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Fluidigm (FLDM) Licenses CFTR Assay From Baylor Genetics – Zacks.com

South San Francisco, CA-based Fluidigm Corporation , a leading player in the analysis of single cells and industrial application of genomics, recently announced that it has entered into a licensing agreement with Baylor Genetics.

Per the agreement, Fluidigm licensed the rights to commercialize the CFTR (cystic fibrosis transmembrane conductance regulator) library prep assay developed by Baylor Genetics for research purposes. This would be used with its proprietary Juno automated microfluidic system. The targeted library prep assay enables accurate identification of variants from each of the 27 exons in the CFTR gene and selected intronic regions. When combined with Fluidigm microfluidics, this solution has the potential to significantly simplify complex labor-intensive laboratory workflows and improve the efficiency of CFTR sequencing. This would invariably improve the efficiency of its Juno automated microfluidic system and help the company to capture a considerable market share.

Next-generation sequencing offers a more comprehensive approach to CFTR genetic analysis by allowing a complete view of the sequence. Targeted sequencing library prep workflows, however, can be very labor-intensive. With the application of Fluidigm automated microfluidics technology, library preparation can be streamlined to provide significant efficiencies.

Over the past one month, Fluidigm has underperformed the broader industry. The stock has shed 7.1%, compared with the industrys decline of 3.1%.

Fluidigm develops, manufactures and markets life science analytical and preparatory systems for markets such as mass cytometry, high-throughput genomics, and single cell genomics. The company caters to leading academic institutions, clinical research laboratories and pharmaceuticals, biotechnology and agricultural biotechnology companies worldwide.

Zacks Rank & Key Picks

Currently, Fluidigm has a Zacks Rank #3 (Hold). A few better-ranked medical stocks are Edwards Lifesciences Corp. (EW - Free Report), Lantheus Holdings, Inc. (LNTH - Free Report) and Align Technology, Inc. (ALGN - Free Report). Edwards Lifesciences and Align Technology sport a Zacks Rank #1 (Strong Buy), while Lantheus Holdings carries a Zacks Rank #2 (Buy). You can see the complete list of todays Zacks #1 Rank stocks here.

Edwards Lifesciences has a long-term expected earnings growth rate of 15.2%. The stock has gained around 3.2% over the last three months.

Lantheus Holdings has a long-term expected earnings growth rate of 12.5%. The stock has gained 66.1% over the last six months.

Align Technology has a long-term expected earnings growth rate of 26.6%. The stock has rallied roughly 29.6% over the last three months.

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Fluidigm (FLDM) Licenses CFTR Assay From Baylor Genetics - Zacks.com

EXCLUSIVE: ‘Grey’s Anatomy’s’ Giacomo Gianniotti Talks Jo and DeLuca: ‘I See Them Having a Relationship’ – Entertainment Tonight

Greys Anatomy star Giacomo Gianniotti is hopeful that Dr. Andrew DeLuca will see happier days in the halls of Grey Sloan Memorial Hospital.

The 28-year-old actor discussed the future of the love triangle his character is currently entangled in with Jo (Camilla Luddington) and her ex, Alex (Justin Chambers). Over the course of the last season, DeLuca began developing strong feelings for Jo, and it appears theres a very real possibility for a deeper connection between the two doctors.

DeLucas attempts to confess his feelings to Jo havent gone so well for him, Gianniotti recently told ET. But personally speaking, I think he jumped the gun a little bit. Shes fresh out of this relationship [with Alex]. I think she just needs a little time to process everything. Its not necessarily that she doesnt have interest and feelings for DeLuca, but she needs some space.

RELATED: 'Grey's Anatomy' Casts DeLuca's Sister for Season 14

They were great friends before and confidantes during a traumatic moment in her life, he added. Theres definitely bonding that happened there regardless. I see them having some kind of a relationship, whether its love or friends.

