Category Archives: Genetics

Genetic Services | Boston Medical Center

Diagnostic genetics services at Boston Medical Center provide expertise in the diagnosis and evaluation of genetic and developmental disorders for patients, including:

Medical geneticist Jodi Hoffman, MD and the genetics teammanagement services for adults who have inherited disorders, genetic conditions, or birth defects. Patients seen in this clinic often have connective tissue disorders (Marfan syndrome and Ehlers Danlos syndrome, etc) as well as neurofibromatosis types 1 and 2, tuberous sclerosis, Down syndrome, rare cancer syndromes, and others. Consultations are provided in the Yawkey Ambulatory Care Clinic, 6th floor. NOTE: This is the same location as pediatric genetics.

For an appointment call 617.414.4841 or fax 617.414.5741

For more information, please call: 617.638.4317

Center of Excellence in Sickle Cell DiseaseHemoglobin Diagnostic Reference LaboratoryFor more information, please call: 617.414.1024.Medical Director: David Chui, MD

Jodi Abbott, MDRobert Blatman, MDPhilip Connors, MS, CGCAviva Lee-Parritz, MDGlenn Markenson, MDLillian Sosa, MS, CGCChristina Yarrington, MD

For an appointment, call 617.414.2000Antenatal Testing Unit: Yawkey5th Floor

Our certified genetic counselors provide consultation and testing for cancer predisposition syndromes for people who have a strong personal or family history of certain types of cancer. Identifying a genetic cause for cancer in a family allows for increased surveillance and earlier detection for at risk family members. The team works with testing companies and insurance to obtain coverage for this testing. Consultations are provided in the Moakley Building, 3rd floor, at 830 Harrison Ave.

For an appointment call: 617.638.6428Referrals can be faxed to: 617.414.1558

Medical geneticist Jodi Hoffman, MD and the genetics teamprovide diagnostic and management services for children who are likely to have inherited disorders, genetic syndromes, or birth defects. Children with unusual physical characteristics, developmental days, autism, or atypical growth are often referred for a genetics evaluation to determine if a genetic condition could explain the constellation of features. A diagnosis may provide information important for future health management as well as connections with support groups, research opportunities, and other families who have children with related conditions. Consultations are provided in the Yawkey Ambulatory Care Clinic, 6th floor.

For an appointment call 617.414.4841 orfax 617.414.5741More information

Certified genetic counselors Philip Connorsand Lillian Sosa provide consultation and counseling in the antenatal unit at Boston Medical Center to women who are pregnant or considering a pregnancy. Reasons for visits include advanced maternal age, abnormal nuchal translucency or maternal serum screening, medication exposures, carrier status, and family history. Clinic is held in Boston Medical Centers Antental Center, Yawkey 5th Floor.

For an appointment call 617.414.2000 orfax 617.414.7657More information

For more information:

Raveen Basran, D.Phil. Director of Diagnostic Molecular Genetics ([emailprotected]: 617.414.5329)Tom Maher, MS, Laboratory Manager of Diagnostic Molecular Genetics ([emailprotected]: 617.414.5312)Dan Remick, MD Medical Director, Diagnostic Molecular GeneticsDownload Diagnostic Genetics Consent Form

Michael OBrien, MD Chief Anatomic PathologyCarl O'Hara, MD - Chief of Laboratory MedicineShi Yang, MD, Scientific DirectorDownload Tissue Based DMP Requisition Form

Nancy Miller, MD, Medical Director Microbiology ([emailprotected])Chris Andry, PhD, Administrative Director and Vice Chair for Pathology Operations and Management ([emailprotected])Neil ONeill, Senior Manager for Laboratory Medicine Operations([emailprotected]: 617.414.4737)

All molecular genetics testing at BMC should be processed via the BMC Laboratory. BMC uses Quest Diagnostics as a reference laboratory and performs some testing in house. Quest Diagnostics' highly trained geneticists and genetic counselors are available at 1.866.GENE.INFO, (1.866.436.3463)

Go here to read the rest:
Genetic Services | Boston Medical Center

18 Things You Should Know About Genetics – YouTube

Gene Screen BC 2011 Participant.18 Things You Should Know About Genetics is an animated film that presents fundamental background information about genetics, as well as offering some quirky but interesting facts about DNA, genes and genetics. It was created to be an upbeat, fun educational short film to initiate and draw interest to this sometimes daunting and seemingly complex subject matter.

The rest is here:
18 Things You Should Know About Genetics - YouTube

Hundreds of Thousands of Species in a Few Thousand Years?

