Associations Between miRNAs and Two Different Cancers: Breast and Colo | CMAR – Dove Medical Press

Berrin Papila Kundaktepe,1 Volkan Sozer,2 Cigdem Papila,3 Sinem Durmus,4 Pinar Cigdem Kocael,1 Gonul Simsek,5 Remise Gelisgen,4 Kagan Zengin,1 Kenan Ulualp,1 Hafize Uzun4

1Department of General Surgery, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey; 2Department of Biochemistry, Yildiz Technical University, Istanbul, Turkey; 3Department of Internal Medicine, Division of Oncology, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey; 4Department of Medical Biochemistry, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey; 5Department of Physiology, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey

Correspondence: Hafize UzunDepartment of Medical Biochemistry, Cerrahpasa Faculty of Medicine, Istanbul University Cerrahpasa, Cerrahpasa, stanbul 34303, TurkeyTel +90 212 414 30 56Fax +90 212 633 29 87Email huzun59@hotmail.com

Objective: Screening approaches using microRNAs (miRNAs) have been gaining increased attention owing to their potential applications in the diagnosis, prognosis, and monitoring of cancer, because aberrant miRNA expression plays a role in the development and advancement of malignancies. The objectives of this study were to characterize mir21, miR31, mir143, mir145, and control RNU43, which are differentially expressed in peripheral blood mononuclear cells (PBMCs) of breast and colorectal cancer patients, compared to that in controls and to establish whether this is specific to breast and colon cancer for use as tumor markers.Methods: Thirty newly diagnosed patients with breast cancer and 30 patients with colorectal cancer were enrolled together with 30 healthy controls. PBMCs were isolated from venous blood samples of individuals. Next, miRNA expression analysis was performed by a two-step method of reverse transcription and qPCR.Results: The expression levels of miR-143 and miR-31 were significantly decreased, whereas the expression levels of miR-145 and miR-21 were significantly increased in breast cancer patients compared to those in healthy subjects. Moreover, the expression levels of miR-143, miR-145, and miR-21 were significantly increased and, in contrast, the changes in the expression levels of miR-31 were not statistically significant in colon cancer compared to those in healthy subjects. miR-21 exhibited the highest increase in both breast and colon cancers. There was a weak positive correlation between miR-145 and CA-15.3 in patients with breast cancer (r = 0.451; p = 0.012). miR-143 was positively correlated with the TNM stage in colon cancer patients (r = 0.568; p = 0.001).Conclusion: A biomarker panel composed of miR-21, miR-31, miR-143, and miR-145 in PBMC may provide a new diagnostic approach for the early detection of breast and colon cancer. As miR-21 expression was found to be the highest among all the miRNAs evaluated, it may represent a new tumor biomarker and a candidate therapeutic drug or gene target in colon and breast cancer.

Keywords: breast cancer, colon cancer, peripheral blood mononuclear cells, mir21, mir31, mir143, mir145

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Associations Between miRNAs and Two Different Cancers: Breast and Colo | CMAR - Dove Medical Press

Bio-Based Platform Chemicals Market and its Key Opportunities and Challenges | Zhejiang Guoguang Biochemistry Co. Ltd, Reverdia, Cargill Incorporated…

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Purdue University to Offer Free Tampons, Pads in Bathrooms – The New York Times

WEST LAFAYETTE, Ind. Purdue University will offer free tampons and other feminine hygiene products in the campus bathrooms in response to student advocates who have been pushing for the move for three years.

University President Mitch Daniels on Thursday credited the University Senate, a faculty-led body, for proposing the initiative in a resolution that described feminine hygiene products as a basic necessity that should be in campus restrooms free of charge. The measure was set to be voted on later this month, but Daniels obtained permission from the University Senate to go ahead and implement it.

"I think people will treat it responsibly," Daniels told WLFI in an interview. "That's what the Purdue family does."

Its not yet clear when the public university will stock its West Lafayette campus bathrooms with free pads, liners and tampons, a university spokesman said.

Alison Rickert, a junior studying neurobiology and physiology at Purdue, founded The Period Project an initiative aimed at providing menstrual products to those who need them both in and out of university walls. She said Purdues decision resulted from she and other students advocating for the same issue.