Adding a wrinkle to Jo and DeLucas blossoming relationship is the return of Jos estranged husband, Dr. Paul Stadler (Matthew Morrison), whom viewers met briefly when Alex tailed him at a Seattle medical conference. Though Gianniotti remained mum when it came to specifics about Stadlers reappearance, which Morrison hinted would be a big role.

I think its a great storyline to explore, Gianniotti said of Morrisons reprisal. We saw him and his existence outside of Seattles Grey Sloan, so if he comes into our world, thats a whole other thing. Thats him meeting the other doctors. Thats him being involved in the lives of everybody, not just Jo, so it definitely raises the stakes having him around in that capacity.

As for DeLuca and Maggies (Kelly McCreary) short-lived romance, Gianniotti says that nothing on Greys is simple -- and he prefers it that way.

RELATED: 'Grey's Anatomy' Cast Kicks Off Season 14 With First Table Read

Its complicated is such a great way to describe a lot of the relationships on Greys Anatomy, he said. We didnt really get much closure, but theyve gotten to the point where they can work together and be in the same room and be cool. But yeah, theres definitely some things left unsaid on both sides.

But Gianniotti promises there will be real closure for the two, romantically, in the new season: We might see a resolution, but it might not be a resolution that you guys thought or hoped for. Its gonna be comical more than dramatic.

He also spoke about the show reaching the impressive 300th episode milestone, which will air as the seventh installment in season 14.

I dont see [the show] stopping anytime soon. The show is still growing very strong, he said, noting that Greys added new producers, new writers this season for a fresh take. Its going to be funnier and sexier and lighter. Were still going to give you the drama. Youre still going to need that tissue box, for sure, but we want our audience to have a little bit more fun this season and enjoy some of our characters being happy.

Greys Anatomy kicks off season 14 with a two-hour premiere on Thursday, Sept. 28 at 8 p.m. ET/PT on ABC.

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EXCLUSIVE: 'Grey's Anatomy's' Giacomo Gianniotti Talks Jo and DeLuca: 'I See Them Having a Relationship' - Entertainment Tonight

New ‘Grey’s Anatomy’ Season 14 Photo Will Keep Fans Guessing – People’s Choice

Johnni Macke 11:17 am on August 17, 2017

(Photo Courtesy: ABC)

The stars ofGreys Anatomy have been teasing the upcoming season since the beginning of August, and now the production team behind the amazing medical drama is jumping in on the fun by giving fans a first look at whats coming up.

While the cast members who make up everyones favorite TV doctors (including Ellen Pompeo, Jesse Williams, Sarah Drew, and more) have been reuniting and sharing on-set pictures for weeks, Shondaland TV (aka Shonda Rhimes production company) has been keeping the new season under wrapsuntil now!

Whos excited for the 14th season of #GreysAnatomy? #shondaland, the production company wrote on Instagram on Wednesday (Aug. 16), along with a behind-the-scenes first look at scene from the new season.

Besides confirming that filming for season 14 is well underway, the photo gives fans a glimpse at a scene from the upcoming two-hour premiere episode while offering just enough clues to keep fans guessing about whats really going on in the scene in question.

In the photo, we can see that there are three people lined up at the hospital (one of whom appears to be Meredith Grey?). Are 0ur favorite docs presenting a united front? Or are we actually looking at a new batch of interns? More importantly, why isnt anyone wearing a lab coat? The photo purposefully keeps things vague.

According to the slate seen in the pic, episode will be directed by Debbie Allen (who has acted on the series since 2011). The premiere will mark the 15th episode shes directed for the series to date.

As previously reported, Greys alum, Krista Vernoff, who is returning to the series as itsshowrunner, wrote the season 14 premiere episode, so clearly there is a LOT of star power both in front of the camera and behind it for this kickoff episode.

Greys Anatomy returns with a two-hour premiere for its 14th season on September 28, 2017 at 8 p.m. on ABC.