A recent1 review paper proposed a controversial claimthat the vast majority of animal species arose contemporary with modern humans. Not surprisingly, this claim was met with backlash from the evolutionary community. On what basis did the authors make this wide-reaching claim? Is their assertion true? Furthermore, what ramifications do their data have for the creationist explanation of the origin of species from the originally created min or kinds?

The main focus of Stoeckle and Thalers paper is genetics. Specifically, they focus on a subset of DNA in human and animal cells, termed mitochondrial DNA (mtDNA). Their analysis of mtDNA is clear, straightforward, and carefully justifiedso much so that I will summarize their arguments by liberally quoting from their paper.

About 15 years ago, DNA barcoding was first proposed as a tool for practical taxonomy.2 Taxonomy is the field of science concerned with the classification of life, and scientists thought that taking small subsets of DNA would aid in identifying and classifying species. The particular mitochondrial sequence that has become the most widely used is the 648 base pair (bp) [think of base pairs as DNA letters] segment of the gene [a subsection of DNA sequence] encoding mitochondrial cytochrome c oxidase subunit I (COI).3

With a subset of a subset of DNA, Skeptics of COI barcoding raised a number of objections about its power and/or generality as a single simple metric applicable to the entire animal kingdom, including: the small fraction of the genome (about 5% of the mitochondrial genome and less than one millionth of the total organisms genome [total DNA in an organism]) might not be sensitive or representative.4

A simple example from humans illustrates this concern. For instance, on average any two humans differ at 0.2%0.5% of their mtDNA base pairs. Theoretically, if all mtDNA differences are evenly distributed around the human mtDNA genome, you would expect 12 mtDNA differences in each individuals 648 bp COI barcode. With numbers this low, one generation of an extra mutation or two in the COI barcode sequence might throw a real classification pattern (i.e., one based on comparisons of hundreds of anatomical and physiological features) into confusion.

However, since the early days of DNA barcoding, such objections have been mostly mollified. I can attest to this from my own experience in handling thousands of mtDNA sequences. As a representative of the mtDNA diversity among species and individuals, a subset of mtDNA sequence is a good first approximation. Though subsets arent always perfect representations of the whole sequence, they are good initial data points.

Furthermore, over several decades of mtDNA barcoding, scientists have discovered a specific clustering pattern among mtDNA barcodes from individuals across diverse species: a general observation is that barcode clusters correspond best to species in well-studied animal groups, where taxonomists have mostly decided and agreed upon what species are. Thus there is good support in several major phyla, including Chordata [e.g., vertebrates and a handful of other species], Arthropoda [e.g., insects, arachnids, and crustaceans], Mollusca [e.g., shellfish, octopi], Echinodermata [e.g., starfish]. We note that these phyla are estimated to contain about 34 of named animal species.5

This fact has two major ramifications: First, the cluster structure of the animal world found in COI barcode analysis is independent of any definition(s) of species. Second, domain experts judgments of species tend to agree with barcode clusters and many apparent deviations turn out to be exceptions that prove the rule.6 In other words, the initial fears of those skeptical of DNA barcoding have not been met. Instead, barcoding has been very successful.

In light of these successes, the authors acknowledge the unexpected implications for explanations for the origin of species: At its origin DNA barcoding made no claim of contributing to evolutionary theory,7 yet the pattern of DNA barcode variance is the central fact of animal life that needs to be explained by evolutionary theory.8

Expanding our scope beyond the narrow evolutionary focus of the authors, we can generalize their statement: These mtDNA barcode patterns need to be explained by any model purporting to account for the origin of species.

The barcode patterns take a very specific form: the clustering structure of COI barcodessmall variance within species and often but not always sequence gaps among nearest neighbor species is the primary fact that a model of evolution and speciation must explain. Furthermore, the average pairwise difference among individuals (APD; equivalent to population genetics parameter ) within animal species is between 0.0% and 0.5%. The most data are available for modern humans, who have an APD of 0.1% calculated in the same way as for other animals.9

Stoeckle and Thaler recognize the sweeping potential in these patterns: The agreement of barcodes and domain experts implies that explaining the origin of the pattern of DNA barcodes would be in large part explaining the origin of species. Understanding the mechanism by which the near-universal pattern of DNA barcodes comes about would be tantamount to understanding the mechanism of speciation.10

In their evolutionary model, Stoeckle and Thaler invoke two hypotheses account for the barcode cluster patterns: Either 1) COI barcode clusters represent species-specific adaptations, OR 2) extant populations have recently passed through diversity-reducing regimes whose consequences for sequence diversity are indistinguishable from clonal bottlenecks.11

Their conclusion? Modern human mitochondria and Y chromosome [another subset of DNA, but inherited paternally] originated from conditions that imposed a single sequence on these genetic elements between 100,000 and 200,000 years ago.12 In other words, to account for human CO barcode patterns, they favor the second hypothesissome sort of population dynamic (contraction) that reduced the genetic diversity of the population.

