Ethan’s Army gets a boost – Brockville Recorder and Times

The Tucker family, from back left, Kadyn 11, mom Shawntel, Jorja 13, and dad Chris, Westyn 3, and Ethan, who will be 15 on Christmas Day, pose in their home. (CATHERINE ORTH/Special to The Recorder and Times)jpg, BT

Ethan Tucker cant swallow. He cant eat. He cant talk. He cant walk. His life as he knew it was taken away from him two years ago this coming January, shortly after his Christmas Day 13th birthday.

And now, a local developers generosity is helping to make his living conditions more bearable.

Ethan did not feel well. It took a couple of trips to the local hospital to find out that Ethan had an aggressive form of brain cancer. He underwent a 30-hour operation to remove only 10 per cent of the tumour, and later, a 17-hour operation that removed 90 per cent of the tumour.

But then, things went very sideways as Ethans body started to react after the fourth chemo treatment. It is believed that the chemo triggered an autoimmune reaction that attacked his brains stem cell. It took a lot to sort this out, but finally a procedure that cleansed Ethans blood fourteen times stopped the attack.

But the effects, by the time it was suppressed, were simply devastating to his body.

Still, Ethan is there, locked in his body, with an intelligent functioning mind that can spell out his thoughts on a word board.

If Ethan had one wish, it would be that he could sit at the table and eat regular food with his family. But he cannot.

This makes him very sad and sometimes he cries.

Ethan, is his familys treasure, their Christmas miracle, said dad, Chris, and mom Shawntel Tucker. They are his champions, his advocates. He is their hero.

They fought sometimes toe-to-toe with doctors who shook their heads and wanted to give up on Ethan. But Ethan did not want to give up. Nor did his parents.

Giving up is unthinkable, said Chris.

And so the family, with love and strength that comes almost mysteriously in these times of misfortune, took each day and adjusted to a new life.

Chris had to leave work and become a single dad to their other three children: Jorja 12, Kadyn, 11 and Westyn, 3. Shawntel moved into Ethans room at the Childrens Hospital of Eastern Ontario (CHEO). Westyn took his first steps in Ethans hospital room, which he called Ethans house.

Ethan is currently cancer-free and scheduled to go to inpatient rehab in Toronto in January.

Its not been easy. But no words of complaint or self pity are expressed by the Tuckers; love for their son and their young family has seen them through.

And generosity from the community.

We found it hard to ask for help, but it came to a point where we had no choice. Thats one thing I would say to any family going through a dramatic change of circumstances: Dont be afraid to ask for help; its there, said Shawntel.

Among the people who have been there for the Tuckers from the get-go is Michelle Robinson. Anyone who knows her will tell you she is a person of energy and ideas. She motivates and helps young parents to get their kids out doors through her Walk-A-Baby program.

The Facebook page Ethans Army and a GoFundMe account were put in place.

Ethan, after a thirteen-month stay at CHEO, was coming home. The Tuckers realized that they could not live in their home as it was. It had to be renovated. But even renovations, it was realized, would not address Ethans needs.

The decision was made to move. And again things fell into place. The Tuckers found a house on the outskirts of town that suited the family, who had always wanted to live in the country. The house, now purchased, required some renovations.

The Tuckers were pretty certain that if they got a team together they could work around schedules and get the renovations done.

Michelle put the call out on the Ethans Army page. It was answered, but not in the way they ever imagined.

Local developer Mapleview Homes, along with EXIT Realty Brockville, came forward to help in what Chris calls above and beyond and beyond. They took on the complete job and absorbed all costs, both materials and labour.

In the next few days, Ethan will have his own room, with all his needs: Laminated flooring for easy moving of his wheelchair, bed and lift in place; and barn doors that slide close for privacy or open to a view of the countryside.

The room was slightly modified and painted. Poignantly, Ethan had just been given his own room, in their former home, six months before he became ill. He will once again have his own room.

The Tuckers dont look back. They are moving forward as a family.

Chris has been able to return to work and has a part, as does daughter Jorja, in the local production of Broadway in Love, in February, presented by the Brockville Operatic Society.

Shawntel, now home, is actively again able to be mom to all her kids.

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Ethan's Army gets a boost - Brockville Recorder and Times

Harvard geneticist George Church’s goal: to protect humans from viruses, genetic diseases, and aging – 60 Minutes – CBS News

Our lives have been transformed by the information age. But what's coming next is likely to be more profound, call it the genetic information age. We have mapped the human genome and in just the last few years we have learned to read and write DNA like software. And you're about to see a few breakthroughs-in-waiting that would transform human health. For a preview of this revolution in evolution we met George Church, a world leading geneticist, whose own DNA harbors many eccentricities and a few genes for genius.

We found George Church in here.

Cory Smith: Most of these are frozen George. Little bits of George that we have edited all in different tubes.

Church threw himself into his work, literally. His DNA is in many of the experiments in his lab at Harvard Medical School. The fully assembled George Church is 6'5" and 65. He helped pioneer mapping the human genome and editing DNA. Today, his lab is working to make humans immune to all viruses, eliminate genetic diseases, and reverse the effects of time.

Scott Pelley: One of the things your lab is working on is reversing aging.

George Church: That's right.

Scott Pelley: How is that possible?

George Church: Reversing aging is one of these things that is easy to dismiss to say either we don't need it or is impossible or both.

Scott Pelley: Oh, we need it.

George Church: Okay. We need it. That's good. We can agree on that. Well, aging reversal is something that's been proven about eight different ways in animals where you can get, you know, faster reaction times or, you know, cognitive or repair of damaged tissues.

Scott Pelley: Proven eight different ways. Why isn't this available?

George Church: It is available to mice.

In lucky mice, Church's lab added multiple genes that improved heart and kidney function and levels of blood sugar. Now he's trying it in spaniels.

Scott Pelley: So is this gene editing to achieve age reversal?

George Church: This is adding genes. So, it's not really editing genes. It's, the gene function is going down, and so we're boosting it back up by putting in extra copies of the genes.