We didnt all know each other, necessarily, Rickert said. But we all were heading to the same place. Thats how movements happen, right?

Rickert added that she expected resistance, but Daniels support reassured her.

Its a lot of work for someone and some money, Rickert said Thursday. But its happening. Finally. What a great day.

The West Lafayette campus has more than 650 womens and gender-neutral bathrooms in the academic and administration buildings, Purdue spokeswoman Rebecca Terry said. That number doesnt include residence halls or athletic facilities.

___

This story corrects the attribution of a statement from Rickert.

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Purdue University to Offer Free Tampons, Pads in Bathrooms - The New York Times

Conquer your health and fitness goals with these subscriptions – ITworld

Its officially 2020, and many of us are trying to kick off the new year by living a healthier and more productive life. But making good on that New Years resolution to eat better and hit the gym is always harder than it sounds, which is why weve rounded up five best-selling diet and fitness products and subscriptions that will help you hit your goals faster and more efficiently. Enjoy.

1. Ultimate Meal Plans: Lifetime Subscription

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When it comes to living a healthier life, the most important thing you can do is eat better. These Ultimate Meal Plans make it easy to fine-tune your diet and lose weight by offering 28 healthy meal plans per week, each of which is fun and easy to make and features an affordable ingredients list.

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Boost not only your health but the health of those around you with this accredited Health & Nutrition Life Coach Certification, which will teach you wholistic ways in which you can build powerful motivational techniques, craft diet and fitness plans, gain an understanding of human physiology, and more.

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This meal-planning system streamlines the process of eating well by combining planning, shopping, and cooking into an all-in-one app. Youll be able to acquire detailed nutritional information based on your unique body, get weekly cooking lists with delicious ingredients, and keep up with detailed stats on your health progress.

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This story, "Conquer your health and fitness goals with these subscriptions " was originally published by TechConnect.

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Virus expert and cancer biologist Harry Rubin dies at 93 – UC Berkeley

Harry Rubin in 1989. (UC Berkeley photo by Jane Scherr)

Harry Rubin, a leader in the search to understand how viruses cause cancer research that ultimately led to the discovery of cancer-causing genes called oncogenes died on Sunday, Feb. 2, at the age of 93. Rubin was a professor emeritus of molecular and cell biology at the University of California, Berkeley.

A veterinarian by training, Rubin began investigating in the 1950s how normal cells turn into cancer cells a process called transformation. This was at a time before genes could be cloned and sequenced, and much of his research relied on manipulating cultured cells in a petri dish.

Many labs were beginning to work with tumor viruses as the only tractable way to understand cancerous transformation, and Rubin chose to focus on a virus known since 1911 to cause cancer in chickens: the Rous sarcoma virus (RSV). RSV is an RNA virus, which means that it carries its genetic instructions in the form of RNA, not DNA. The virus tricks cells into reverse transcribing its RNA into DNA and integrating it into its own genome.

At that time, there was really no way of studying the molecular or genetic basis of cancer by studying cancer cells, because the genome of the cell is so enormous, said G. Steven Martin, one of Rubins former postdoctoral fellows and a UC Berkeley professor emeritus of molecular and cell biology. Before the advent of cloning and genetic sequencing, we couldnt look into the cancer cell and find the genes involved in cancer. Since tumor viruses have such small genomes and carry only a few genes, it was clear that studying tumor viruses would provide an entry point into the basic mechanisms of cancer.

Between 1953 and 1958, Rubin worked as a postdoctoral fellow and, later, as a research fellow in the lab of virologist Renato Dulbecco at the California Institute of Technology in Pasadena. In 1955, Rubin showed that every cell in an RSV-induced tumor was capable of releasing the virus, implying that RSV was permanently associated with the host cell and suggesting that it plays a direct and continuing role in perpetuating the cell in its malignant state.

Then, working with Caltech graduate student Howard Temin, Rubin developed a way to measure the amount of infectious virus using cultured fibroblast cells from chicken embryos. This opened the way for quantitative studies of the mechanism by which RSV transforms normal cells into cancerous cells.

