Manizheh Narimani,1 Mohammadreza Sharifi,2 Ali Jalili1

1Cancer and Immunology Research Center, Institute of Research for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran; 2Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Correspondence: Ali JaliliCancer and Immunology Research Center, Institute of Research for Health Development, Kurdistan University of Medical Sciences, Sanandaj, IranTel +98-9183771862Email Ali130@gmail.com

Introduction: Human Baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC5) which encodes survivin exhibits multiple biological activities, such as cell proliferation and apoptosis. Survivin is overexpressed in numerous malignant diseases including acute myeloid leukemia (AML). Recent studies have shown that the CRISPR/Cas9 nuclease-mediated gene-editing systems are suitable approachsfor editing or knocking out various genes including oncogenes.Methods and materials: We used CRISPR-Cas9 to knockout the BIRC5 in the human leukemic cell line, HL60, and KG1, and these cell lines were transfected with either the Cas9- and three sgRNAs expressing plasmids or negative control (scramble) using Lipofectamine 3000. The efficacy of the transfection was determined by quantitative reverse transcription-polymerase chain (RT-qPCR) and surveyor mutation assays. Cell proliferation and apoptosis were measured by MTT assay and flow cytometry, respectively.Results: We have successfully knocked out the BIRC5 gene in these leukemic cells and observed that the BIRC5-knocked out cells by CRISPR/Cas9 showed a significant decrease (30 folds) of survivin at mRNA levels. Moreover, cell death and apoptosis were significantly induced in BIRC5-CRISPR/Cas9-transfected cells compared to the scramble vector.Conclusion: We demonstrated for the first time that targeting BIRC5 by CRISPR/Cas9 technology is a suitable approach for the induction of apoptosis in leukemic cells. However, further studies targeting this gene in primary leukemic cells are required.

Keywords: BIRC5, survivin, CRISPR/Cas9 nuclease, AML, KG1 cells, HL60 cell

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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Knockout Of BIRC5 Gene By CRISPR/Cas9 Induces Apoptosis And Inhibits C | BLCTT - Dove Medical Press

University of Iowa professor Gail Bishop has been named a fellow of the American Association for the Advancement of Science (AAAS), the worlds largest general-scientific society and publisher of the journal Science. Election as an AAAS Fellow is an honor bestowed upon AAAS members bytheirpeers.

As part of the Biological Sciences Section, Bishop,a professor of microbiology and immunology at the UI Roy J. and Lucille A. Carver College of Medicine, was selected for her distinguished contributions to the field of immunology, particularly for insights into regulation of T and B lymphocyteactivation.

This year, 443 members were awarded this honor by the AAAS because of their scientifically or socially distinguished efforts to advance science or itsapplications.

I am very honored by this recognition from my scientific colleagues,says Bishop, who also is associate director for basic science research at Holden Comprehensive Cancer Center at the UI, and a professor of internalmedicine.

Bishop joined the UI in 1989. Her research focuses on the molecular mechanisms that regulate the function of blood cells known as lymphocytes in normal immunity, inflammatory disease, and cancer. In particular, Bishop and her team are investigating lymphocyte signaling and interactions between innate and adaptive immune receptors. Her work has implications for treating B-cell cancers, including multiple myeloma, and developing cancervaccines.

She received a doctoral degree in cellular and molecular biology from the University of Michigan in 1983 and performed postdoctoral research at the University of North Carolina, Chapel Hill, focusing on understanding the molecular mechanisms of B lymphocyte activation and interactions between B cells and Tcells.

Bishop has served in many roles during her 30-year UI career. She was appointed as endowed College of Medicine Distinguished Professor of Microbiology in 2001 and Holden Chair of Cancer Biology in 2004; from 1998 to 2013, she directed the Immunology Graduate Program; and in 2004, she was appointed associate director for basic science research of Holden Comprehensive CancerCenter.

This is such a well-deserved honor for Dr. Bishop, who exemplifies the values that we believe make the University of Iowa great, says Brooks Jackson, UI vice president for medical affairs and the Tyrone D. Artz Dean of the UI Carver College of Medicine. As her election to the AAAS demonstrates, she is an established leader in her field of immunology, and she has coupled that scientific success with a deep commitment to training and mentoring the next generation of scientists. Her leadership within our research community has helped to shape an environment where collaboration and collegiality are valued andfostered.