Scott Pelley: What's the time horizon on age reversal in humans?

George Church: That's in clinical trials right now in dogs. And so, that veterinary product might be a couple years away and then that takes another ten years to get through the human clinical trials.

Human trials of a personal kind made George Church an unlikely candidate to alter human evolution. Growing up in Florida, Church was dyslexic, with attention deficit, and frequently knocked out by narcolepsy.

Scott Pelley: What was it that made you imagine that you could be a scientist?

George Church: The thing that got me hooked was probably the New York World's Fair in 1964. I thought this is the way we should all be living. When I went back to Florida, I said, "I've been robbed," you know? "Where is it all?" So, I said, "Well, if they're not going to provide it, then I'm gonna provide it for myself."

With work and repetition, he beat his disabilities and developed a genius for crystallography, a daunting technique that renders 3D images of molecules through X-rays and math. But in graduate school at Duke, at the age of 20, his mania for the basic structures of life didn't leave time for the basic structure of life.

Scott Pelley: You were homeless for a time.

George Church: Yeah. Briefly.

Scott Pelley: Six months.

George Church: Six months.

Scott Pelley: And where were you sleeping when you were homeless?

George Church: Well, yeah. I wasn't sleeping that much. I was mostly working. I'm narcoleptic. So, I fall asleep sitting up anyway.

His devotion to crystallography was his undoing at Duke.

George Church: I was extremely excited about the research I was doing. And so, I would put in 100-plus hours a week on research and then pretty much didn't do anything else.

Scott Pelley: Not go to class.

George Church: I wouldn't go to class. Yeah.

Duke kicked him out with this letter wishing him well in a field other than biology. But, it turned out, Harvard needed a crystallographer. George Church has been here nearly 40 years. He employs around 100 scientists, about half-and-half men and women.

Scott Pelley: Who do you hire?

George Church: I hire people that are self-selecting, they see our beacon from a distance away. There are a lot of people that are a little, you know, might be considered a little odd. "Neuroatypicals," some of us are called.

Scott Pelley: "Neuroatypical?"

George Church: Right.

Scott Pelley: Unusual brains?

George Church: Right, yeah.

Parastoo Khoshakhlagh: One thing about George that is very significant is that he sees what you can't even see in yourself.

Parastoo Khoshakhlagh and Alex Ng are among the "neuroatypicals." They're engineering human organ tissue.

Cory Smith: I think he tries to promote no fear of failure. The only fear is not to try at all.

Cory Smith's project sped up DNA editing from altering three genes at a time to 13,000 at a time. Eriona Hysolli went to Siberia with Church to extract DNA from the bones of wooly mammoths. She's editing the genes into elephant DNA to bring the mammoth back from extinction.

Eriona Hysolli: We are laying the foundations, perhaps, of de-extinction projects to come.

Scott Pelley: De-extinction.

Eriona Hysolli: Yes.

Scott Pelley: I'm not sure that's a word in the dictionary yet.

Eriona Hysolli: Well, if it isn't, it should be.

Scott Pelley: You know there are people watching this interview who think that is playing God.

George Church: Well, it's playing engineer. I mean, humans have been playing engineer since the dawn of time.

Scott Pelley: The point is, some people believe that you're mucking about in things that shouldn't be disturbed.

George Church: I completely agree that we need to be very cautious. And the more powerful, or the more rapidly-moving the technology, the more cautious we need to be, the bigger the conversation involving lots of different disciplines, religion, ethics, government, art, and so forth. And to see what it's unintended consequences might be.

Church anticipates consequences with a full time ethicist in the lab and he spends a good deal of time thinking about genetic equity. Believing that genetic technology must be available to all, not just those who can afford it.

We saw one of those technologies in the hands of Alex Ng and Parastoo Khoshakhlagh. They showed us what they call "mini-brains," tiny dots with millions of cells each. They've proven that cells from a patient can be grown into any organ tissue, in a matter of days, so drugs can be tested on that patient's unique genome.

Scott Pelley: You said that you got these cells from George's skin? How does that work?

Alex Ng: We have a way to reprogram essentially, skin cells, back into a stem cell state. And we have technologies where now we can differentiate them into tissue such as brain tissue.

Scott Pelley: So you went from George's skin cells, turned those into stem cells, and turned those into brain cells.

Alex Ng: Exactly. Exactly.

Scott Pelley: Simple as that.

Organs grown from a patient's own cells would eliminate the problem of rejection. Their goal is to prove the concept by growing full sized organs from Church's DNA.

George Church: It's considered more ethical for students to do experiments on their boss than vice versa and it's good to do it on me rather than some stranger because I'm as up to speed as you can be on the on the risks and the benefits. I'm properly consented. And I'm unlikely to change my mind.

Alex Ng: We have a joke in the lab, I mean, at some point, soon probably, we're going to have more of his cells outside of his body than he has himself.

Church's DNA is also used in experiments designed to make humans immune to all viruses.

George Church: We have a strategy by which we can make any cell or any organism resistant to all viruses by changing the genetic code. So if you change that code enough you now get something that is resistant to all viruses including viruses you never characterized before.

Scott Pelley: Because the viruses don't recognize it anymore?

George Church: They expect a certain code provided by the host that they replicate in. the virus would have to change so many parts of its DNA or RNA so that it can't change them all at once. So, it's not only dead. But it can't mutate to a new place where it could survive in a new host.

Yes, he's talking about the cure for the common cold and the end of waiting for organ transplants. It's long been known that pig organs could function in humans. Pig heart valves are routinely transplanted already. But pig viruses have kept surgeons from transplanting whole organs. Church's lab altered pig DNA and knocked out 62 pig viruses.

Scott Pelley: What organs might be transplanted from a pig to a human?

George Church: Heart, lung, kidney, liver, intestines, various parts of the eye, skin. All these things.

Scott Pelley: What's the time horizon on transplanting pig organs into human beings?

George Church: you know, two to five years to get into clinical trials. And then again it could take ten years to get through the clinical trials.