Dulbecco and Temin later shared the 1975 Nobel Prize in Physiology or Medicine for their work on tumor-causing viruses.

When Rubin moved to UC Berkeley in 1958 to join the Department of Virology, he continued work on RSV and developed other assays, including one to detect avian leukosis virus in vaccines, such as the measles vaccine, that are produced in chicken cell cultures.

Harry Rubin and his wife Dorothy.

He also showed that one strain of RSV was a replication-defective virus that could transform normal cells into cancer cells, but required a leukosis virus a helper virus to replicate and spread. In other words, the RSV could transform, but not replicate, itself, while the helper virus could replicate, but not transform.

This was one of the very first observations to suggest that the virus might carry information about cell transformation and tumorigenesis that was separate from the information needed for the replication cycle of the virus, Martin said.

Rubins work on RSV earned him a prized Lasker Award in 1964.

The work of Drs. Rubin and Dulbecco proves that cells can carry, for many generations, a foreign nucleic acid, whether RNA or DNA, that is responsible for the malignant properties of these cells, the Lasker Foundation wrote in giving them the award in clinical research.

Rubin also received the 1961 Eli Lilly Award in Bacteriology and Immunology and the 1963 Merck Research Award for his work on RSV and was elected to the National Academy of Sciences in 1978.

In 1970, a viral gene responsible for cancerous transformation, now known as viral src, or v-src, was identified through genetic and biochemical studies on RSV carried out by Martin, who was then in the Rubin lab, Peter Vogt at the University of Washington in Seattle and Peter Duesberg at UC Berkeley. This allowed Harold Varmus and Michael Bishop of UC San Francisco to identify an analogous gene in the cellular genome a gene evidently stolen by the Rous sarcoma virus. Called cellular src, or c-src, it was the first known proto-oncogene, that is, a normal gene that, when mutated, can trigger cancer. Many more proto-oncogenes have been discovered since then. The discovery won Bishop and Varmus the 1979 Nobel Prize in Physiology or Medicine.

The significance of the work on the Rous sarcoma virus is that it led to the work on cellular genes that can cause cancer, Martin said. The idea that, by studying the virus, one could get an insight into the cellular and genetic mechanism of carcinogenesis was, in fact, vindicated.

Although Rubins research set the stage for the discovery of oncogenes, by the early 1970s he had switched his focus from viruses to the biology of transformed cells, looking at the mechanisms of growth control and, in particular, the role of inorganic ions in cellular regulation. In later years, he studied the origin of spontaneous transformation of animal cells in culture, using this system as a model for tumor progression.

Harry Rubin was born in New York City on June 23, 1926, the son of Russian Jewish immigrants. His father ran a grocery store in Manhattan. As a teenager, he worked on farms in upstate New York and at 16 enrolled in the veterinary school at Cornell University. Upon graduation in 1947 with a D.V.M. degree, he went to Mexico to help with an outbreak of hoof-and-mouth disease, then joined the U.S. Public Health Service in Montgomery, Alabama, to work on viral diseases, including rabies and Eastern equine encephalitis. In a 1991 profile in California Monthly magazine, he referred to it as time spent chasing cows and horses in Mexico and Louisiana.

Seeking new challenges, he enrolled at New York University and, a year later, in 1952, convinced Nobel Prize winner Wendell Stanley to let him work in his Virus Laboratory at UC Berkeley. Rubin transferred to Caltech in 1953, returning to join the UC Berkeley faculty in 1958, where he eventually occupied Stanleys old office. He retired as an emeritus professor in 2001.

Rubin is survived by his wife, Dorothy, of Berkeley; three children, Andrew, Janet and Clinton Rubin; six grandchildren; and six great-grandchildren. He and his wife were longtime members of Congregation Beth Israel in Berkeley.

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Virus expert and cancer biologist Harry Rubin dies at 93 - UC Berkeley

Is There Any Science Behind Beauty Sleep? – Labmate Online

A new study from the University of Manchester suggests the popularised term "beauty sleep" could be more than just a saying. After analysing body clocks of mice, a team of biologists maintain a good night's sleep plays an important role in preparing the body for the day ahead and replenishing cell structures.