For the latest pop culture news and voting, make sure to sign up for the Peoples Choice newsletter!

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New 'Grey's Anatomy' Season 14 Photo Will Keep Fans Guessing - People's Choice

New Magic Mushrooms Discovery Could Reveal How to Make Your Own Drugs – Newsweek

Scientists have long wondered how and why magic mushrooms create psilocybin, a psychoactive chemical that causes hallucinations when ingested. Two new papers published this month provide some answers, one of which paves the way for an easier way to create the psychedelic compound.

Around 200 types of mushrooms produce psilocybin, and theyve been used ceremonially for millennia. Since trip-inducing fungi were introduced to Western audiences by financier and author Gordon Wasson in a Life magazine article in 1957, people have been using them for recreational purposes throughout the world. Albert Hofmann, the Swiss chemist who synthesized LSD, identified psilocybin as the active ingredient in magic mushrooms and determined its structure in 1959. At that time, he also figured out how to synthesize it using biochemistry.

However, nobody knewuntil nowhow mushrooms themselves make psilocybin. In a study published in the journal Angewandte Chemie, Dirk Hoffmeister and colleagues sequenced and mapped the genes in the magic mushroom Psilocybe cubensis. Scientists have known for a while that these genes produce several enzymes that combine to create psilocybin, but nobody knew the sequence and order of this seemingly mystical process. Through a series of trial-and-error type tests, Hoffmeister and colleagues figured out the correct order. There was some Wow! in the air when the team finally figured it out, says Hoffmeister, with the University of Jena in Germany.

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One of the most surprising findings is the simplicity of the process, says David Sherman, a medicinal chemist at the University of Michigan who wasnt involved in the paper. In only five steps, the mushrooms enzymes convert tryptophan, a widely occurring amino acid (a building block of protein) into psilocybin.

The paper could pave the way for people without advanced knowledge to produce psilocybin on their own, using commercially available synthetic biology kits, Sherman says.

Magic mushrooms, pictured here in Amsterdam, create the psychedelic psilocybin in an "elegant" process. Jerry Lampen / REUTERS

Hoffmeister says the finding could theoretically make the mass-production of psilocybin easier and less expensive, though he expects it will take quite some effort until we make headway. He also notes that this scientific study was done for the purpose of better understanding natures elegant way of making psilocybin, and is not intended as a drug endorsement or "get-high-quick" kind of thing. Using naturally occurring enzymes would avoid the expensive and difficult biochemical tools currently required to make the compound.

In another study published this month in the online journal bioRXiv, though not yet peer-reviewed, researchers sequenced genomes from three different mushroom species and found the cluster of psilocybin-producing genes in each. The way the small cluster apparently traveled between species, without alteration, suggests that it was passed through a peculiar process called horizontal gene transfer. In this process, a gene can literally move between different species by physical contact, Sherman explains. This transfer could have happened when, for example, a spore of a psilocybin-producing mushroom physically landed on top of another mushrooms species, and was incorporated into its genome, Sherman says. Because the gene cluster is so small, it can be absorbed and then passed on.

Sherman says horizontal gene transfer of psilocybin-producing genetic bits still happens and will likely enable more mushrooms to produce this psychedelic compound.

Its wide distribution in unrelated species and endurance over time suggests thatthe psilocybin gene may give mushrooms a survival advantage, says Jason Slot, an assistant Professor at the Ohio State University and study lead author. Other research shows that psilocybin confuses predators by mimicking the neurotransmitter serotonin, and that its effects in humans is an coincidental byproduct of this ability.

Sherman marveled at how simple it is for mushrooms to make psilocybin, especially considering many useful compounds like antibioticsderived from fungi and bacteriatake more than 50 steps. Mother nature makes it quite elegantly, Hoffmeister says.