Bishop also is the recipient of many awards and honors for service to the field of immunology. She served as both a section editor of The Journal of Immunology, and is on the current editorial board of the Journal of Leukocyte Biology. She has served as a grant reviewer for the National Science Foundation, the American Heart Association, and the National Institutes of Health, serving as chair of the NIH Tumors, Tolerance and Transplantation studysection.

In 2003, she received the UI Graduate Mentoring Award, and in 2009 was awarded the Iowa Technology Associations Woman of Innovation award for academic research innovation and leadership. Bishop served as president of the American Association of Immunologists in 201213, and is the director of the UI Center for Immunology and Immune-Based Diseases. She was elected as a Distinguished Fellow of the American Association of Immunologists in2019.

This years AAAS Fellows will be formally announced in the AAAS News and Notes section of the journal Science on Nov.29.

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Bishop named 2019 fellow of the American Association for the Advancement of Science - Iowa Now

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Newswise Structural immunologist Dr. Erica Ollmann Saphire is available to discuss Lassa virus and current efforts to develop much-needed antibody therapies to treat often lethal Lassa infections.

A Dutch doctor, who was evacuated from Sierra Leone after contracting Lassa fever, died on November 23, while being treated at Leiden University Medical Center. A second Dutch doctor and a Sierra Leonean anesthetist have also been infected. Other Dutch and British medical personnel have been evacuated.

Lassa typically causes flu-like symptoms but can be deadly in about a quarter of infected people. There is no vaccine.

Earlier this year, Dr. Ollmann Saphire and her team identified the molecular properties shared by antibodies that are particularly efficient at inactivating Lassa virus. The beauty of structural biology is that it gives you the ability to directly see how these therapies work, says Dr. Ollmann Saphire. These high-resolution images become blueprints to engineer potent antibody therapeutics or a vaccine that elicits the desired immune response.

Bio:

Erica Ollmann Saphire, Ph.D. is a Professor of the La Jolla Institute for Immunology. Her research explains, at the molecular level, how and why viruses like Ebola and Lassa are pathogenic and provides the roadmap for medical defense. Her team has solved the structures of the Ebola, Sudan, Marburg, Bundibugyo and Lassa virus glycoproteins, explained how they remodel these structures as they drive themselves into cells, how their proteins suppress immune function and where human antibodies can defeat these viruses.

Dr. Ollmann Saphire also directs the Viral Hemorrhagic Fever Immunotherapeutic Consortium (VIC), which unites 43 academic, industrial and government labs across five continents. The consortiums goal is to understand which antibodies are most effective in patients and to streamline the research pipeline to provide antibody therapeutics against Ebola, Marburg, Lassa and other viruses.

Dr. Ollmann Saphire is available via email, phone and Skype.

Watch Dr. Ollmann Saphire discuss Ebola in the Democratic Republic of Congo.

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Expert available to discuss Lassa virus and antibody therapies against the virus - Newswise

Surprisingly, the antiviral cytokine type I interferon (IFN-I) was found to be a master regulator of metabolic pathways in liver cells. The researchers focused on the urea cycle, a central metabolic node, and found that it is disrupted by IFN-I during viral infection. This led to altered serum metabolite concentrations which regulated antiviral immunity and reduced liver pathology.

The liver is a crucial organ for systemic metabolism in our body. Apart from the turnover of biomolecules and drug metabolism, the liver's main function is the removal of toxic substances from the organism. Hepatocytes, or liver cells, are the most abundant cell type and functional unit of the liver. They are metabolic powerhouses in the healthy organism, but they also serve as important immune signaling platforms during infections. As such, they have the potential to react to a range of cytokines - small molecules that are essential for the coordination of immune responses.

Previous studies in the field of immunology and metabolism, or immunometabolism, unveiled groundbreaking mechanisms about how cells of the immune system need to adjust their metabolism to perform their functions to fight pathogens and cancer. Building on this, Andreas Bergthaler and his group at CeMM aimed to study the immunometabolic changes that occur in the whole organism during infection. They particularly focused on the liver due to its important role in controlling systemic metabolism.

To dissect the involved complex processes, the authors took advantage of the benchmark model of chronic infection, the lymphocytic choriomeningitis virus (LCMV). Research with LCMV had already led to fundamental insights into immunology over the past 80 years, and notably contributed to three Nobel Prizes. Among them is the 2018 Nobel Prize in Physiology or Medicine, which was awarded to James Allison and Tasuku Honjo for their discoveries relating to the revolutionary new cancer immunotherapies which exploit the body's own immune killer cells, or CD8 T cells.