The findings were published in the journal Nature Cell Biology and explain how body clock mechanisms support the extracellular matrix (ECM), a three-dimensional network of macromolecules that build connective tissue cells such as skin, bone, cartilage and tendons. Professor Karl Kadler, lead author of the study, argues that understanding the importance of the body clock and the extracellular matrix could shed new light on the ageing process.

Kadler explains that more than half the body is made up of matrix. Of this matrix, 50% is collagen, a key extracellular matrix structural protein and major component of connective tissues. Roles of collagen include providing the skin with structure and elasticity and strengthening bones. By the time the body reaches the age of 17 collagen has fully formed, suggesting the body starts to slowly deteriorate moving forward.

"Collagen provides the body with structure and is our most abundant protein, ensuring the integrity, elasticity and strength of the body's connective tissue," says Kadler.

Collagen is made up of rope-like structures called fibrils, which are woven together by cells to create tissues. During the research, the biologists discovered two types of fibrils. The first were relatively thick, measuring around 200 nanometres in diameter. They form by the age of 17 and stay with the body throughout its lifespan. The second type of fibril was thinner, measuring just 50 nanometres in diameter. As the body is put through its daily paces these thinner fibrils snap and become damaged. They are automatically repaired and replenished at night, with the team asserting that sleep plays a critical role in supporting this process.

"It's intuitive to think our matrix should be worn down by wear and tear, but it isn't and now we know why: our body clock makes an element which is sacrificial and can be replenished, protecting the permanent parts of the matrix."

Kadler says detailed knowledge of how the body clock influences the extracellular matrix could help scientist understand human biology at its most fundamental level. "It might, for example, give us some deeper insight into how wounds heal, or how we age," he predicts.

From exploring the role of the body clock to analysing interactions between different species, science is continually offering new insight into how the world works. To find out more about the cutting-edge composition-gradient multi-angle light scattering (CG-MALS) technique, don't miss 'Fusion Protein Complexes Analysed by CG-MALS - Non-equivalent, Multivalent Interactions.'

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Is There Any Science Behind Beauty Sleep? - Labmate Online

When rocket blasts off for space station, EVMS will be along for the ride – Daily Press

Just days before a planned rocket launch, a crate the size of a dishwasher destined for the International Space Station had been routed to the wrong Norfolk address.

The mysterious wooden box held equipment for scientists at Eastern Virginia Medical School who needed to prepare it to be shot into orbit from Wallops Island on Sunday.

Instead, it sat at a senior high-rise, intriguing elderly residents with its many Hawaii labels.

The delivery mishap gave Northrop Grumman project manager JoElla Delheimer a dose of last-minute anxiety. The stress lifted when she learned that the box was only a couple of blocks away from the EVMS campus.

One thing about flying a rocket to space is that you cant be five minutes late, she said.

Through a multimillion-dollar contract, scientists are using the Norfolk medical schools laboratories and supplies to prepare experiments for astronauts. And while certain studies are done in orbit, scientists down below will conduct control experiments at EVMS.

The partnership with NASA contractor Northrop Grumman began with a mission last fall and will continue for at least three years, aiding five more space launches out of Wallops Island.

Weather permitting, Northrop Grumman plans to send up its unmanned Antares rocket and Cygnus spacecraft, carrying more than 8,000 pounds of cargo, at 5:39 p.m. Sunday from the Virginia flight facility.

So long as the Cygnus is on schedule, it will dock at the station Tuesday.

Bill Wasilenko, the vice dean of research at EVMS, said one reason the school got involved was that it would bring in researchers from around the world. On a later mission, for example, the school will host some Japanese scientists through the contract.

A lot of biomedical benefit is likely to come out of doing the research that we do up there, in terms of drug development. There are ways in which crystals develop in space that are different that could lead to new pharmaceuticals, new therapeutics, he said. The hope is our medical students will mingle around the scientists, learn about what were doing from mission to mission, come to our seminars. Maybe some of them will get interested in space medicine.

Two research teams were at the Norfolk campus this week preparing experiments and hardware for liftoff.