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New Magic Mushrooms Discovery Could Reveal How to Make Your Own Drugs - Newsweek

Allahabad University’s aging-related studies to be showcased in international meet – Hindustan Times

A team of scientists at the Allahabad University engaged in finding clues to brain ageing and devising anti-ageing strategies is getting international recognition.

Three scientists from AUs biochemistry department, who are a part of the study team led by Prof SI Rizvi, have been invited by the International Society of Neurochemistry to present their findings at the meeting of the European Society for Neurochemistry to be held in Paris (France) from August 20-24.

Abhishek Kumar Singh, a Kothari fellowship awardee, would present his research findings on the anti-aging effect of a compound rapamycin on rat brain through activation of a mechanism based on self-destruction of cells, scientifically known as autophagy.

Another researcher Sandeep Singh is slated to showcase his research findings on the use of a compound spermidine which is a caloric restriction mimetic.

Caloric restriction is a strategy to enhance lifespan by reducing food intake.

Since the strategy is difficult to implement on humans, scientists find ways to mimic this effect through specific drugs. Spermidine is one such drug which is being tested by the research team.

Researcher Geetika Garg will present her findings on possible anti-aging effect of whey protein. Recent scientific evidence has shown that whey comprising of protein obtained after milk is made into curd, has an abundance of sulphur containing amino acids which can be beneficial for human health, especially during the old age.

Whey contains an amino acid cysteine which is not only an important constituent of proteins but is also important for the formation of an antioxidant molecule glutathione in the human cell, she said.

Glutathione is the most abundant antioxidant in the body that protects us from damage due to toxins and free radicals. It is found in the highest concentration in brain and liver, Geetika explained.

During aging, the capacity of red blood cells to transport cysteine to all parts of the body decreases. This results in deficiency of cysteine for the synthesis of glutathione which makes the body prone to damages caused by oxidative stress leading to aging. A high cysteine diet can offset these alterations since the red blood cells would then transport more cysteine to other cells of the body, she said.

Our research findings opens up new strategy for formulation of anti-aging food supplementations based on high cysteine intake, Geetika added.

The three scholars have been given fellowships from International Society of Neurochemistry and department of science and technology, Government of India.

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Allahabad University's aging-related studies to be showcased in international meet - Hindustan Times

Linking seizures, heart health and sleeping sickness to bacteria and shape-shifting parasites in the mouth and gut – UB News Center

BUFFALO, N.Y. Four studies focused on improving ourunderstanding of the human genome and microbiome were awardedfunding through the third round of research pilots supported by theUniversity at Buffalos Community of Excellence in Genome,Environment and Microbiome (GEM).

The projects, which total $150,000, will study how therelationship between the human body and the collection ofmicroorganisms that reside on or within it affect our risk forcertain diseases.

Understanding the connection these microorganisms have with ourbodies may enable the development of precision medicine and empowerindividuals to have greater control over their health.

The pilot grants award researchers from a variety of disciplinesup to $50,000 to develop innovative projects focused on themicrobiome. The funds support up to one year of research.

The awards are provided through GEM, an interdisciplinarycommunity of UB faculty and staff dedicated to advancing researchon the genome and microbiome. GEM is one of UBs threeCommunities of Excellence, a $9 million initiative to harness thestrengths of faculty and staff from fields across the university toconfront the challenges facing humankind through research,education and engagement.

Changes in the genome our own or those of themicrobes in, on or around us have a tremendous impact onhuman health and our environment, says Jennifer Surtees,PhD, GEM co-director and associate professor in the Department ofBiochemistry in the Jacobs School of Medicine and BiomedicalSciences at UB.

With these newest projects, UB scientists from acrossdisciplines have come together to dig deeper into these changes andto help establish the infrastructure necessary for advancedprecision medicine.

Along with Surtees, GEM is led by Timothy Murphy, MD, executivedirector and SUNY Distinguished Professor in the UB Department ofMedicine; and Norma Nowak, PhD, co-director, professor in theDepartment of Biochemistry, and executive director of UBsNew York State Center of Excellence in Bioinformatics and LifeSciences.