Church is a role model for the next generation. He has co-founded more than 35 startups. Recently, investors put $100 million into the pig organ work. Another Church startup is a dating app that compares DNA and screens out matches that would result in a child with an inherited disease.

George Church: You wouldn't find out who you're not compatible with. You'll just find out who you are compatible with.

Scott Pelley: You're suggesting that if everyone has their genome sequenced and the correct matches are made, that all of these diseases could be eliminated?

George Church: Right. It's 7,000 diseases. It's about 5% of the population. It's about a trillion dollars a year, worldwide.

Church sees one of his own genetic differences as an advantage. Narcolepsy lulls him several times a day. But he wakes, still in the conversation, often, discovering inspiration in his twilight zone.

Scott Pelley: If somebody had sequenced your genome some years ago, you might not have made the grade in some way.

George Church: I mean, that's true. I would hope that society sees the benefit of diversity not just ancestral diversity, but in our abilities. There's no perfect person.

Despite imperfection, Church has co-authored 527 scientific papers and holds more than 50 patents. Proof that great minds do not think alike.

The best science can tell, it was about 4 billion years ago that self-replicating molecules set off the spark of biology. Now, humans hold the tools of evolution, but George Church remains in awe of the original mystery: how chemistry became life.

Scott Pelley: Is the most amazing thing about life, then, that it happened at all?

George Church: It is amazing in our current state of ignorance. We don't even know if it ever happened ever in the rest of the universe. it's awe-inspiring to know that it either happened billions of times, or it never happened. Both of those are mind boggling. It's amazing that you can have such complex structures that make copies of themselves. But it's very hard to do that with machines that we've built. So, we're engineers. But we're rather poor engineers compared to the pseudo engineering that is biological evolution.

Produced by Henry Schuster. Associate producer, Rachael Morehouse. Broadcast associate, Ian Flickinger.

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Harvard geneticist George Church's goal: to protect humans from viruses, genetic diseases, and aging - 60 Minutes - CBS News

Start-up to research on degenerative eye disease – Deccan Herald

A city-based medical science startup is gearing up to halt the progress of degenerative eye disease in Indians after trials in blind rats showed the creatures regaining their sight in a few months.

Age-Related Macular Degeneration (AMD) is a form of blindness that affects a segment of the adult population after they reach the age of 50. It accounts for 8.7% of all blindness worldwide. Retinitis Pigmentosa (RP), meanwhile, is a rare genetic disorder, which affects one child in 4,000.

There is no known cure for the diseases. However, Dr Jogin Desai, whose startup, Eyestem, which has been under incubation by the governments Centre for Cellular and Molecular Platforms (C-Camp) for the past three years, believes its work can halt the progression of the diseases by using genetically modified stem cells to restore the pigment epithelium in the cornea.

The pigment epithelium, which is only 1.5 mm thick, performs critical functions that support photoreceptor health and integrity. It was likened to the foundation of a building. The therapy will also seek to restore the photoreceptor cells in the retina, which were likened to buildings. Phase 1 human clinical trials are set to start within two-and-half months.

Existing research postulates that using biodegradable scaffolding upon which modified cells are stacked can help rebuild the pigment epithelium. However, Dr Desai said that current work delivering modified Eycyte-RPE (or Retinal Pigment Epithelium) cells, which are suspended in the liquid, is even more effective.

We have found that cells delivered in this way automatically seek out their body niche and assimilate into the system, he said, adding that trials in blind lab rats had showed the animals regaining their vision over a two-month period.

Most discoveries fail

Desai, however, cautioned that no amount of promise can legitimise an idea if its time has not yet come. In fact, just one of 1,600 scientific discoveries made in research labs makes it into a fully fledged development where it can impact peoples lives, he explained.

Most scientific discoveries are weeded out in exacting, three-phased clinical trials, based on the criteria of safety, scalability and effectiveness.

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Start-up to research on degenerative eye disease - Deccan Herald

Global Stem Cell Antibody Market Executive Summary and Analysis by Top Players 2019-2025 : Thermo Fisher Scientific, Inc., Merck Group, Abcam plc,…

Global Stem Cell Antibody Market Executive Summary and Analysis by Top Players 2019-2025 : Thermo Fisher Scientific, Inc., Merck Group, Abcam plc, Becton  Industry News Hour

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Global Stem Cell Antibody Market Executive Summary and Analysis by Top Players 2019-2025 : Thermo Fisher Scientific, Inc., Merck Group, Abcam plc,...

R&D Activities to Fast-track the Growth of the Stem Cell Assay Market Between 2018 2028 – Kentucky Reports

TMRR, in its latest market intelligence study, finds that the global Stem Cell Assay market registered a value of ~US$ xx Mn/Bn in 2018 and is spectated to grow at CAGR of xx% during the foreseeable period 2019-2029. In terms of product type, segment holds the largest share, while segment 1 and segment 2 hold significant share in terms of end use.

The Stem Cell Assay market study outlines the key regions Region 1 (Country 1, Country 2), region 2 (Country 1, Country 2), region 3 (Country 1, Country 2) and region 4 (Country 1, Country 2). All the consumption trends and adoption patterns of the Stem Cell Assay are covered in the report. Prominent players, including player 1, player 2, player 3 and player 4, among others, account for substantial shares in the global Stem Cell Assay market.

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growth drivers and lists down the major restraints. Additionally, the report gauges the effect of Porters five forces on the overall stem cell assay market.

Global Stem Cell Assay Market: Key Market Segments

For the purpose of the study, the report segments the global stem cell assay market based on various parameters. For instance, in terms of assay type, the market can be segmented into isolation and purification, viability, cell identification, differentiation, proliferation, apoptosis, and function. By kit, the market can be bifurcated into human embryonic stem cell kits and adult stem cell kits. Based on instruments, flow cytometer, cell imaging systems, automated cell counter, and micro electrode arrays could be the key market segments.

In terms of application, the market can be segmented into drug discovery and development, clinical research, and regenerative medicine and therapy. The growth witnessed across the aforementioned application segments will be influenced by the increasing incidence of chronic ailments which will translate into the rising demand for regenerative medicines. Finally, based on end users, research institutes and industry research constitute the key market segments.