Stoeckle and Thaler then extrapolate their conclusions to controversial heights. To justify their extrapolation, they caution that one should not as a first impulse seek a complex and multifaceted explanation for one of the clearest, most data rich and general facts in all of evolution. Then they draw a parallel: The simple hypothesis is that the same explanation offered for the sequence variation found among modern humans applies equally to the modern populations of essentially all other animal species. Namely that the extant population, no matter what its current size or similarity to fossils of any age, has expanded from mitochondrial uniformity within the past 200,000 years.13 In other words, based on mtDNA barcodes, Stoeckle and Thaler claim that the vast majority of species have originated contemporary with modern humans.

Though Stoeckle and Thaler dont perform this step, lets revisit their data and take their results to the next logical conclusion. We can do this because creationists have no problems with the observations that Stoeckle and Thaler describe. Ive already mentioned that my own experience with mtDNA matches theirsbarcodes are a useful first approximation and should be treated as such. Yet this first approximation has revealed a consistent patternlow numbers of mtDNA differences within species and higher numbers of mtDNA differences between species.

Furthermore, since Stoeckle and Thaler explore the origin of individual speciesrather than the origin of whole classification groups, like mammalstheir reasoning applies almost seamlessly to the creationist explanation for the origin of species. Their claim that species arose recently is one that focuses on species within kindsnot one that explores changes from one kind into another. In other words, for Stoeckle and Thalers particular question, evolutionists and creationists agree on the question of common ancestry.

Nevertheless, they differ sharply on the question of timewhen these individual species arose. Unlike Stoeckle and Thaler, creationists invoke not two, but three potential explanations for low numbers of mtDNA sequence differences within species: (1) species-specific adaptations; (2) changing population sizes or past bottlenecks (see especially the discussion of American bison (Bison bison) mtDNA and African buffalo (Syncerus caffer) mtDNA in this paper; (3) time recent origin (e.g., within the last 4,5006,000 years).

We now have two decades worth of direct measurements of the rate at which human mtDNA mutates, and it matches exactly the 6,000-year timescale and rejects the evolutionary timescale (see Genetics Confirms the Recent, Supernatural Creation of Adam and Eve and references therein). Thus, taking Stoeckle and Thalers results to their logical conclusion, we can revise their statement to Modern human [mitochondrial DNA] originated from conditions that imposed a single sequence on these genetic elements14 about 6,000 years ago.

Lets now re-extrapolate these results to other species. The simple hypothesis is that the same explanation offered for the sequence variation found among modern humans applies equally to the modern populations of essentially all other animal species. Namely that the extant population, no matter what its current size or similarity to fossils of any age, has expanded from mitochondrial uniformity within the past 6,000 years.

We can refine this conclusion even more, with more spectacular implications for the creationist model: In the last two decades, the mtDNA mutation rate in a handful of invertebrate species has also been directly measured, and these rates14 are around 10 times higher (or more!) than the human mtDNA mutation rate (again, see this article and references therein). This would imply that multiple species within a genus (or perhaps even a family) have originated within the last 6,000 years.

In other words, these broad mtDNA barcode results suggest that, in general, the predictions15 I made for mtDNA mutation rates in diverse species are likely to be fulfilled. This is good evidence that Darwins ideas are well on their way to being replaced.

As this article was going to press, the theistic evolutionary organization BioLogos posted a critique of Stoeckle and Thalers paper. More specifically, BioLogos posted a critique of creationist responses to Stoeckle and Thaler. BioLogos took strong exception to the type of thesis that I advanced above. For example, consider the following quote from BioLogos: "Did Stoeckel [sic] and Thaler conclude that 90% of animal species appeared at same time as humans? The answer is No [emphasis theirs].

Did I miss a key element of the Stoeckle and Thaler paper?

Lets take a look at the BioLogos article, which was written by PhD biologist and professor Joel Duff. Duff clearly desired to minimize the implications of Stoeckle and Thalers paper. For example, Duff characterized the journal in which it was published as a low-profile Italian journal. He also downplayed the impact, saying that the extended press release didnt generate much reaction inside or outside of the scientific community. More strongly, Duff denounced claims like the one I made above as mischaracterization of the original research. He said it was an incorrect claim that most species originated about the same time.