The funded projects involve faculty teams from the Jacobs Schoolof Medicine and Biomedical Sciences, the UB School of Public Healthand Health Professions, and the UB School of Dental Medicine.

Can organisms in the gut increase vulnerability toseizures?

Inflammation in the central nervous system can increasesusceptibility to seizures.

Given the role that the intestinal microbiome plays in shapinginflammation in the body, UB researchers believe that the tinyorganisms may have an impact on the onset, strength and duration ofseizures.

The study, led by Ira J. Blader, PhD, professor in the UBDepartment of Microbiology and Immunology, and Alexis Thompson,PhD, senior research scientist in the UB Research Institute onAddictions, will examine in mice the composition of the microbiomeand which of its components affect seizures.

If correct, this may suggest the gut microbiome as a therapeutictarget for the treatment of seizures and epilepsy.

Researchers lay groundwork for UB genomic research with SpitFor Buffalo

To better understand how the human genome and microbiomeinteract to influence health, UB researchers will establish SpitFor Buffalo, a project that will collect DNA samples from volunteerUBMD patients for use in future studies.

The researchers will collect saliva samples, anonymously linkthe samples to each patients electronic medical record, andsequence the genome and oral microbiome. By determining which genesare associated with which diseases, new connections betweenspecific genes and diseases will be made.

Samples are currently being collected from patients in the UBMDNeurology, Internal Medicine and OBGYN clinics in the ConventusCenter For Collaborative Medicine.

The project will provide an infrastructure resource for genomeand microbiome investigations at UB.

The research is led by Richard M. Gronostajski, PhD, professorin the Department of Biochemistry and director of both the WNY StemCell Culture and Analysis Center and the Genetics, Genomics andBioinformatics Graduate Program; Gil I. Wolfe, MD, professor andIrvin and Rosemary Smith Chair of the UB Department of Neurology;Michael Buck, PhD, associate professor in the Department ofBiochemistry and director of the WNY Stem CellSequencing/Epigenomics Center; and Nowak.

Solving how RNA provides a parasite with shape-shiftingabilities

The parasite Trypanosoma brucei, the cause of HumanAfrican Trypanosomiasis commonly known as sleeping sickness radically alters its physiology and morphology as it movesbetween insect and mammal over the course of its life cycle.

These changes, researchers found, are caused by various RNAbinding proteins, allowing the organism to survive in environmentsthat range from the human bloodstream to the insect gut. UBresearchers will examine how these proteins regulate theparasites transformations.

The study is led by Laurie K. Read, PhD, professor in theDepartment of Microbiology and Immunology; and Jie Wang, PhD,research assistant professor in the Department of Biochemistry.

Pinpointing the potential effects of oral and gut bacteria onheart health

UB researchers will investigate the connection between oral andgut bacteria and the onset and progression of atheroscleroticcardiovascular disease (CVD), or the buildup of plaque around theartery walls, eventually blocking blood flow.

The study will seek to understand how the microbes in the bodycontribute to plaque formation in the arteries, providing the basisfor interventions that reduce the effects of the microorganisms onCVD.

Previous studies have found microbes present in arterialplaques, but have not provided conclusive links to the parts of thebody where the microbes originate. Researchers will usenext-generation sequencing and advanced bioinformatics analysismethods to identify and characterize microorganisms in the arterywalls and compare the bacteria with those present in oral, gut andskin microbiomes.

Environmental factors such as smoking, blood cholesterol andperiodontal disease status will also be examined as potentialfactors that influence the bacteria-CVD relationship.

The research is led by Robert J. Genco, DDS, PhD, SUNYDistinguished Professor in the UB Department of Oral Biology andDepartment of Microbiology and Immunology, and director of the UBMicrobiome Center; and Michael J. LaMonte, PhD, research associateprofessor in the UB Department of Epidemiology and EnvironmentalHealth.