The report includes a detailed assessment of the various factors influencing the markets expansion across its key segments. The ones holding the most lucrative prospects are analyzed, and the factors restraining its trajectory across key segments are also discussed at length.

Global Stem Cell Assay Market: Regional Analysis

Regionally, the market is expected to witness heightened demand in the developed countries across Europe and North America. The increasing incidence of chronic ailments and the subsequently expanding patient population are the chief drivers of the stem cell assay market in North America. Besides this, the market is also expected to witness lucrative opportunities in Asia Pacific and Rest of the World.

Global Stem Cell Assay Market: Vendor Landscape

A major inclusion in the report is the detailed assessment of the markets vendor landscape. For the purpose of the study the report therefore profiles some of the leading players having influence on the overall market dynamics. It also conducts SWOT analysis to study the strengths and weaknesses of the companies profiled and identify threats and opportunities that these enterprises are forecast to witness over the course of the reports forecast period.

Some of the most prominent enterprises operating in the global stem cell assay market are Bio-Rad Laboratories, Inc (U.S.), Thermo Fisher Scientific Inc. (U.S.), GE Healthcare (U.K.), Hemogenix Inc. (U.S.), Promega Corporation (U.S.), Bio-Techne Corporation (U.S.), Merck KGaA (Germany), STEMCELL Technologies Inc. (CA), Cell Biolabs, Inc. (U.S.), and Cellular Dynamics International, Inc. (U.S.).

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The Stem Cell Assay market research answers important questions, including the following:

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TMRR stays aligned with the fact the organization lands among the leading market research firms in India. Our analysts work irrespective of the time-zone, the result, we are being recognized worldwide. We abide by the notion that each client has his/her own set of requirements. With extensive primary and secondary research, our experts churn out the most accurate information regarding the desired the market.

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R&D Activities to Fast-track the Growth of the Stem Cell Assay Market Between 2018 2028 - Kentucky Reports

IFN-: The T cell’s license to kill stem cells in the inflamed intestine – Science


IFN- produced by T cells directly induces intestinal stem cell death upon inflammation-induced intestinal injury (see the related Research Article by Takashima et al.).

Intestinal regeneration upon tissue damage is fueled by intestinal stem cells (ISCs) residing in the crypt bottom of the epithelium and marked by the gene Lgr5 (1, 2). There is growing evidence that tissue repair is at least partially mediated by a regenerative inflammatory response (3, 4). How inflammation-induced intestinal injury influences ISCs and their microenvironment (stem cell niche) remains poorly understood. In this issue of Science Immunology, Takashima et al. (5) explore the changes in the ISC niche in vivo upon T cellmediated injury as a model of graft-versus-host disease (GVHD) and in vitro using organoid T cell cocultures. Although earlier studies already implicated interferon- (IFN-) as a negative regulator of intestinal epithelial homeostasis (68), Takashima et al. now demonstrate that IFN- directly acts on ISCs by triggering apoptosis.

In an allogeneic bone marrow transplant (BMT) model, Takashima and colleagues found that ISC numbers per intestinal crypt were markedly reduced in mice receiving bone marrow alone or bone marrow and T cells when compared with normal control mice. While the ISCs in the mice receiving only bone marrow recovered 7 days later, the ISC numbers remained reduced in those mice also transplanted with donor T cells. Of note, Paneth cell numbers were also reduced after ISC depletion. The numbers of organoids established from the intestines of mice 10 days after BMT recovered back to that of control mice, whereas the organoid forming capacity from crypts of mice after combined transplantation of bone marrow and T cells remained significantly lower. Similar in vivo and in vitro results were obtained when autoreactive T cells were transplanted, pointing to a common feature of T cellmediated intestinal injury.

As seen by three-dimensional confocal microscopy, intraepithelial T cells (CD3+ IELs) preferentially localized to the villus region, whereas lamina propriaassociated T cells (CD3+ LPLs) were equally distributed along the crypt-villus axis of control mice (Fig. 1A). Conversely, mice receiving bone marrow and allogeneic T cells showed a progressive increase in the density of both CD3+ LPLs and CD3+ IELs in the crypt region.

To identify signaling molecules that cause the loss of ISCs in this model, Takashima and colleagues performed several elegant murine and human epithelial organoid coculture experiments. Murine nave allogeneic T cells did not impair murine intestinal organoid numbers, whereas alloreactive T cells effectively reduced organoid numbers. Likewise, human allogeneic cytotoxic T cells robustly inhibited human intestinal organoid forming efficiency. Even bead-activated autologous T cells suppressed human intestinal organoid growth. The authors then proceeded to screen for potential pathways mediating cytotoxicity. Organoids cocultured with T cells in the presence of antiIFN- neutralizing antibodies showed normal growth. Although IFN- receptor (IFN-R)depleted T cells were still able to affect organoid viability, IFN-Rdepleted organoids were resistant to T cellmediated killing. Organoid toxicity by IFN- was also observed in the absence of T cells. Live imaging confirmed the progressive ISC depletion upon organoid exposure to IFN-. Treatment of organoids with the immunosuppressive JAK1/2 inhibitor ruxolitinib robustly preserved numbers of both organoids and ISCs in the presence of IFN-, irrespective of whether the organoids were cultured alone or together with T cells. The authors additionally demonstrated that JAK1-depleted organoids are resistant to IFN- treatment. Further downstream, ruxolitinib prevented STAT1 phosphorylation by IFN- in intestinal crypts, and, in line, STAT1-depleted organoids were resistant to growth suppression in response to IFN- treatment.

IFN-treated organoids showed reduced expression of ISC marker genes. ISCs underwent apoptosis in vitro in a direct response to IFN-. Next, the authors confirmed in vivo that ISC numbers did not change upon transplanting allogeneic bone marrow and T cells when treating mice with IFN- neutralizing antibodies. Likewise, ruxolitinib treatment protected ISCs from T cellmediated killing in vivo. Donor T cells, particularly T helper 1 cells, were activated and IFN-+. Transplanting IFN-depleted allogeneic T cells robustly reduced the ISC loss and allowed epithelial cell proliferation to increase.