One group from Hawaii plans to run a tissue-culturing study in a device it developed called the Mobile SpaceLab. The equipment has a sort of set-it-and-forget-it capability: Once its at the space station, it will perform biology tests without crew. The device will take pictures of the cell activity every six minutes for four weeks.

Devin Ridgley, chief biologist for the Scorpio-V division of HNu Photonics, said the automation frees up the crew to work on other things and eliminates some of the potential for mistakes.

Weve been trained with this equipment and cell biology for many years now, but the crew may not be as well-trained, he said. Some are fighter pilots deservedly crew, but maybe not the best at doing cell biology experiments.

On Thursday at EVMS, Ridgley started growing a type of cancer cell, neuroblastoma, for the experiment. The study will look at the effects of microgravity the weak gravitational conditions of the space station at the subcellular level.

The second team, from BioServe Space Technologies based at the University of Colorado, was busy in a different lab preparing kits for another microgravity-related study. Mark Rupert, associate director of BioServe, said the hardware sort of like petri dishes that work without gravity will facilitate research on bone loss using osteoblast cells.

On Earth there is a way to levitate organisms with strong magnets, which may provide a way to study the bone loss that happens in space, he said. But its unclear if that simulation is a good substitute. The experiment, run by a researcher at the University of Minnesota, will compare the methods. If the magnet technique is suitable, it could be a cheaper way to study the problem in the future than running more tests at the space station.

Because astronauts experience bone loss in orbit, researchers want to learn more about it, not only to help future space travelers but to better understand a wide range of disorders, such as osteoporosis.

To get ready for its supporting role for NASA, EVMS sent staff down to the Kennedy Space Center in Florida to tour the facility and observe operations. There they saw things like researchers who were growing lettuce talk to an astronaut, who was also growing the leafy vegetable at the space station.

The laboratories that are needed for the pre-launch preparation of experiments primarily occur at the Kennedy Space Center, but theyre overwhelmed. They have a backlog of experiments, Wasilenko said.

That makes EVMS, a two-hour drive from the Wallops Island launchpad, well-positioned for providing similar services, especially for experiments that involve live tissue or rodents that must be packed at the last minute. Though no critters will board the Cygnus this time, about 40 mice, born and raised on campus, flew in the previous mission that took off in November.

Northrop Grumman said that no other place it considered was large enough or had the capabilities of EVMS.

One of the primary things that brought us here, of course, was the animal care facility, Delheimer said. Their reputation is tremendous.

Separate from the Northrop Grumman contract, EVMS has two NASA-funded studies. Richard Britten, an associate professor of radiation oncology and biophysics, is examining the effects of galactic cosmic radiation on brain function. And Larry Sanford, professor of pathology and anatomy, is studying in-flight stress and sleep disturbances on brain function.

EVMS administrators hope the schools new role will open opportunities for more of its own biomedical research. Wasilenko thinks its an interesting coincidence that a lot of the research coming out of EVMS right now happens to be on similar subjects as those being studied in the space station.

Diabetes, obesity, circadian rhythm work and now the bone thing, he said. "Theres a lot of overlap, and thats the appeal of researchers coming here and mingling with our researchers. If they hit it off, they could work together on some future projects.

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When rocket blasts off for space station, EVMS will be along for the ride - Daily Press

Pedal to the Metal: Speeding Up Treatments for ALS – UANews

A therapeutic intervention for amyotrophic lateral sclerosis, better known as ALS or Lou Gehrig's disease, could be on the horizon thanks to unexpected findings by University of Arizona researchers.

ALS is the progressive degeneration of motor neurons that causes people to lose the ability to move and eventually speak, eat and breathe.

Within the neuronal cells of patients with ALS and other neurodegenerative diseases, two proteins TDP-43 and FUS are often found in bundles of molecular junk called aggregates, which can accumulate to deadly levels.

Its not clear yet if TDP-43 aggregates themselves are truly toxic or a sign that things have gotten really bad in a cell, and this is its last Hail Mary trying to keep things in order, said Ross Buchan, assistant professor of molecular and cellular biology and a member of the BIO5 Institute. These aggregates could possibly be toxic because they are trapping other useful molecules and not letting them do their job.