Why?

To support his assertion, Duff proposed an examination of the original intent of the authors of this paper. Since an authors intent is invisible unless the author clearly states it, Duffs suggested methodology to justify his strong critique is a creative way to tackle a scientific controversy.

After examining Stoeckle and Thalers intent to Duffs satisfaction, Duffs journalism gets more questionable. Weve already examined his emphatic assertion: Did Stoeckel [sic] and Thaler conclude that 90% of animal species appeared at same time as humans? The answer is No. Duff justifies his forceful condemnation with a quote from Stoeckle and Thalers paper: the extant population, no matter what its current size or similarity to fossils of any age, has expanded from mitochondrial uniformity within the past 200,000 years.16 In light of this quote, Duff concludes, In other words, the genetic diversity observed in mitochondrial genomes of most species alive today can be attributed to the accumulation of mutations from an ancestral genome within the past 200,000 years, and Duff asserts that the authors never claim that most species came into existence within the past 200,000 years.

For a critique that began with a proposal to examine intent, Duff seems to have missed the actual intent of the authors. The title of their paper is, Why should mitochondria define species? After discussing and justifying at length the observation that mtDNA differences do, in fact, delineate species, the authors then make a startling statement: The pattern of DNA barcode variance is the central fact of animal life that needs to be explained by evolutionary theory17 [emphasis theirs]. In case the intent of their statement wasnt transparent, the authors make it explicit: The agreement of barcodes and domain experts implies that explaining the origin of the pattern of DNA barcodes would be in large part explaining the origin of species. Understanding the mechanism by which the near-universal pattern of DNA barcodes comes about would be tantamount to understanding the mechanism of speciation.18 They then spend the next chunk of their paper discussing what mtDNA barcodes imply about the mechanism of speciation. Clearly, Stoeckle and Thaler are concerned with much more than just the accumulation of mutations from an ancestral genome within the past 200,000 years. Instead, they have a strong focus on the origin of species.

But did the authors never claim that most species came into existence within the past 200,000 years? In one sense, if we split hairs, Duff is technically correct: In their paper, Stoeckle and Thaler never say so explicitly. Yet as weve just observed, the conclusion about the timing of the origin of species is implied. Furthermore, Thaler makes the conclusion explicit in the press releasethe very one that Duff cited:

Our paper strengthens the argument that the low variation in the mitochondrial DNA of modern humans also explains the similar low variation found in over 90% of living animal specieswe all likely originated by similar processes and most animal species are likely young19. [emphasis added]

How did Biologos miss this?

Duff advances a second argument in his critique of the implications of Stoeckle and Thalers paper. He says that the mtDNA results at best, [tell] us the minimum age of the species. It tells us little to nothing about the maximum age of a species [emphasis his]. For the maximum age, Duff thinks the fossil record is essential. Furthermore, he states that an examination of the mitochondrial genome of any species will only tell us when the common ancestor of all modern members of this species existed, which will almost invariably occur after the evolutionary origin of the species.

But how does Duff know that this is true? Ive already documented that fossils do not directly record genealogical relationships; only DNA does. Why would Duff defer the genealogical question of ancestry (a.k.a. the question of the origin of species) to an indirect field of science (paleontology) when a direct field (geneticsmtDNA) gives a clear answer?

Ive also documented that the process of speciation involves several stepsat a minimum, (1) the formation of one or more distinct individuals, (2) the multiplication of these distinct individuals into a population, and (3) the isolation of this distinct population from the parent species. How does Duff know that the supposed ancestors (recorded by fossils) of modern species were isolated enough from the other populations alive at the time to be called a new species? Duff is trying to win a scientific argument, not by data and by experimentation, but by assertion. This is not a scientific way to resolve the controversy.

BioLogos response is sad, if not ironic. Weve already documented the fact that our evolutionary opponents dont read our literature (Duff included , despite BioLogos professed commitment to dialogue with those who hold other views); yet they call us liars. Sometimes I wonder if they carefully read even the evolutionary literature. Either way, BioLogos main critique (of the implications of Stoeckle and Thalers paper) amounts to misrepresentation and speculation even approaching outright denial. If this is the best that the evolutionary community can do, then perhaps my scientific conclusions (above) are even stronger than they first appear.

Here is the original post:
Hundreds of Thousands of Species in a Few Thousand Years?

