the primary driver of R&D expense and the increase over the first quarter of 2016 reflects investments in 22ME, 33A and our broad pipeline. SG&A expenses were $38 million in the first quarter, also in line with our expectations.

Now I'd like to turn the call over to Jonathan.

Jonathan Drachman, M.D. - Seattle Genetics, Inc.

Thanks Todd. We are positioned for several very important activities this year with ADCETRIS 33A and enfortumab vedotin. We're also advancing and expanding our pipeline and conducting innovative research to remain the industry leader in ADC technology. With ADCETRIS, we're preparing the supplemental BLA submission for labeling CTCL. Our ALCANZA data were remarkable, and we believe ADCETRIS can make a meaningful difference for CTCL patients who requires systemic therapy to treat this debilitating disease.

In collaboration with Takeda, we're also preparing for top line data from our phase 3 ECHELON-1 trial in frontline Hodgkin lymphoma. This large global trial has the potential to redefine the way newly diagnosed patients, mostly young adults are treated by adding ADCETRIS and removing bleomycin from the standard regimen. It is exciting that this year we expect data that could drive improved outcomes for patients with advanced Hodgkin lymphoma.

With 33A, our development focus is on myeloid malignancies, including AML and MDS. We are encouraged by the significant percentage of MRD or minimal residual disease negative remissions achieved by patients in our phase 1 AML trials. MRD-negative remissions are more stringent and deeper than traditional response criteria and have been associated with better patient outcome. As we reported at ASH from our phase 1 trial, interim data suggest that patients who achieve MRD-negative status live longer than those who did not, regardless of whether they achieve a CR or a CRI. We will be evaluating MRD status in our CASCADE trial for older unfit patients and in our planned phase 2 randomized trial in frontline younger AML patients.

With enfortumab vedotin, we're working with regulators on refining our development plan for this program in metastatic urothelial cancer and look forward to initiating a registrational trial later this year. In addition, at the upcoming ASCO Annual Meeting in Chicago follow-up data in patients with metastatic urothelial cancer from the phase 1 trail of 22ME will be featured in an oral presentation. We're also evaluating additional tumor types in the ongoing phase 1 trial, including ovarian and non-small cell lung cancer. And lastly, we and Astellas recently initiated a phase 1 trial of 22ME in Japan. This trial will enable future studies and regulatory submission in Japan.

We and Astellas believe that enfortumab vedotin has the potential to become an important therapy around the globe for patients with urothelial cancer. In addition to our lead programs, we are advancing several other clinical stage programs, notably SGN-LIV1A and ADC in development for metastatic breast cancer, including triple negative disease. We are continuing to optimize the dosing schedule in phase 1 and expect to report additional data from SGN-LIV1A later this year. We are enthusiastic about the opportunity for SGN-LIV1A in triple negative breast cancer and we are evaluating next steps for this program, including potential registrational approaches and combination regimens.

At AACR earlier this month, we showcased our advances in research and preclinical development. Some notable presentations included reporting preclinical data demonstrating that ADCETRIS induces immunogenic cell death resulting in an inflammatory tumor microenvironment and added activity when combined with inhibitors of the PD-1, PD-L1 pathway. Under our collaboration with Bristol-Myers Squibb we're conducting clinical trials with ADCETRIS and nivolumab in multiple Hodgkin and non-Hodgkin lymphoma setting.

In support of our own immuno-oncology portfolio, we reported preclinical data on SEA-CD40 that demonstrate activation of an antitumor immune response and potential for combination with checkpoint inhibitors. SEA-CD40 is an immuno-oncology agent that is in a phase 1 trial for the treatment of both solid tumors and hematologic malignancies. In addition, preclinical data were presented supporting the ongoing phase 1 study of SGN-2FF for patients with advanced solid tumors, including non-small cell lung cancer. SGN-2FF is an oral, small molecule immuno-oncology agent that has been shown to inhibit fucosylation of protein, and thereby stimulate the immune system to slow the growth and spread of cancer. There were also several presentations that highlighted advancements in linker technologies for payloads which enable development of novel ADCs, including the planned clinical program SGN-CD48A for multiple myeloma.

And finally, Unum Therapeutics reported preclinical data with our sugar-engineered antibodies in combination with engineered antibody-coupled T cell receptor, or ACTR cells. Under our collaboration, Unum plans to initiate a phase 1 trial for patients with multiple myeloma targeting BCMA.

Seattle Genetics is built on innovation and scientific excellence. I'm proud that, even as we are advancing multiple exciting programs into registrational studies, we continue to focus on maintaining our leadership in the ADC field and broadening our pipeline by advancing multiple immuno-oncology programs into clinic.

Now I'll turn the call back over to Clay.

Clay B. Siegall - Seattle Genetics, Inc.

Thanks Jonathan. Before we open the line for questions, I'll summarize our key upcoming activities.