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Linking seizures, heart health and sleeping sickness to bacteria and shape-shifting parasites in the mouth and gut - UB News Center

Peroxisomes identified as ‘fighters’ in the battle against bacterial infections – Medical Xpress

Research associate Francesca Di Cara (front), associate professor Andrew Simmonds and Richard Rachubinski, professor and chair of the Department of Cell Biology, discovered that peroxisomes are necessary for proper functioning of the innate immune system. Credit: Melissa Fabrizio

A new addition to the fight against bacteria comes in the unlikely form of an organelle that previously had no link to the immune response. University of Alberta researchers have found that peroxisomes are required for cells in the innate immune response to bacteria and fungi.

The discovery was first made in fruit flies. Research Associate Francesca Di Cara, together with Richard Rachubinski, professor and chair of the Department of Cell Biology, and Andrew Simmonds, cell biology associate professor, partnered to create fruit flies that could be used specifically for studying peroxisomal disorders, which are rare genetic diseases affecting humans.

Di Cara found that peroxisomes are necessary for proper functioning of the innate immune system, the body's first line of defense against microorganisms. The innate immune system is an ancient system of immunity that identifies, captures and processes a pathogen, and then presents it to the acquired immune system.

The peroxisomes also communicate to other organs that there is an infection. The team discovered that when the organelle's basic function is altered, this communication is lost and the organism does not fight the bacteria.

"Understanding how the body fights infection has an impact on human health," says Di Cara. "We have to understand who the 'fighters' in the organism are before we can identify what's failing in the battle against bacterial infections."

Peroxisomes are 'chemical factories' that process complex fat molecules into simple forms and modify reactive oxygen molecules, which together act to signal to cells and tissues to respond appropriately to changes in their environment.

Along with their collaborator Nancy Braverman from McGill University, the researchers used a mouse model to confirm that what they observed in the flies also occurred in a mammalian system.

"To find organelles like peroxisomes that had no link whatsoever to fighting bacterial infections was a critical discoveryit will help expand the roles of what this important organelle does in innate immunity against bacterial and fungi, and its involvement in viral signaling and the lethal peroxisome genetic diseases," says Rachubinski. "As the threat of bacterial infections continues to grow, this discovery can help move our understanding of immunity forward."

The work was recently published in Immunity.

Explore further: Drosophila innate immunity: Another piece to the puzzle

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Peroxisomes identified as 'fighters' in the battle against bacterial infections - Medical Xpress

Two-step process leads to cell immortalization and cancer – Medical Xpress

Human chromosomes (grey) capped by telomeres (white). Credit: PD-NASA; PD-USGOV-NASA

A mutation that helps make cells immortal is critical to the development of a tumor, but new research at the University of California, Berkeley suggests that becoming immortal is a more complicated process than originally thought.

The key to immortalization is an enzyme called telomerase, which keeps chromosomes healthy in cells that divide frequently. The enzyme lengthens the caps, or telomeres, on the ends of chromosomes, which wear off during each cell division.

When the telomeres get too short, the ends stick to one another, wreaking havoc when the cell divides and in most cases killing the cell. The discovery of telomerase and its role in replenishing the caps on the ends of the chromosomes, made by Elizabeth Blackburn and Carol Greider at UC Berkeley and John Szostak at Harvard University in the 1980s, earned them a Nobel Prize in Physiology or Medicine in 2009.

Because telomeres get shorter as cells age, scientists theorized that cancer cells - which never age - become immortalized by turning on production of telomerase in cells that normally don't produce it, allowing these cells to keep their long telomeres indefinitely. An estimated 90 percent of all malignant tumors use telomerase to achieve immortality, and various proposed cancer therapies focus on turning down the production of telomerase in tumors.

The new research, which studied the immortalization process using genome-engineered cells in culture and also tracked skin cells as they progressed from a mole into a malignant melanoma, suggests that telomerase plays a more complex role in cancer.