New hybrid whale-dolphin discovered in Hawaii

Last year, a team of scientists spotted what they believed was a hybrid animal off the coast of Kauai, Hawaii.A new report from Cascadia Research Collectiveconfirms they did and the new sea creature is the result of a whale and a dolphin mating, the teams head researcher told CBS News.

What the researchers discovered was a hybrid of a melon-headed whale and a rough-toothed dolphin. In an interview with local newspaperThe Garden Island,the head of the project said the discovery is their most unusual finding. We had the photos and suspected it was a hybrid from morphological characteristics intermediate between species, Robin Baird said.

During their two-week project, scientists were able to get a biopsy sample from the creature and study its genetics. They were able to confirm that the animal was a hybrid. Based on the genetics, the father was a rough-toothed dolphin and the mother a melon-headed whale, Baird told CBS News via email.

One of the species that makes up this hybrid is very rare in Hawaii. Melon-headed whales usually dont swim in these waters, so when scientists spotted the whale, they put satellite tags on the animal. During this two-week study, scientists also spotted another rare species in the water, pantropical spotted dolphins, which they also tagged.

Bairds research team is going to be back in Kauais waters next month, when they hope to get more photos of the new hybrid whale-dolphin and water samples. They also hope to do testing on other species in the area.

Were hoping that just by talking to some tour operators and fishermen we might get tips and encounter something like pilot whales, Baird said.

More here:
New hybrid whale-dolphin discovered in Hawaii

TOday’s Movers: Seattle Genetics (NASDAQ:SGEN) Stock …

July 27, 2018 - By Vernon Prom

Investors sentiment increased to 1.61 in Q1 2018. Its up 0.38, from 1.23 in 2017Q4. It is positive, as 24 investors sold Seattle Genetics, Inc. shares while 53 reduced holdings. 31 funds opened positions while 93 raised stakes. 159.52 million shares or 12.47% more from 141.83 million shares in 2017Q4 were reported.

California State Teachers Retirement System reported 165,312 shares. 13,084 are held by Bluecrest Cap Ltd. Pictet Asset invested in 0.1% or 786,323 shares. Swiss Bankshares owns 0.02% invested in Seattle Genetics, Inc. (NASDAQ:SGEN) for 349,100 shares. Keybank National Association Oh invested in 0% or 8,414 shares. 4,998 were accumulated by Shell Asset Mngmt Company. Pnc Financial holds 6,727 shares. Utah Retirement Sys holds 0.02% of its portfolio in Seattle Genetics, Inc. (NASDAQ:SGEN) for 19,600 shares. Wells Fargo And Co Mn, a California-based fund reported 306,681 shares. The Connecticut-based Bridgewater Associate L P has invested 0.01% in Seattle Genetics, Inc. (NASDAQ:SGEN). Amundi Pioneer Asset Management has 21,523 shares. National Bank Of America Corp De accumulated 496,573 shares. Daiwa Securities accumulated 4,395 shares. Zurcher Kantonalbank (Zurich Cantonalbank), Switzerland-based fund reported 23,953 shares. Pub Employees Retirement Association Of Colorado invested in 20,183 shares or 0.01% of the stock.

Since February 1, 2018, it had 3 buys, and 12 sales for $266.62 million activity. Cline Darren S also sold $497,983 worth of Seattle Genetics, Inc. (NASDAQ:SGEN) shares. The insider SIEGALL CLAY B sold 18,832 shares worth $951,393. The insider HIMES VAUGHN B sold 5,000 shares worth $290,604. 10,457 shares were sold by DRACHMAN JONATHAN G, worth $552,452.

JP Morgan now has a $77 target on the $11.55 billion market cap company or 5.51 % upside potential. In analysts note issued to clients on Friday, 27 July, Seattle Genetics (NASDAQ:SGEN) shares have had their Overweight Rating kept by professional analysts at JP Morgan.

Among 8 analysts covering Seattle Genetics (NASDAQ:SGEN), 7 have Buy rating, 0 Sell and 1 Hold. Therefore 88% are positive. Seattle Genetics has $77.0 highest and $60.0 lowest target. $68.13s average target is -6.65% below currents $72.98 stock price. Seattle Genetics had 12 analyst reports since January 31, 2018 according to SRatingsIntel. SunTrust maintained it with Hold rating and $60.0 target in Wednesday, February 7 report. The stock of Seattle Genetics, Inc. (NASDAQ:SGEN) earned Buy rating by Needham on Wednesday, February 7. J.P. Morgan upgraded the shares of SGEN in report on Wednesday, February 14 to Buy rating. The rating was maintained by Morgan Stanley on Wednesday, March 21 with Overweight. The firm has Buy rating by RBC Capital Markets given on Tuesday, March 20. The firm has Buy rating given on Monday, June 11 by SunTrust. The company was maintained on Wednesday, February 7 by H.C. Wainwright. On Thursday, February 1 the stock rating was maintained by H.C. Wainwright with Buy. The stock of Seattle Genetics, Inc. (NASDAQ:SGEN) has Neutral rating given on Wednesday, February 7 by Bank of America. The firm has Overweight rating by JP Morgan given on Wednesday, February 14.