The present study by Alexander Lercher, Anannya Bhattacharya et al. is the result of cross-disciplinary collaborations with researchers from the Medical University of Vienna and the University of Veterinary Medicine in Vienna (Austria), as well as from the Hannover Medical School (Germany), the Cantonal Hospital St. Gallen (Switzerland) and the company Bio-Cancer Treatment International Ltd (China). The study was designed as an integrative unbiased approach to investigate the molecular changes in the liver during chronic infection. Next to expected inflammatory changes, the authors identified intriguing changes in hepatocyte metabolism. Many central metabolic pathways, among them the urea cycle, were found to be repressed upon infection. The urea cycle is essential to remove toxic ammonia from the body to prevent brain damage. Surprisingly, the researchers identified the antiviral cytokine signaling pathway of type I interferons (IFN-I) as a regulator of the urea cycle. This resulted in altered blood concentrations of the amino acids arginine and ornithine. "A key experiment for us was that when we removed the receptor for IFN-I on the surface of hepatocytes, we didn't see these metabolic changes anymore", says Alexander Lercher, first author of the study and PhD student in the laboratory of CeMM Principal Investigator Andreas Bergthaler. The systemic changes of arginine and ornithine were found to inhibit antiviral CD8 T cell responses and to reduce liver damage.

One of the most important revelations of this study was the identification of IFN-I signaling as a master regulator for the repression of metabolic processes in hepatocytes upon infection. "We were really surprised that an antiviral molecule affects such vital biological processes as the urea cycle during infection", says Michael Trauner, co-author of the study and head of the Department of Gastroenterology and Hepatology at the Medical University of Vienna. Together, these findings shed new light on how the body's immune system evolved to regulate liver metabolism that modulate CD8 T cell responses and reduce collateral tissue damage during infection. Andreas Bergthaler: "We regard this study an important contribution to the field of systemic immunometabolism. It also highlights the central role of the liver for our immune system and how organs of the body communicate through metabolites." In the future, such findings may be exploited to therapeutically intervene with the regulation of metabolic processes to modulate CD8 T cell responses in diverse diseases such as infection, cancer and autoimmunity.

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Immunity -- master regulator of liver metabolism identified during infection - Science Codex

1.7 million. That's how many people are infected with the human immunodeficiency virus (HIV) each year worldwide. 1.7 million people who are condemned to lifelong antiretroviral therapy (ART) or risk developing fatal AIDS . Out of the 37.9 million people living with HIV (PLWH), 22.3 million have access to ART, allowing them to have an almost normal lifespan. Unfortunately, however, the medications only go so far: they don't reach the cells where the virus lies dormant for years. Moreover, potential long-term adverse effects of these medications remain unknown.

Still, HIV research has been making steady strides to help the large number of PLWH. HIV laboratories around the globe are trying to unlock the "secrets" of the virus and find its weak spots in order to prevent or cure the infection. At the Montreal Clinical Research Institute (IRCM), scientists ric A. Cohen and Tram NQ Pham have recently identified a way to thwart HIV infection at its very early stages. Their discovery is the subject of an article in the scientific journal Cell Reports.

Contrary to popular belief, HIV is not so easily transmitted. We are studying the window of vulnerability of the virus, meaning the moments in the infection process when it could be weakened or attacked. We focused on the very early stages following viral invasion.

ric Cohen, director of the Human Retrovirology Research Unit at the IRCM and a virology professor in the Department of Microbiology, Infectious Diseases and Immunology at Universit de Montral

Once transmitted, HIV does not immediately spread through the body. It initially has to multiply locally, mainly in the genital tissues. It is only after this initial, local expansion that the virus spreads. This localized expansion offers a very brief window of vulnerability before the virus efficiently establishes a systemic infection.

The immune response is like an armed struggle: an enemy infiltrates and the body defends itself. Viruses are the intruders, and white blood cells are soldiers trying to hold down the fort. The white blood cells are equipped with their own "infantry units": lymphocytes, phagocytes, granulocytes and others. The phagocyte group has an even more specialized unit known as 'plasmacytoid dendritic cells' (PDCs). These small, round-shaped cells patrol the body, specializing in both pathogen detection and antiviral response orchestration. In other words, they are the whistleblowers, the ones through which the entire defence process is set into motion. When they detect a threat, they change shape and develop protuberances called dendrites. "Most importantly, they start producing large amounts of interferon, a protein that triggers a state of infection resistance in other cells," Cohen explained.