"Our findings have implications for how to think about the earliest processes that drive cancer and telomerase as a therapeutic target. It also means that the role of telomere biology at a very early step of cancer development is vastly underappreciated," said senior author Dirk Hockemeyer, a UC Berkeley assistant professor of molecular and cell biology. "It is very likely that what we find in melanoma is true for other cancer types as well, which would warrant that people look more carefully at the role of early telomere shortening as a tumor suppressing mechanism for cancer."

The results will be reported online August 17 as a "first release" publication from the journal Science.

From nevus to cancer

Hockemeyer and his UC Berkeley colleagues, in collaboration with dermatopathologistBoris Bastian and his colleagues at UCSF, found that immortalization is a two-step process, driven initially by a mutation that turns telomerase on, but at a very low level. That mutation is in a promoter, a region upstream of the telomerase gene - referred to as TERT - that regulates how much telomerase is produced. Four years ago, researchers reported that some 70 percent of malignant melanomas have this identical mutation in the TERT promoter.

The TERT promoter mutation does not generate enough telomerase to immortalize the pre-cancerous cells, but does delay normal cellular aging, Hockemeyer said, allowing more time for additional changes that turns telomerase up. He suspects that the telomerase levels are sufficient to lengthen the shortest telomeres, but not keep them all long and healthy.

If cells fail to turn up telomerase, they also fail to immortalize, and eventually die from short telomeres because chromosomes stick together and then shatter when the cell divides. Cells with the TERT promoter mutation are more likely to up-regulate telomerase, which allows them to continue to grow despite very short telomeres.

Yet, Hockemeyer says, telomerase levels are marginal, resulting is some unprotected chromosome ends in the surviving mutant cells, which could cause mutations and further fuel tumor formation.

"Before our paper, people could have assumed that the acquisition of just this one mutation in the TERT promoter was sufficient to immortalize a cell; that any time when that happens, the telomere shortening is taken out of the equation," Hockemeyer said. "We are showing that the TERT promoter mutation is not immediately sufficient to stop telomeres from shortening."

It is still unclear, however, what causes the eventual up-regulation of telomerase that immortalizes the cell. Hockemeyer says that it's unlikely to be another mutation, but rather an epigenetic change that affects expression of the telomerase gene, or a change in the expression of a transcription factor or other regulatory proteins that binds to the promoter upstream of the telomerase gene.

"Nevertheless, we have evidence that the second step has to happen, and that the second step is initiated by or is occurring at a time where telomeres are critically short and when telomeres can be dysfunctional and drive genomic instability," he said.

In retrospect, not a surprise

Though most cancers seem to require telomerase to become immortal, only some 10 to 20 percent of cancers are known to have a single-nucleotide change in the promoter upstream of the telomerase gene. However, these include about 70 percent of all melanomas and 50 percent of all liver and bladder cancers.

Hockemeyer said that the evidence supporting the theory that the TERT promoter mutation up-regulated telomerase has always been conflicting: cancer cells tend to have chromosomes with short telomeres, yet have higher levels of telomerase, which should produce longer telomeres.

According to the new theory, the telomeres are short in precancerous cells because telomerase is turned on just enough to maintain but not lengthen the telomeres.

"Our paper reconciles contradictory information about the cancers that carry these mutations," Hockemeyer said.

The finding also resolves another recent counterintuitive finding: that people with shorter telomeres are more resistant to melanoma. The reason, he said, is that if a TERT promoter mutation arises to push a precancerous lesion - the mole or nevus - toward a melanoma, the chances are greater in someone with short telomeres that the cell will die before it up-regulates telomerase and immortalizes the cells.

The study also involved engineering TERT promoter mutations in cells differentiated from human pluripotent stem cells and following their progression toward cellular immortality. The results were identical to the progression seen in human skin lesions obtained from patients in UCSF's Helen Diller Family Comprehensive Cancer Center and examined in the Clinical Cancer Genomics Laboratory, which Bastian directs.