Takashima and colleagues lastly investigated whether IFN- directly induces ISC apoptosis. Using tissue-specific depletion of IFN-R1, the authors found that epithelial loss of the receptor protects from the immune-mediated GVHD phenotype. IFN-R1 is expressed by both ISCs and Paneth cells, the epithelial component of the ISC niche (9). However, Paneth celldeficient organoids remained sensitive to both IFN- and allogeneic T cellmediated cytotoxicity. Likewise, T cells were able to reduce the number of organoids containing IFN-R1deficient Paneth cells, whereas organoids containing IFN-R1deficient ISC were protected from cytotoxicity. The authors demonstrated in further experiments that IFN- directly induces ISC apoptosis independent of Paneth cells (Fig. 1, B and C).

The study by Takashima et al. extends our knowledge on signaling between ISCs and immune cells, identifying ISCs as direct targets of IFN- secreted by T cells in immune-mediated intestinal damage (as caused by GVHD). In the 2015 study by Lindemans et al., this group already identified that interleukin-22 (IL-22) secreted by group 3 innate lymphoid cells (ILC3s) directly stimulates ISCs to proliferate and regenerate the intestinal epithelium upon inflammation-induced intestinal injury (4). Modulating the effects of T cellderived IFN- on ISC, for instance, by suppressing JAK/STAT signaling via ruxolitinib treatment, may provide a new therapeutic avenue to reducing GVHD-induced damage of the intestinal epithelium (10).

(A) ISCs maintain adult homeostasis of the intestinal epithelium. T lymphocytes patrol the intestine. (B) Takashima et al. show that in GVHD as modeled by BMT and aberrant activation of T lymphocytes, T cellderived IFN- directly acts on ISCs and induces apoptosis via JAK/STAT signaling. (C) Disease progression results in marked intestinal damage due to loss of ISCs and their niche.

Acknowledgments: Funding: K.K. is a long-term fellow of the Human Frontier Science Program Organization (LT771/2015). Competing interests: H.C. and K.K. are named inventors on patents or patents pending on Lgr5 stem cellbased organoid technology.

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IFN-: The T cell's license to kill stem cells in the inflamed intestine - Science

Movies opening in L.A. this week: ‘Bombshell,’ ‘Jumanji: The Next Level’ and more – Los Angeles Times

Black ChristmasUpdate of the 1974 holiday horror classic about sorority sisters stalked by a masked killer. With Imogen Poots, Aleyse Shannon, Lily Donoghue, Cary Elwes. Written by Sophia Takal, April Wolfe. Directed by Takal. (1:38) PG-13.

BombshellCharlize Theron, Nicole Kidman and Margot Robbie play Fox News employees whose allegations of sexual harassment help topple network founder Roger Ailes. With John Lithgow, Allison Janney, Connie Britton, Kate McKinnon. Written by Charles Randolph. Directed by Jay Roach. (1:48) R.

CunninghamDocumentary profile of influential dancer-choreographer Merce Cunningham includes archival footage plus re-creations of his works. Directed by Alla Kovgan. (1:33) PG.

The Death & Life of John F. DonovanAn actor recalls the letters he exchanged with a long-dead American television star. With Kit Harington, Natalie Portman, Jacob Tremblay, Susan Sarandon, Kathy Bates, Thandie Newton, Sarah Gadon. Written by Xavier Dolan, Jacob Tierney. Directed by Dolan. (2:03) R.

The Disappearance of My MotherWriter-director Beniamino Barrese profiles his reclusive mother, 1960s-era supermodel turned feminist activist Benedetta Barzini. In English and Italian with English subtitles. (1:34) NR.

First LoveThe brother of a famous but troubled actress is torn between selling his explosive tell-all book about their childhood or helping her after she suffers a nervous breakdown. With Annie Heise, Aaron Costa Ganis, Arye Gross, Mia Barron. Written and directed by Michael Masarof. (1:20) NR.

The Great WarAmerican soldiers during WWI go behind enemy lines to try to rescue a lost platoon. With Ron Perlman, Billy Zane, Bates Wilder. Written and directed by Steven Luke. (1:48) R.

Hell on the BorderA former slave gets a job as a lawman and goes on a manhunt in his fact-based western about the first black marshal in the Wild West. With David Gyashi, Frank Grillo, Ron Perlman. Written and directed by Wes Miller. (1:50) R.

A Hidden LifeWriter-director Terrence Malicks fact-based drama about an Austrian farmer who refused to fight for Nazis during WWII. With August Diehl, Valerie Pachner, Bruno Ganz, Matthias Schoenaerts. In English, German, Italian with English subtitles. (2:53) R.

Jumanji: The Next LevelDanny Glover and Danny DeVito join Dwayne Johnson, Jack Black, Kevin Hart and Karen Gillan in this sequel to the 2017 action adventure hit about young people trapped in a videogame. With Nick Jonas, Awkwafina. Written by Jake Kasdan, Jeff Pinkner, Scott Rosenberg; based on the book by Chris Van Allsburg. Directed by Kasdan. (1:54) PG-13.

Line of DescentAn organized-crime family in Delhi deals with threats from without and within. With Brendan Fraser, Max Beesley, Abhay Deol. In Hindi and English with English subtitles. (1:48) NR.

Midnight FamilyDocumentary about a family-run private ambulance service in Mexico City. Directed by Luke Lorentzen. In Spanish with English subtitles. (1:30) NR.

Mob TownMafia figures assemble for a summit in upstate New York in 1957 in this fact-based crime drama. With David Arquette, Jennifer Esposito, Jamie-Lynn Sigler, Robert Davi, Nick Cordero. Written by Jon Carlo and Joe Gilford. Directed by Danny A. Abeckaser. (1:30) R.