Buchan and his team set out to investigate how healthy cells clear harmful aggregates from the cell.

What they found was that the aggregates were being removed via endocytosis, which was surprising for two reasons. First, the textbook definition of endocytosis is a process in which proteins, nutrients and chemical signals from outside the cell are brought inside to be degraded and recycled by the lysosome. But in this case, endocytosis was working on aggregates that were already inside the cell. And second, theres already a mechanism, called autophagy, in place for recycling junk that originated from within a cell, yet endocytosis was doing what autophagy should have been doing instead.

Autophagy and also likely, although its still uncertain, endocytosis often slows as we age, and there are genes that are mutated in that pathway that are associated with some neurodegenerative diseases. So people thought the reason aggregates form when we get old, or when you have these diseases, is because that pathway isnt working very well, Buchan said.

Additionally, the accumulation of aggregates slows the endocytosis pathway further, creating a negative feedback loop within the cell.

If we genetically or chemically impede the pathway, then the TDP-43 protein accumulates and becomes super toxic. The cool thing, as far as a therapy for ALS is concerned, is that we can also do the reverse, Buchan said. We can make the endocytosis pathway work better by over-expressing parts of it, like putting the gas pedal down so it goes really fast. When we do that, then the TDP-43 aggregates are cleared really efficiently and its no longer toxic.

Many of the papers experiments were performed in yeast cells, but the general findings are likely translatable to human cells based on initial findings. Buchan called yeast a powerful genetic tool, for understanding cellular processes, including those in human disease.

While the results from Buchans lab are unexpected If I were to pull a textbook off the self, it would say endocytosis is for things that are outside the cell, not inside, so its still pretty heretical, he said there are other labs with data suggesting endocytosis can also clear already internalized proteins.

The next step is to determine how TPD-43 and FUS enter the endocytic pathway, and then to develop ways to make endocytosis work better in these cells.

There are genetic ways to do that, but not chemically at the moment, Buchan said. We think if we have a drug that inhibits the negative regulators of endocytosis, the pathway will go faster as a result. We have a couple ideas of where to start next.

The findings were published in the journal Molecular and Cellular Biology. Buchans co-authors include undergraduate Amanda Warner, former post-doctoral fellow Guangbo Liu, graduate student Aaron Byrd, former graduate student Fen Pei, assistant research scientist Eman Basha and former lab technician Allison Buchanan.

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Pedal to the Metal: Speeding Up Treatments for ALS - UANews

Sonoma Biotherapeutics launches with $40 million in Series A funding to advance regulatory T cell therapy in autoimmune and degenerative diseases -…

Company founded by four pioneers of Treg cell biology and cell therapy and financed by a syndicate of leading biotech investors

SOUTH SAN FRANCISCO, Calif. and SEATTLE, Feb. 6, 2020 /PRNewswire/ -- Sonoma Biotherapeutics, a privately held company developing regulatory T cell (Treg) therapies for autoimmune and degenerative diseases, launched today in South San Francisco, CA and Seattle, WA with $40 million in its Series A financing. Sonoma brings together next-generation research, development and manufacturing capabilities in cell therapy and genetic engineering with an accomplished team of executives, scientists, board members and investors with extensive experience in the fields of cell therapy and drug discovery.

"With this team and our assembled expertise and technologies, we are in an ideal position to move adoptive cell therapy beyond cancer, to establish safe, effective and long-lasting treatments for a range of conditions where current drugs and biologics are simply not good enough," said founder and CEO Jeffrey Bluestone, PhD. "As the immune system's master regulators of protecting the body against self-destruction, Treg cell therapy is perhaps the ideal means to shut down unwanted immune reactions and provide meaningful treatment for patients."

The financing involves an investor syndicate that includes Lyell Immunopharma, ARCH Venture Partners, Milky Way Ventures and 8VC. "Treg therapies have the potential to transform the treatment of autoimmune and degenerative diseases," said Robert Nelsen, managing partner and co-founder of ARCH Ventures Partners. "Sonoma Biotherapeutics has assembled the team and capabilities required to make this vision a reality for patients and their families."