For ADCETRIS, these include submitting a supplemental BLA to the FDA for CTCL in mid 2017, reporting data from the phase 3 ECHELON-1 trial in frontline Hodgkin lymphoma this year, and reporting data from the phase 3 ECHELON-2 trial in frontline MTCL in 2018. For 33A, we are advancing the phase 3 CASCADE trial in frontline older AML, and a phase 1/2 trial in frontline MDS. In addition, we plan to initiate a randomized phase 2 trial in the second half of the year in frontline younger AML patients. Lastly, for 22ME, together with Astellas, we plan to initiate a pivotal phase 2 monotherapy trial in the second half of 2017 for metastatic urothelial cancer patients, who had previously been treated with a checkpoint inhibitor. We are also planning a trial in combination with a checkpoint inhibitor to begin later this year. And we will report additional phase 1 data at ASCO. We will keep you updated on our progress, as well as activities across our earlier stage pipeline programs.

At this point, we will open the line for Q&A. Operator, please open the call for questions.

Question-and-Answer Session

Operator

Thank you. We will take our first question from Michael Schmidt with Leerink Partners.

Michael Schmidt - Leerink Partners LLC

Thanks for taking my questions, and congrats on a good first quarter. I had a follow-up question on your ASG-22ME discussions with the FDA. And just wondering if you could provide some more color there in terms of the feedback that you received, for example, number of patients, what is the potential size of the phase 2 study, which endpoints could be used here, and what is the approval hurdle potentially?

Clay B. Siegall - Seattle Genetics, Inc.

Okay, Michael, thank you very much for the questions. So, what I would say is, it was a positive meeting with the FDA. The trial you asked about, and at this point, what we're saying is that the modestized (23:11) trial with a relatively rapid timeframe. We mentioned it's a single-arm monotherapy trial of patients who previously had been treated with checkpoint inhibitors. And this would be under the accelerated approval pathway within the FDA.

So overall, we're really excited with the data from 22ME. We previously presented data. At ASCO this year, you'll be hearing more data, and in fact it's an oral presentation. So that was fantastic. And so there'll be a lot of data that will be presented. And we are also going to do we said we're going to start a trial of 22ME with checkpoint inhibitors. And the thing that I really like about that is, you have the high overall response rate of an ADC, and then you have this long durability of a checkpoint and together that could be really exciting. And we've seen evidence of that with ADCETRIS, OPDIVO. We're excited with that. But for the approval trial that is the single arm monotherapy.

Michael Schmidt - Leerink Partners LLC

Okay, great, thanks. And then I had a follow up regarding Hodgkin lymphoma in particular around your activities and in second line Hodgkin lymphoma potentially, I was just wondering if you could just provide some more color there on your activities and sort of what your strategy and next steps are regarding the second line Hodgkin lymphoma setting? Thank you.

Clay B. Siegall - Seattle Genetics, Inc.

Sure. So we've previously presented quite a lot of data in second line. As you know in frontline, we're trying to really redefine frontline with ADCETRIS every day and that's the E-1 trial. But in second line, I think when you look at what we've done historically, I think we've taken two approaches, we had ADCETRIS plus bendamustine. We had quite a lot of data there with a CR rate over 80%. So that is a one way to consider, although bendamustine does have some toxicities that are well known.

The other approach which we've done of late and perhaps I'm even more interested in is ADCETRIS plus checkpoint inhibitors, and we've put data out on ADCETRIS plus OPDIVO at the appropriate cancer conferences and the data looks really good. At this point, we haven't said anything specific on how we're going to follow it up. I mean those trials also were done with in partnership with Bristol-Myers Squibb. So they were done together with them. We've had a good relationship. We started out with two trials. We added a third trial in our relationship, so I think that's good. And I would say stay tuned for more information as soon as we can provide it in that area, but something that we're very keen to look at.

Michael Schmidt - Leerink Partners LLC

Okay. Great. Thanks, Clay. Thanks for that.

Operator

We'll take our next question from Geoff Meacham with Barclays.

Paul Choi - Barclays Capital, Inc.

Hi, everyone. It's Paul Choi. Thanks for taking our questions. Could you maybe provide a little bit of color on your perhaps pre-CTCL activities in terms of physician awareness and how they're thinking about current standard of care versus what you could do with ADCETRIS?

Clay B. Siegall - Seattle Genetics, Inc.

Sure. I'd be delighted to talk about that, but probably better for Darren to talk about what our commercial team is doing to prep for CTCL based on this fantastic data, remarkable data that we had with ALCANZA.

Darren S. Cline - Seattle Genetics, Inc.