RabidA fashion designer experiences a horrifying transformation after undergoing an experimental stem-cell treatment following a car accident. With Laura Vandervoort, Benjamin Hollingsworth, Phil Brooks. Written by the Soska Sisters, John Serge; story by Serge. Directed by the Soska Sisters. (1:47) NR.

Richard JewellClint Eastwood directs this fact-based drama about the security guard falsely accused in the Centennial Park bombing during the 1996 Olympics in Atlanta. With Paul Walter Hauser, Sam Rockwell, Kathy Bates, Jon Hamm, Olivia Wilde, Ian Gomez. Written by Billy Ray; based on an article by Marie Brenner. (2:09) R.

SebergFrench New Wave actress Jean Seberg is targeted by the FBI for her political and romantic involvement with civil-rights activist Hakim Jamal during the 1960s in this fact-based drama. With Kristen Stewart, Anthony Mackie, Jack OConnell, Margaret Qualley, Zazie Beetz, Vince Vaughn. Written by Joe Shrapnel, Anna Waterhouse. Directed by Benedict Andrews. (1:36) R.

6 UndergroundRyan Reynolds stars in this Michael Bay action flick about a globe-trotting team of untraceable operatives dedicated to saving the world. With Mlanie Laurent, Corey Hawkins, Adria Arjona, Dave Franco. Written by Paul Wernick, Rhett Reese. (2:05) R.

Uncut GemsAdam Sandler stars as a desperate New York City jeweler juggling numerous deals in this crime thriller. With Lakeith Stanfield, Julia Fox, Kevin Garnett, Idina Menzel, Eric Bogosian, Judd Hirsch. Written by Josh Safdie, Benny Safdie, Ronald Bronstein. Directed by the Safdies. (2:15) R.

What She Said: The Art of Pauline KaelDocumentary on the longtime firebrand film critic of the New Yorker. With Alec Baldwin, Quentin Tarantino, David O. Russell, Francis Ford Coppola and Sarah Jessica Parker as the voice of Kael. Directed by Rob Garver. (1:38) NR.

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Movies opening in L.A. this week: 'Bombshell,' 'Jumanji: The Next Level' and more - Los Angeles Times

Updated Clinical Data from Phase 2 SPiReL Study Evaluating DPX-Survivac as a Combination Therapy in r/r DLBCL Presented at 61st American Society of…

DARTMOUTH, Nova Scotia--(BUSINESS WIRE)--IMV Inc. (Nasdaq: IMV; TSX: IMV), a clinical-stage biopharmaceutical company pioneering a novel class of immunotherapies, today announced that updated results from SPiReL, an ongoing Phase 2 investigator-sponsored study of DPX-Survivac in combination with pembrolizumab in patients with recurrent/refractory diffuse large B-cell lymphoma (r/r DLBCL), were presented in a poster session at the 61st American Society of Hematology (ASH) Annual Meeting in Orlando, FL. The poster, which included additional data collected between the abstract submission and the presentation, continued to demonstrate a favorable therapeutic profile and treatment-associated clinical benefit in r/r DLBCL patients who received the DPX-Survivac combination regimen.

These updated data show encouraging clinical activity in patients treated with a DPX-Survivac combination regimen for recurrent/refractory diffuse large B-cell lymphoma, said Neil Berinstein, MD, FFCPC, ABIM, hematologist at Sunnybrook Health Sciences Centre and lead investigator for the clinical trial. In contrast, both to standard-of-care treatments and other immunotherapeutic approaches in development, to observe this clinical benefit alongside a favorable safety profile highlights DPX-Survivacs potential to reach this patient population in dire need of better treatment options.

These results demonstrate a robust response in evaluable patients who received the combination regimen including DPX-Survivac, which continues to exhibit a promising therapeutic profile for patients with hard-to-treat cancers, said Joanne Schindler, M.D., D.V.M., Chief Medical Officer of IMV. These data further validate DPX-Survivacs novel mechanism, extending previously documented results in solid cancers now to survivin-expressing hematologic malignancies, and support the hypothesis that our lead candidate works well in combination with checkpoint inhibitors. We believe this represents a potentially meaningful alternative to more toxic chemotherapy regimens; and, with this foundation, we look forward to topline results from this study as we prepare to launch an IMV-sponsored study in r/r DLBCL in 2020.

Updated Clinical Data from the SPiReL Study

In the poster presentation at ASH, Dr. Berinstein reported updated clinical results from the ongoing Phase 2 SPiReL study. Highlights of this preliminary data are outlined below:

As of December 1, 2019, 17 subjects have been enrolled in the study.

Conference Call Information:

IMV will host a conference call and webcast on Monday, December 9, 2019 at 8:00 a.m. EST to discuss the DPX-Survivac clinical results presented at ASH.

Financial analysts are invited to join the conference call by dialing (866) 211-3204 (U.S. and Canada) or (647) 689-6600 (International) using the conference ID number: 8796370. Other interested parties will be able to access the live audio webcast at this link:

The webcast will be recorded and available on the IMV website for 30 days following the call. The poster and the webcast will available on the Investors section of the companys website, under Events, Webcasts & Presentations.

About the SPiReL Study

SPiReL is a Phase 2 non-randomized, open label, efficacy and safety study. Eligible subjects have persistent or recurrent/refractory DLBCL, confirmed expression of survivin and are not eligible for curative therapy. Study treatment includes administering two doses of 0.5 mL of DPX-Survivac 3 weeks apart followed by up to six 0.1 mL doses every 8 weeks. Intermittent low dose cyclophosphamide is administered orally at 50 mg twice daily for 7 days followed by 7 days off. Pembrolizumab 200 mg is administered every 3 weeks. Study participants continue active therapy for up to one year or until disease progression, whichever occurs first.

The primary objective of this study is to document the response rate to this treatment combination using modified Cheson criteria. Secondary objectives include duration of response and safety. Exploratory endpoints include T cell response, tumor immune cell infiltration, and gene expression analysis.