Explore further: Unraveling the mystery of why cancer cells survive and thrive

More information: K. Chiba el al., "Mutations in the promoter of the telomerase gene TERT contribute to tumorigenesis by a two-step mechanism," Science (2017). science.sciencemag.org/lookup/ 1126/science.aao0535

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Two-step process leads to cell immortalization and cancer - Medical Xpress

Anatomy Lab Live comes to Manchester with dinner, drinks – and a live post-mortem – Manchester Evening News

An interactive autopsy show which dissects a semi-synthetic human cadaver is coming to Manchester.

Anatomy Lab Live is a touring hands-on post-mortem suite, which serves a sumptuous two-course dinner to guests before the gory procedure begins.

After its UK tour last year the show returns bigger and better in 2018, with a string of dates including a show in the Village Hotel Ashton on January 27.

Those attending will be given mortuary wear including protective surgical hats, masks and aprons as well as scalpels, scissors, forceps and bone saws.

A team of human anatomists, medics and physiologists will accompany host and science teacher Samuel Piri as they carry out a real post-mortem.

The cadaver - known as VIVIT - is the next best thing to a real human cadaver and houses real internal organs from pigs, chosen for their anatomical similarity to humans.

Visitors will also be given a set of case notes to look over before then starting procedures for themselves, which could include a real head and brain sample, the pulmonary system, the gastrointestinal tract, or the heart and greater blood vessels.

There will also be Q&A time as the floor opens for questions from the audience.

According to organisers, this event is a high-level interactive experience for level 4 and above, and the content is aimed at those studying towards graduate professions. However, the wider public is welcome to attend and the event will allocate some anatomy pods especially for those with a general interest.

Tickets for the dinner and dissection are 79 general admission, with discounts available for students. Book online via eventbrite.co.uk .

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Anatomy Lab Live comes to Manchester with dinner, drinks - and a live post-mortem - Manchester Evening News

Netflix signs Grey’s Anatomy creator Shonda Rhimes to multi-year deal – The Verge

Acclaimed television writer and producer Shonda Rhimes has signed a multi-year deal with Netflix, where shell produce new series and work on other projects for the streaming company. The deal means Rhimes, known for her work as the creator and show runner of Greys Anatomy and Scandal, will depart ABC after 15 years with the broadcaster. She will be reportedly paid around $10 million a year at Netflix, and will be accompanied in the move by longtime collaborator Betsy Beers.

Shonda Rhimes is one of the greatest storytellers in the history of television, said Ted Sarandos, chief content officer at Netflix, in a press statement. Her work is gripping, inventive, pulse-pounding, heart-stopping, taboo-breaking television at its best. Shows from ShondaLand Rhimes production company including Greys Anatomy, Scandal, and How to Get Away with Murder will continue to air on ABC. These shows are also available to stream on Netflix (depending on your region.)

The move to Netflix means Rhimes will be able to work in a wider range of genres and formats, according to Variety. "ShondaLands move to Netflix is the result of a shared plan Ted Sarandos and I built based on my vision for myself as a storyteller and for the evolution of my company, said Rhimes. Ted provides a clear, fearless space for creators at Netflix. He understood what I was looking for the opportunity to build a vibrant new storytelling home for writers with the unique creative freedom and instantaneous global reach.

This deal marks another step in a content arms race where companies like Netflix and Amazon are carving up exclusive deals that would usually only be available to TV networks at least back in their heyday. Just last week, Amazon pinched The Walking Dead creator Robert Kirkman from AMC. While a single show might be valuable, having a creator on board where all their new shows will be exclusive to one platform is especially lucrative. Netflix currently has 104 million subscribers in over 190 countries, so the appetite for high-quality, original content remains huge.

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Netflix signs Grey's Anatomy creator Shonda Rhimes to multi-year deal - The Verge