Yeah. Thanks. And as I alluded to in the prepared remarks that we've been doing a lot of market research around the ALCANZA data and physicians are quite frankly stunned at the results. And if you think about the CTCL patient population, there're about 2,000 that get systemic therapy annually in the U.S. about a 1,000 that express CD30, but as we think about the label, the implications, we're focused on identifying who the appropriate treaters are. Again, because this is somewhat of a rare disease and it's really been segmented with a few key physicians and treatment sites throughout the United States, so we're focusing on that.

Our marketing team is preparing and doing message testing, et cetera to quickly upon approval get the datasets in front of the patient or excuse me, the physicians. So we'll have the rapid uptake with these physicians.

So we're excited, the physician community is excited. They're most excited for a new option that if you think about cutaneous T-cell lymphoma, it's a very visible disease to both obviously the patients and the physicians, and I think with data like ADCETRIS in the setting, we're going to see I think patients are going to see remarkable results. And so, we're excited about it, physicians are and so our patient.

Clay B. Siegall - Seattle Genetics, Inc.

And I want to add one thing about CTCL. So we have Breakthrough Designation from our ALCANZA trial. And so, we have had a good opportunity to collaborate and discuss with FDA all of our data. And you may recall from earlier conference calls that we initially had guided that we would be submitting earlier in this year. And then we changed our guidance at our last conference call to mid-year. And that was because of our discussions with the FDA based on other data that we've had from investigator-sponsored trials, specifically two of them which showed strong activity in CTCL with patients that were below the histology cut off that we used in our ALCANZA trial and with patients that were in other subtypes of CTCL.

So our goal in presenting our data, ultimately submitting a supplemental BLA is to try to get the it will help the most patient that we can and that might be with helping all patients with CTCL. It's not clear that based on histology is the right way to select the patients, and that in fact our data says otherwise. And when you look at the listing in compendia, that does not have a CD30 cut off. So we think that we're in a good position to submit all our data, ALCANZA and from two other trials to try to get the broadest label that we can and help the most patients we can. But that's been our goal and we've been talking about that.

Paul Choi - Barclays Capital, Inc.

Great. Thank you very much.

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Seattle Genetics (SGEN) Q1 2017 Results - Earnings Call Transcript - Seeking Alpha

NSA Looked for ‘Nefarious’ Genetics Projects – GenomeWeb

More than 10 years ago, the US National Security Agency was monitoring international research projects with the aim of spotting "nefarious" genetic engineering projects, Gizmodo reports.

A new document from the trove leaked by Edward Snowden in 2013 claims that the signals intelligence program was sifting through electronic and communication data it collected for information on genetic sequencing efforts, it adds.

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NSA Looked for 'Nefarious' Genetics Projects - GenomeWeb

One Mind: Looking at genetics and environment – The Knox Student

Like any aspect of medicine or biology, mental health is quite a complex subject and there isnt really any one thing that can improve or worsen it. In most cases, genetics is a key factor. A lot of mental conditions, or even just mental health issues in general, tend to be rather common in some families. Obviously, genetics is a complex subject, and family history can only explain so much of it. For instance, Down Syndrome, one of the most common mental health conditions, is caused by an abnormality in the number of chromosomes a person has. Schizophrenia has been traced to one very specific gene. Autism, on the other hand, is largely genetic, but has been linked to hundreds, perhaps even thousands of genes, and there isnt one or even a specific set of these genes that seem to cause it.

Confused yet? Believe me, it gets weirder. Many of these autism genes have been traced to pre-evolution, meaning that humans have had them before they were human. The number of autistic genes has since increased. This, combined with a possible occurrence of a few of these genes in child prodigies, has led some to believe that autism was a positive mutation for humanity at some point and played a small role in species survival. Also, even though autism is highly genetic and can run in families family members almost never have the same autistic symptoms, nor do they fall on the same place on the spectrum.

Schizophrenia is just as complex and surprising. For instance, that one gene that has been linked to Schizophrenia has been named DIS (Disrupted in Schizophrenia). The reason for this is because scientists still have no idea what the gene is supposed to do. They only know that its malfunction results in Schizophrenia. Another weird statistic is that Schizophrenia seems to be slightly more common in gay men than most other groups, and the scientific community still has no idea why.

Perhaps strangest of all is that despite all of this genetic complexity, the mentally ill and those with physical disabilities are still a minority population-wise. The mentally ill make up only about one-fifth of the American populace. Most people are able-bodied and neurotypical despite literally thousands of interconnected parts designed to fit together in one specific way. One of my personal favorite biology facts is that evolution functions on genetic diversity. Literally every creature that exists today does so because somebody was born different from everyone else, and, miracle of miracles, that individual had an easier go at life than all the others, and so that became the new normal. Take us, for example. We have opposable thumbs, are mostly hairless, walk on two feet, stand up straight, live in communities, etc., and the basic reason for all of it? Well it worked for that first guy.

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One Mind: Looking at genetics and environment - The Knox Student