About DPX-Survivac

DPX-Survivac is the lead candidate in IMVs new class of immunotherapies that programs targeted T cells in vivo. It has demonstrated the potential for industry-leading targeted, persistent, and durable CD8+ T cell generation. IMV believes this mechanism of action (MOA) is key to generating durable solid tumor regressions. DPX-Survivac consists of survivin-based peptides formulated in IMVs proprietary DPX drug delivery platform. DPX-Survivac is designed to work by eliciting a cytotoxic T cell immune response against cancer cells presenting survivin peptides on their surface.

Survivin, recognized by the National Cancer Institute (NCI) as a promising tumor-associated antigen, is broadly over-expressed in most cancer types, and plays an essential role in antagonizing cell death, supporting tumor-associated angiogenesis, and promoting resistance to chemotherapies. IMV has identified over 20 cancer indications in which survivin can be targeted by DPX-Survivac.

DPX-Survivac has received Fast Track designation from the U.S. Food and Drug Administration (FDA) as maintenance therapy in advanced ovarian cancer, as well as orphan drug designation status from the U.S. FDA and the European Medicines Agency (EMA) in the ovarian cancer indication.

About IMV

IMV Inc. is a clinical stage biopharmaceutical company dedicated to making immunotherapy more effective, more broadly applicable, and more widely available to people facing cancer and other serious diseases. IMV is pioneering a new class of immunotherapies based on the Companys proprietary drug delivery platform. This patented technology leverages a novel mechanism of action that enables the programming of immune cells in vivo, which are aimed at generating powerful new synthetic therapeutic capabilities. IMVs lead candidate, DPX-Survivac, is a T cell-activating immunotherapy that combines the utility of the platform with a target: survivin. IMV is currently assessing DPX-Survivac in advanced ovarian cancer, as a single regimen, as well as a combination therapy in multiple clinical studies with Merck. Connect at

IMV Forward-Looking Statements

This press release contains forward-looking information under applicable securities law. All information that addresses activities or developments that we expect to occur in the future is forward-looking information. Forward-looking statements are based on the estimates and opinions of management on the date the statements are made. In the press release, such forward-looking statements include, but are not limited to, statements regarding the FDA potentially granting accelerated regulatory approval of DPX-Survivac. However, they should not be regarded as a representation that any of the plans will be achieved. Actual results may differ materially from those set forth in this press release due to risks affecting the Corporation, including access to capital, the successful design and completion of clinical trials and the receipt and timely receipt of all regulatory approvals. IMV Inc. assumes no responsibility to update forward-looking statements in this press release except as required by law. These forward-looking statements involve known and unknown risks and uncertainties and those risks and uncertainties include, but are not limited to, our ability to access capital, the successful and timely completion of clinical trials, the receipt of all regulatory approvals and other risks detailed from time to time in our ongoing quarterly filings and annual information form Investors are cautioned not to rely on these forward-looking statements and are encouraged to read IMVs continuous disclosure documents, including its current annual information form, as well as its audited annual consolidated financial statements which are available on SEDAR at and on EDGAR at

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Updated Clinical Data from Phase 2 SPiReL Study Evaluating DPX-Survivac as a Combination Therapy in r/r DLBCL Presented at 61st American Society of...

Stem Cell Alopecia Treatment Market 2019 Business Growth, Size and Comprehensive Research Study Forecast to 2026 – Montana Ledger

New Jersey United States, The report offers an all-inclusive and accurate research study on theStem Cell Alopecia Treatment Market while chiefly focusing on current and historical market scenarios. Stakeholders, market players, investors, and other market participants can significantly benefit from the thorough market analysis provided in the report. The authors of the report have compiled a detailed study on crucial market dynamics, including growth drivers, restraints, and opportunities. This study will help market participants to get a good understanding of future development of the Stem Cell Alopecia Treatment market. The report also focuses on market taxonomy, regional analysis, opportunity assessment, and vendor analysis to help with comprehensive evaluation of the Stem Cell Alopecia Treatment market.

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Market players need to have a complete picture of the competitive landscape of the Stem Cell Alopecia Treatment market as it forms an essential tool for them to plan their future strategies accordingly. The report puts forth the key sustainability strategies taken up by the companies and the impact they are likely to have on the Stem Cell Alopecia Treatment market competition. The report helps the competitors to capitalise on opportunities in the Stem Cell Alopecia Treatment market and cope up with the existing competition. This will eventually help them to make sound business decisions and generate maximum revenue.

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1 Introduction of Stem Cell Alopecia Treatment Market

1.1 Overview of the Market 1.2 Scope of Report 1.3 Assumptions

2 Executive Summary

3 Research Methodology of Verified Market Research

3.1 Data Mining 3.2 Validation 3.3 Primary Interviews 3.4 List of Data Sources

4 Stem Cell Alopecia Treatment Market Outlook

4.1 Overview 4.2 Market Dynamics 4.2.1 Drivers 4.2.2 Restraints 4.2.3 Opportunities 4.3 Porters Five Force Model 4.4 Value Chain Analysis

5 Stem Cell Alopecia Treatment Market, By Deployment Model

5.1 Overview

6 Stem Cell Alopecia Treatment Market, By Solution 6.1 Overview

7 Stem Cell Alopecia Treatment Market, By Vertical

7.1 Overview

8 Stem Cell Alopecia Treatment Market, By Geography 8.1 Overview 8.2 North America 8.2.1 U.S. 8.2.2 Canada 8.2.3 Mexico 8.3 Europe 8.3.1 Germany 8.3.2 U.K. 8.3.3 France 8.3.4 Rest of Europe 8.4 Asia Pacific 8.4.1 China 8.4.2 Japan 8.4.3 India 8.4.4 Rest of Asia Pacific 8.5 Rest of the World 8.5.1 Latin America 8.5.2 Middle East

9 Stem Cell Alopecia Treatment Market Competitive Landscape

9.1 Overview 9.2 Company Market Ranking 9.3 Key Development Strategies

10 Company Profiles

10.1.1 Overview 10.1.2 Financial Performance 10.1.3 Product Outlook 10.1.4 Key Developments

11 Appendix

11.1 Related Research

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Celgene Gave This Tech Back to Editas Medicine, but It Could Prove Valuable – The Motley Fool

In the middle of November, Editas Medicine (NASDAQ:EDIT) and Celgene (NASDAQ:CELG) announced changes to a development pact originally formed in 2015 with Juno Therapeutics, which is now part of Celgene. The agreement was amended in 2018, too, so the fact that changes were made wasn't necessarily big news. Editas received a $70 million upfront payment for executing the amended agreement, which was interpreted as the main takeaway from the announcement.