The stock increased 2.43% or $1.73 during the last trading session, reaching $72.98. About 1.60M shares traded or 72.55% up from the average. Seattle Genetics, Inc. (NASDAQ:SGEN) has declined 15.50% since July 28, 2017 and is downtrending. It has underperformed by 28.07% the S&P500.

Seattle Genetics, Inc., a biotechnology company, develops and commercializes targeted therapies to treat cancer worldwide. The company has market cap of $11.55 billion. It markets ADCETRIS, an antibody-drug conjugate for relapsed Hodgkin lymphoma and relapsed systemic anaplastic large cell lymphoma. It currently has negative earnings. The firm also develops SGN-CD33A that is in Phase III clinical trial to evaluate SGN-CD33A in combination with hypomethylating agents in previously untreated older patients, as well as in Phase 1/2 clinical trial for patients with relapsed or refractory acute myeloid leukemia ; ASG-22ME, which is in Phase I clinical trial for Nectin-4-positive solid tumors, including bladder cancer; SGN-LIV1A that is in Phase 1 clinical trial for patients with LIV-1-positive metastatic breast cancer; and SGN-CD19A, which is in Phase II clinical trial for patients with relapsed DLBCL, as well as in Phase II trial for patients with newly diagnosed DLBCL.

More notable recent Seattle Genetics, Inc. (NASDAQ:SGEN) news were published by: Streetinsider.com which released: Seattle Genetics (SGEN) Adcetris On-going Launch in 1L cHL is Positive Says SunTrust. on July 02, 2018, also Benzinga.com with their article: Benzingas Daily Biotech Pulse: Biogen, AC Immune Slip Despite Positive Trials, Sarepta Slapped With Clinical Hold published on July 26, 2018, Seekingalpha.com published: Mid-stage study underway for Seattle Genetics tisotumab vedotin in solid tumors; shares up 1% premarket on July 12, 2018. More interesting news about Seattle Genetics, Inc. (NASDAQ:SGEN) were released by: Seekingalpha.com and their article: Dont Sell Axon Enterprise Cramers Lightning Round (7/11/18) published on July 12, 2018 as well as Benzinga.coms news article titled: Benzingas Daily Biotech Pulse: Achaogen To Trim Workforce By 28%, Amgens Beat-And-Raise Quarter with publication date: July 27, 2018.

Receive News & Ratings Via Email - Enter your email address below to receive a concise daily summary of the latest news and analysts' ratings with our FREE daily email newsletter.

Go here to read the rest:
TOday's Movers: Seattle Genetics (NASDAQ:SGEN) Stock ...

Seattle Genetics (SGEN) "Buy" Rating Reaffirmed Today By H …

July 27, 2018 - By Mona Holcomb

Investors sentiment increased to 1.61 in Q1 2018. Its up 0.38, from 1.23 in 2017Q4. It is positive, as 24 investors sold Seattle Genetics, Inc. shares while 53 reduced holdings. 31 funds opened positions while 93 raised stakes. 159.52 million shares or 12.47% more from 141.83 million shares in 2017Q4 were reported.

Pub Employees Retirement Association Of Colorado holds 20,183 shares. Jgp Global Gestao De Recursos Ltda reported 22,334 shares or 0.47% of all its holdings. Jane Street Gru Limited Company invested in 3,903 shares or 0% of the stock. Prudential Fincl, New Jersey-based fund reported 6,451 shares. 7,900 were reported by Ellington Management Grp. Caisse De Depot Et Placement Du Quebec reported 5,300 shares or 0% of all its holdings. D E Shaw & stated it has 168,554 shares. Td Asset owns 0.01% invested in Seattle Genetics, Inc. (NASDAQ:SGEN) for 154,016 shares. Virtu Fincl Ltd Liability Corporation reported 10,922 shares stake. Stratos Wealth Limited holds 0% of its portfolio in Seattle Genetics, Inc. (NASDAQ:SGEN) for 1,213 shares. World Asset Inc stated it has 3,870 shares. State Of Alaska Department Of Revenue reported 9,710 shares stake. Franklin Res has 108,400 shares for 0% of their portfolio. Zurcher Kantonalbank (Zurich Cantonalbank) owns 23,953 shares. 205,300 are owned by California Pub Employees Retirement.