As its name implies, HIV preferentially targets the immune system: it attacks and weakens the body's own defences, and the infected person becomes susceptible to the slightest infection. As soon as it arrives, HIV gets PDCs out of the way and prevents them from sounding the alarm. "The virus doesn't seem to kill them directly, but it makes them disappear in a way that is still not understood," said Pham, the senior research associate in the Human Retrovirology Research Unit. "The loss of PDCs from both the infection site and throughout the body helps establish the infection."

"Given what HIV does to PDCs, we wondered what would happen if we boosted PDC levels and their function both prior to and during infection," said Cohen. To test this, the scientists used a special protein known as Flt3 receptor ligand to stimulate the production of PDCs from the bone marrow of humanized mice. These rodents are engineered to have a human immune system in place of the mouse's own machinery. Consequently, in an infected humanized mouse, HIV behaves as it otherwise would in a human host.

Administration of this special protein maintained high levels of PDCs in these mice and produced some striking results: 1) the initial number of infected mice was reduced; 2) the time it took for the virus to be detectable in the blood was lengthened; and 3) the amount of virus in the blood, also known as viremia, was significantly reduced. "We observed up to a 100-fold decrease in viremia," Pham noted. "In other words, the initial infection is suppressed by maintaining a high level of PDCs."

This seminal work also showed that the injection of the Flt3 receptor ligand not only increased PDC abundance, but also boosted their ability to detect the virus and produce interferon following its detection.

Of course, HIV infection normally goes unnoticed and by the time the viremia is detectable, it is a little too late. In this context, the discovery by Cohen and Pham is highly important in terms of prevention and a potential cure. "These new findings will be crucial in the design of an HIV vaccine, which is basically aimed at teaching the immune system to defend itself by introducing it to a weakened form of the virus," said Cohen. "We can now focus on PDCs in order to control the seeding and expansion of the virus at the early stage of infection."

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New way to thwart HIV infection at early stages - News-Medical.net

SAN DIEGO--(BUSINESS WIRE)--

Gossamer Bio, Inc. (GOSS), a clinical-stage biopharmaceutical company focused on discovering, acquiring, developing and commercializing therapeutics in the disease areas of immunology, inflammation and oncology, today announced that members of the management team will participate in the following investor conferences:

A live webcast of the presentations will be available on the Events and Presentations page in the Investors section of the companys website at https://ir.gossamerbio.com. A replay of the webcast will be archived on the companys website for 90 days following the presentation.

About Gossamer Bio

Gossamer Bio is a clinical-stage biopharmaceutical company focused on discovering, acquiring, developing and commercializing therapeutics in the disease areas of immunology, inflammation and oncology. Its goal is to be an industry leader in each of these therapeutic areas and to enhance and extend the lives of patients suffering from such diseases.

View source version on businesswire.com: https://www.businesswire.com/news/home/20191126005147/en/

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Gossamer Bio Announces Participation in Upcoming Investor Conferences - Yahoo Finance

AbbVie's (NYSE:ABBV) third-quarter earnings call reminded investors about the transformative potential of the Allergan acquisition for the pharma giant. Management reiterated that they continue to expect the deal to close by the end of the first quarter of 2020. This is promising for investors, as the combined entity will allow AbbVie to gain a more diversified foothold in faster-growing therapeutic areas such as Botox and neuroscience while expanding its immunology portfolio with the addition of Allergan's Linzess and Viberzi.

AbbVie CEO Richard Gonzalez said on the earnings call that "the Allergan transaction will make us even stronger and more diversified." Let's see why.

Photo Credit: Getty Images

The new AbbVie will have a strong market leadership position in a number of therapeutic areas. AbbVie would be No. 1 in immunology, supported by its flagship arthritis treatment, Humira, but investors are also excited about potential approvals following results of ongoing Phase 3 clinical trials of Skyrizi in psoriasis and Upadacitinib in rheumatoid arthritis before the end of 2020. Not surprisingly, AbbVie will also have a market leadership position in medical aesthetics, with a product suite covering Botox, the CoolSculpting fat removal system, and Juvederm dermal fillers, which are used to help conceal wrinkles. Medical aesthetics is still a rapidly growing market, especially internationally. Management cited a Markets and Markets Medical Aesthetics report from September 2018 that cited the aesthetics addressable market being $12B at the time and "growing."