The announcement barely registered with investors and few gave it much thought for too long, especially after promising early results from the first clinical trials using a CRISPR-based medicine were announced by CRISPR Therapeutics days later.

But revisiting the amended collaboration agreement, and specifically what changes were made, hints at the long-term development plans of Editas Medicine. In short, it now has full control over an important class of immune cells. Whether that means the gene-editing pioneer lands another major development partner or goes full-steam ahead alone, investors can't overlook the significance.

Image source: Getty Images.

The basic scientific goal of the collaboration hasn't changed. Editas Medicine will use its gene-editing technology platform to engineer T cell receptors (TCR), while Juno Therapeutics will leverage its immunotherapy leadership to develop the engineered cellular medicines in clinical trials.

Why engineer TCRs? Immune cells rely on their receptors to identify targets, such as pathogenic bacteria and cancer cells. But immune cell receptors can be confused by molecules secreted within the tumor microenvironment, forcing them to halt their attack. They can also incorrectly attack an individual's own cells to trigger an autoimmune disease. A more recent concern stems from cellular medicines derived from a donor. Since the donor cells present different receptors compared to what the recipient's native T cells carry, the recipient's immune system (correctly) identifies the immunotherapy as a foreign substance, attacks it, and renders it less effective and less safe.

Therefore, it makes sense to engineer TCRs to create more potent and stealthier immunotherapies that are less likely to be tricked. Editas Medicine and Celgene still intend to do just that, albeit with subtle, yet important, differences to their development agreement.


Previous Agreement (2015, 2018)

Amended Agreement (2019)



Cancer and autoimmune diseases

Types of cells

CAR-T cells, alpha-beta T cells, gamma-delta T cells

Alpha-beta T cells

Juno Therapeutics exclusivity

Editas Medicine prohibited from all other work with CAR-T and TCRs in oncology

Editas Medicine prohibited from all other work on alpha-beta T cells and T cells derived from pluripotent stem cells

Upfront payment

$57.7 million (includes milestones collected under agreement)

$70 million

Milestone potential

$920 million plus tiered royalties

$195 million plus tiered royalties

Data source: SEC filings.

Essentially, Editas Medicine and Celgene have scaled back their original agreement in cancer and expanded their work to include autoimmune diseases. The most important detail is that the amended agreement allows the gene-editing pioneer to pursue the development of gamma-delta T cells, which were previously under the exclusive control of Juno Therapeutics. What does that mean?

Image source: Getty Images.

Without getting too far into the weeds, there are two main types of TCRs: alpha-beta and gamma-delta. The name refers to the molecular structure of the receptor, but that's not the important part.

Gamma-delta T cells, which comprise only about 5% of the T cells in your body, are thought to be one of the missing links in our understanding of the immune system. They're a mysterious bunch, but there could be significant value residing in the knowledge gaps.

These unique immune cells are governed by their own unique set of rules (relative to their alpha-beta peers) and straddle the innate immune system (what we're programmed with at birth) and adaptive immune systems (what's programmed as we encounter new environments throughout life). Gamma-delta T cells could be tinkered with in gut microbiome applications, to treat cardiovascular diseases, and to neutralize antibiotic-resistant infections. But the nearest commercial target of the mysterious immune cells is likely to be treating solid tumor cancers.

They possess potent anti-tumor activity where current immunotherapies fail, such as attacking cancer cells that lack tumor-specific antigens to target or that have become immune to checkpoint inhibitors. In fact, there's a link between certain cancer outcomes and the activity of specific gamma-delta T cells.

Given that, why would Celgene amend the agreement to ditch the rare subset of immune cells? Well, in August 2019, Celgene inked with a start-up called Immatics to develop engineered TCRs. The start-up's platform is based on gamma-delta tech.

Don't feel too bad for Editas Medicine, though. SEC filings reveal that the gene-editing pioneer didn't receive any money from the original collaboration deal with Celgene in the first nine months of 2019. That suggests the work had stalled or that the amendment was being hammered out for some time. The gene-editing pioneer wrestled back control of the tech and took a $70 million upfront payment to boot. While the potential milestone payments in the amended agreement are significantly lower than the originally promised bounty, Editas Medicine can offset that by signing a lucrative collaboration deal with a new partner.

There should be plenty of interest. Fellow gamma-delta T cell developer Adicet Bio recently landed an $80 million series B round funded in part by Johnson & Johnson, Regeneron,Samsung Biologics(not the same company as the electronics powerhouse), and Novartis. There's also Immatics, GammaDelta Therapeutics, and a handful of other start-ups making noise in the space.

Some competitors are directly engineering gamma-delta cells, and others are developing molecules to trigger the immune cells into action. Editas Medicine believes it has the edge, as it has a relatively precise and efficient method for engineering immune cells: gene editing.

The amended collaboration deal between Editas Medicine and Celgene received relatively little attention from investors. Perhaps that was a good thing, as Wall Street likely would have overreacted to the reduced scope of development and milestones. But investors that take the time to understand the details might be intrigued by the new research avenue for the gene-editing stock.

Can Editas Medicine become a leading force in gamma-delta T cell development? Perhaps. While it isn't the only company wielding a gene-editing platform, and CRISPR gene editing isn't the only type of gene editing, the company is well-positioned to take advantage of the opportunity. Investors will have to wait to see how (or if) the development strategy evolves around the new tech.

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Celgene Gave This Tech Back to Editas Medicine, but It Could Prove Valuable - The Motley Fool