Since February 1, 2018, it had 3 insider buys, and 12 insider sales for $266.62 million activity. $936,818 worth of stock was sold by SIEGALL CLAY B on Friday, February 9. On Thursday, March 15 HIMES VAUGHN B sold $290,604 worth of Seattle Genetics, Inc. (NASDAQ:SGEN) or 5,000 shares. On Wednesday, May 9 the insider Cline Darren S sold $497,983. DRACHMAN JONATHAN G sold $552,452 worth of stock or 10,457 shares.

EU: In an analyst report issued to investors and clients on 27 July, H.C. Wainwright reiterated their Buy rating on Seattle Genetics (SGEN) shares. They now have a $98.0 target price on the firm. H.C. Wainwrights target indicates a potential upside of 37.54 % from the companys last price.

The stock increased 2.04% or $1.45 during the last trading session, reaching $72.7. About 995,861 shares traded or 7.56% up from the average. Seattle Genetics, Inc. (SGEN) has declined 15.50% since July 27, 2017 and is downtrending. It has underperformed by 28.07% the S&P500.

Seattle Genetics, Inc., a biotechnology company, develops and commercializes targeted therapies to treat cancer worldwide. The company has market cap of $11.50 billion. It markets ADCETRIS, an antibody-drug conjugate for relapsed Hodgkin lymphoma and relapsed systemic anaplastic large cell lymphoma. It currently has negative earnings. The firm also develops SGN-CD33A that is in Phase III clinical trial to evaluate SGN-CD33A in combination with hypomethylating agents in previously untreated older patients, as well as in Phase 1/2 clinical trial for patients with relapsed or refractory acute myeloid leukemia ; ASG-22ME, which is in Phase I clinical trial for Nectin-4-positive solid tumors, including bladder cancer; SGN-LIV1A that is in Phase 1 clinical trial for patients with LIV-1-positive metastatic breast cancer; and SGN-CD19A, which is in Phase II clinical trial for patients with relapsed DLBCL, as well as in Phase II trial for patients with newly diagnosed DLBCL.

More notable recent Seattle Genetics, Inc. (NASDAQ:SGEN) news were published by: Streetinsider.com which released: Seattle Genetics (SGEN) Adcetris On-going Launch in 1L cHL is Positive Says SunTrust. on July 02, 2018, also Seekingalpha.com with their article: Dont Sell Axon Enterprise Cramers Lightning Round (7/11/18) published on July 12, 2018, Seekingalpha.com published: Mid-stage study underway for Seattle Genetics tisotumab vedotin in solid tumors; shares up 1% premarket on July 12, 2018. More interesting news about Seattle Genetics, Inc. (NASDAQ:SGEN) were released by: Benzinga.com and their article: Benzingas Daily Biotech Pulse: Biogen, AC Immune Slip Despite Positive Trials, Sarepta Slapped With Clinical Hold published on July 26, 2018 as well as Benzinga.coms news article titled: Benzingas Daily Biotech Pulse: Achaogen To Trim Workforce By 28%, Amgens Beat-And-Raise Quarter with publication date: July 27, 2018.

Receive News & Ratings Via Email - Enter your email address below to receive a concise daily summary of the latest news and analysts' ratings with our FREE daily email newsletter.

Read the original:
Seattle Genetics (SGEN) "Buy" Rating Reaffirmed Today By H ...

The Genetics Of Becoming An Ant Queen – sciencefriday.com

Clonal raider ants carrying and grooming larvae. Ants were tagged with colored dots to allow for behavioral observation. Credit: Daniel Kronauer

Many ant species have a queen, the member of the colony that lays eggs. The rest of the ants are divided into different roles that support the queen and the colony. So what ants become queens versus workers? Scientists found that the gene ilp2 that regulates insulin played a role in determining what ant becomes the queen. Their results were published in the journal Science.

[What is the origin of the word quark? Well, let us tell you the tale of particle physics, Aristotle, and James Joyce]

Biologist Ingrid Fetter-Pruneda, an author on that study, talks about how this gene works in determining a queen and what this can tell us about the evolution of societies in insects and beyond.

Continued here:
The Genetics Of Becoming An Ant Queen - sciencefriday.com

LR hospital hires cancer institute chief – arkansasonline.com

The outgoing director of the Winthrop P. Rockefeller Cancer Institute at the University of Arkansas for Medical Sciences has accepted a job at CHI St. Vincent.