The goal of Treg therapy is to restore a state of self-tolerance by halting harmful inflammatory responses in autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease and multiple sclerosis, along with degenerative diseases including amyotrophic lateral sclerosis (ALS) and Alzheimer's. Over 50 million Americans currently live with an autoimmune disease, and millions more with some form of degenerative diseases. For many, existing therapies are ineffective at controlling their disease.

Tregs have a clear role in many of these conditions. These cells' natural ability to migrate to inflamed tissues and control harmful immune responses make them ideal for treating a range of conditions. In addition, the ability to engineer Treg cells to target specific disease-causing antigens reduces the potential for unwanted systemic effects. The role of Tregs in tissue maintenance and repair offers the potential for effective, durable and restorative treatments.

Sonoma Biotherapeutics is co-founded by four of the foundational scientists in the Treg field:

Collectively, the founding team brings expertise and proprietary methodologies across the Treg drug discovery and development process, including selection, manipulation, editing, regulation and translation for clinical use. Together, Drs. Bluestone and Tang have pioneered adoptive Treg cell therapy in some of its first clinical uses in type 1 diabetes, lupus and organ transplantation. Drs. Rudensky and Ramsdell co-discovered FOXP3, a critical transcription factor for Treg development and function, and in 2017 were awarded the Crafoord Prize by the Royal Swedish Academy of Sciences for their landmark studies. They are complemented by an experienced senior management team and seasoned board of directors.

"The Sonoma Biotherapeutics leadership are responsible for a significant portion of our understanding of the nature of Treg cells, their role in disease and their potential for use as a cell therapy," said Dr. Rick Klausner, CEO of Lyell Immunopharma and newly appointed Chair of the Sonoma Biotherapeutics Board of Directors. "Perhaps more importantly, they understand the requirements of a successful cell therapeutic and the corresponding challenges in defining the pathway to market. We look forward to a strong partnership between Lyell and Sonoma Biotherapeutics."

In this regard, Sonoma Biotherapeutics has entered into a strategic partnership with Lyell that provides both parties with access to technologies and know-how to enhance the durability, stability and specificity of cell therapies in their respective indications of focus. This partnership will further enable Sonoma's rapid translation of Treg therapies from target identification and discovery, through preclinical and clinical development.

Senior Management Team

Jeffrey Bluestone, PhD, Founder, CEO & PresidentFred Ramsdell, PhD, Founder & CSOPeter DiLaura, Chief Business & Strategy OfficerJoshua Beilke, MBA, PhD, VP Translational Development

Board of Directors

Rick Klausner, MD (Chair) Founder & CEO, Lyell Immunopharma, Inc.Maggie Wilderotter CEO, Grand Reserve Inn; former board member, Juno TherapeuticsToni Hoover, PhD Director, Strategy, Planning and Management for Global Health, Bill & Melinda Gates FoundationTerry Rosen, PhD CEO, Arcus BiosciencesDavid Moskowitz, PhD Principal, 8VC (observer)Jeffrey Bluestone, PhD, CEO & President, Sonoma Biotherapeutics

About Sonoma Biotherapeutics

Sonoma Biotherapeutics is a privately held, San Francisco and Seattle-based company leading the development of adoptive Treg therapies cell for autoimmune and degenerative diseases. Using next generation genome editing and target-specific cell therapy, Sonoma is focused on developing its best-in-class platform across the entire spectrum of Treg cell therapeutic capabilities. Founded by pioneers in Treg biology and cell therapy, the company brings together leading expertise and proprietary methodologies for the discovery and development of disease modifying and curative therapies.

Contact: media@sonomabio.com

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Sonoma Biotherapeutics launches with $40 million in Series A funding to advance regulatory T cell therapy in autoimmune and degenerative diseases -...

Trillium Therapeutics Announces Changes to Its Board of Directors – BioSpace

CAMBRIDGE, Mass., Feb. 07, 2020 (GLOBE NEWSWIRE) -- Trillium Therapeutics Inc.. (Trillium or the Company) (NASDAQ/TSX: TRIL), a clinical stage immuno-oncology company developing innovative therapies for the treatment of cancer, today announced that Paul Walker has been appointed to the Companys Board of Directors, and Dr. Ali Behbahani has been appointed as a Board Observer, effective February 6, 2020.

We are delighted to welcome Mr. Walker to the Board of Directors and Dr. Behbahani as a Board Observer, and look forward to their guidance as we work to bring to patients our CD47 programs, stated Dr. Robert Kirkman, Executive Chair of Trillium Therapeutics.

We are excited about Trilliums recent progress and look forward to working with the leadership team as they expand their clinical development program, said Paul Walker.

Mr. Walker and Dr. Behbahani are general partners with New Enterprise Associates (NEA), a global venture capital firm with more than $20 billion of cumulative committed capital invested in healthcare and technology companies. Prior to joining NEA, Paul worked at MPM Capital as a General Partner with the MPM BioEquities Fund, where he specialized in public, PIPE and mezzanine-stage life sciences investing. Previously, he was a portfolio manager at Franklin Templeton Investments. Paul received a BS in Biochemistry and Cell Biology from the University of California at San Diego, and holds the Chartered Financial Analyst (CFA) designation.

Dr. Behbahanis previous positions include a consultant in business development at The Medicines Company, a Venture Associate at Morgan Stanley Venture Partners and as a Healthcare Investment Banking Analyst at Lehman Brothers. He concurrently earned his MD degree from The University of Pennsylvania School of Medicine and his MBA degree from The University of Pennsylvania Wharton School.

The Company also announced that Dr. Robert Uger, Trilliums Chief Scientific Officerhas resigned from the Board of Directors effective February 6, 2020.

About Trillium Therapeutics

Trillium is an immuno-oncology company developing innovative therapies for the treatment of cancer. The Companys two clinical programs, TTI-621 and TTI-622,target CD47, a do not eat signal that cancer cells frequently use to evade the immune system.

The Companys pipeline also includes a preclinical STING (stimulator of interferon genes) agonist program. As previously announced, the program is earmarked for out-licensing.

For more information visit: http://www.trilliumtherapeutics.com

Caution Regarding Forward-Looking Information

This press release contains forward-looking statements within the meaning of applicable United States securities laws and forward-looking information within the meaning of Canadian securities laws (collectively, forward-looking statements). Forward-looking statements in this press release include statements about, without limitation, the belief that Trilliums programs could achieve best-in-class status for CD47 blocking agents and Trilliums future plans and objectives for its CD47 programs. With respect to the forward-looking statements contained in this press release, Trillium has made numerous assumptions regarding, among other things: the effectiveness and timeliness of clinical trials; and the completeness, accuracy and usefulness of the data. While Trillium considers these assumptions to be reasonable, these assumptions are inherently subject to significant scientific, business, economic, competitive, market and social uncertainties and contingencies. Additionally, there are known and unknown risk factors that could cause Trilliums actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements contained in this press release. Factors that may cause such a difference include, without limitation, risks and uncertainties related to the reliance on positive results of preclinical and early clinical research as such results are not necessarily predictive of results of later-stage clinical trials. A further discussion of risks and uncertainties facing Trillium appears in Trilliums Form 20-F for the year ended December 31, 2018 is filed with Canadian securities authorities and with the U.S. Securities Exchange Commission, each as updated by Trilliums continuous disclosure filings, which are available at http://www.sedar.comand at http://www.sec.gov. Forward-looking statements are not guarantees of future performance and accordingly undue reliance should not be put on such statements due to the inherent uncertainty therein. All forward-looking statements herein are qualified in their entirety by this cautionary statement, and Trillium disclaims any obligation to revise or update any such forward-looking statements or to publicly announce the result of any revisions to any of the forward-looking statements contained herein to reflect future results, events or developments, except as required by law.

Company Contact:James ParsonsChief Financial OfficerTrillium Therapeutics Inc.416-595-0627 x232james@trilliumtherapeutics.com

Media Contact:Mike BeyerSam Brown Inc.312-961-2502mikebeyer@sambrown.com

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Trillium Therapeutics Announces Changes to Its Board of Directors - BioSpace