Dr. Peter Emanuel turned in his resignation letter on May 4. His last day at UAMS is Tuesday.

Emanuel, 59, will join CHI St. Vincent on Sept. 1, according to a statement from the hospital. His position was not specified.

At the time of his resignation, he declined to give the reason for his departure, only citing unspecified challenges. He could not be reached for comment Friday afternoon.

UAMS is conducting a national search for a new cancer institute director, said Leslie Taylor, vice chancellor of communications and marketing. Dr. Laura Hutchins was appointed interim director in June. Hutchins is a professor in the College of Medicine Division of Hematology/Oncology, where she was division director from 1998 until September 2013.

Emanuel is a widely recognized expert in leukemia and lymphoma, a UAMS website states. He joined UAMS in 2007 after leaving the University of Alabama at Birmingham, where he was a professor of medicine, genetics and biochemistry.

From 2004 to 2006 he was the acting director of the National Cancer Institute-designated Comprehensive Cancer Center at the Alabama university.

During his time at UAMS, he oversaw the addition of the cancer institute's 12-story research and treatment tower, which opened in 2010. His annual salary was $500,000.

His resignation in May followed UAMS' decision to temporarily suspend its cardiac surgery program due to lead surgeon Dr. Gareth Tobler's retirement. That program restarted at the beginning of July, with the hospital contracting with four new physicians.

UAMS also laid off almost 260 employees in January to curb an anticipated $72.3 million deficit. Those layoffs included one full-time physician -- a general ear, nose and throat doctor who did not work at the cancer institute.

News of Emanuel's new role comes one day after an invoice that his wife, Carla Emanuel, sent seeking reimbursement from the Winthrop P. Rockefeller Cancer Institute became public.

The $4,000 bill lists events that she attended, phone calls she made and work she did to resolve problems with donors. Taylor said UAMS was not going to pay the bill because state procedures regarding vendors and invoices were not followed.

Taylor added that the invoice was the first one she was aware of from a spouse, and the institution does not normally reimburse people for attending fundraising events.

The Arkansas Times first reported on the invoice on Thursday.

Metro on 07/28/2018

See the article here:
LR hospital hires cancer institute chief - arkansasonline.com

Genetics | Children’s Hospital of Pittsburgh

The Division of Medical Genetics at UPMC Children's Hospital of Pittsburgh is committed to the treatment and study of genetic disorders in children, providing advanced patient care of the highest quality and an active research program dedicated to providing a deeper understanding of the fundamental issues underlying these disorders and developing better therapeutic approaches.

Clinical services, a critical part of the comprehensive care offered by the Division of Medical Genetics, include diagnosis, evaluation, treatment and management of a range of genetic conditions, such as birth defects, chromosomal abnormalities, specific genetic syndromes and inborn errors of metabolism. These services are organized under two programs:an Inborn Errors of Metabolism Clinic and a General Genetics Clinic. Both offer an experienced team of faculty and staff, including physician geneticists, genetic counselors, a nurse practitioner, metabolic dietitian and social worker.

The Inborn Errors of Metabolism Clinic at Childrens Hospital provides diagnostic services, evaluation, treatment management, genetic counseling and other support to children with these inherited disorders and to their families. A Phenylketonuria Clinic specializes in the diagnosis, treatment and management of one of the most common inborn errors of metabolism.

Counseling, education and other support services to address all of the needs of patients and their families are also provided. Genetic counselors are available to help to identify families at risk, serve as patient advocates, help families understand genetic disorders and their consequences, provide supportive counseling and counsel families who may be at risk for inherited conditions. Division staff members also help families arrange for physical, occupational and speech therapists, comprehensive developmental assessments and other services and support.

Research within the division is providing new insight into genetic disorders from which new and better therapies can be developed. The laboratory research program focuses on discovering the underlying causes of genetic diseases, understanding the clinical implications of mutations in genes, and development of novel approaches for treatment of genetic disorders. An active clinical research program collaborates with other genetic programs world wide to evaluate new therapies for genetic disease.

Referrals from primary care physicians, medical and social agencies or other Childrens Hospital specialty services are helpful, but not necessary. Authorization from the patients insurance provider and/or primary care physician may be needed for insurance coverage. The Division of Medical Genetics staff can help with these matters. Medical records from previous medical evaluations may be requested. For more information, please call the office number listed.

Read more here:
Genetics | Children's Hospital of Pittsburgh