Investors should be encouraged by Gonzalez's comments on the call that, "Based on the uniqueness of this particular molecule, we have come to the conclusion that it would be extremely difficult to create a biosimilar version of Botox, and I would tell you, we looked at this very extensively with a lot of outside expertise and we feel very confident that that's the case." This should create a steady stream of earnings and cash flow to AbbVie to help support other therapeutic areas without the worry of generic competition.

The scale and synergies of the acquisition are another bright spot for investors in a world where size matters more than ever to fend off competition.

Let's start with scale. Using full-year 2018 financials, adding AbbVie and Allergan gives us an entity that would have trailed only Johnson & Johnson, Roche, and Pfizer in revenue, lagging only the first two in operating cash flow. With the company's new scale, management believes it can achieve high-single-digit revenue growth.

With respect to the synergies, management expects the combined entity to lower costs and increase returns. Total savings are expected to top $2 billion over a three-plus-year period: 50% from R&D efficiency; 40% from selling, general, and administrative expenses as the footprint of the combined organization becomes leaner; and 10% from greater manufacturing efficiency. Those savings should show up quickly: Earnings per share are expected to get a 10% boost in year one and eventually top 20%. This will help support the increase of an already generous 5%-plus dividend yield, coupled with the promise of further shareholder-friendly actions as the company reduces its debt load. Gonzalez said that "combined, we will generate significant earnings and cash flow to enhance our innovative R&D platform support a strong and growing dividend and rapidly pay down debt."

Year to date, AbbVie's stock price has been more or less flat, lagging the S&P 500. As a result, it's sporting a forward price-to-earnings multiple of roughly 10 times consensus estimates. That's not a steep price for an attractive dividend yield coupled with the prospect of accelerating revenue and earnings growth.

As closure of the acquisition draws near, any negative investor sentiment should begin to abate, allowing for the prospects of multiple expansion. Gonzalez said on the call, "Our model is more conservative than what the Allergan current performance is and certainly more conservative than their longer-range forecast, but it still does project growth for Botox going forward." Thus, this multiple expansion should be led by reduced fears around competition, realized cost synergies, and potential for increased earnings guidance.

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AbbVie Shareholders Have a Lot to Look Forward To With Allergan - The Motley Fool

by Alex Kekauoha on November 24, 2019 10:31 am

Dorothy Tovar, PhD student in microbiology and immunology, is among those selected to be an IF/THEN ambassador. (Courtesy Dorothy Tovar)

Three Stanford students and one postdoctoral scholar have been selected to the first class of IF/THEN ambassadors for the American Association for the Advancement of Science. Each will provide support and mentorship to young girls interested in pursuing STEM fields.

Catie Cuan

Graduate students CATIE CUAN and DOROTHY TOVAR, postdoctoral scholar HELEN TRAN and undergraduate ERIN SMITHare among 125 women selected to serve as ambassadors.

The ambassadors recently attended the IF/THEN Summit in Dallas, Texas, where they participated in a full-body scan that produced life-sized 3D-printed statues of the ambassadors the largest collection of statues of women. Ambassadors will also work with Bay Area Girl Scout troops, appear on the network television series Mission Unstoppable about women working on cutting-edge STEM projects and participate in media campaigns.

The IF/THEN initiative is based on the idea that if women in STEM fields are supported, then they can change the world. The program is supported by a $25 million commitment from Dallas-based Lyda Hill Philanthropies. It is also a partnership with the American Association for the Advancement of Science, which works to advance science, engineering and innovation throughout the world for the benefit of all people.

Catie Cuan is a PhD candidate in the Department of Mechanical Engineering. Growing up in Berkeley, California, she loved math and science, but had few female role models in those fields.

Helen Tran

This resulted in a self-imposed narrowing of what my future possibilities were, she said.

Cuan earned a bachelors degree from the University of California, Berkeley, and has had a career as a dancer and choreographer. After making performances and art installations with robots, she decided to pursue a graduate degree in mechanical engineering.Cuan is currently designing physical interactions between humans and robots, as well as haptic devices to tele-operate robots.

Helen Tran is the Intelligence Community postdoctoral fellow in the lab of Professor Zhenan Bao in the Department of Chemical Engineering.

A native of San Jose, California, science was not on Trans radar until college. She earned a bachelors degree in chemistry from the University of California, Berkeley, and a PhD in chemistry from Columbia University. She joined Stanford in 2016 and is currently researching biodegradable stretchable electronics.

Through the IF/THEN program, Tran has enjoyed learning about the quantitative studies on the importance of media representation of women in media.

Dorothy Tovar is a PhD student studying microbiology and immunology.

Erin Smith

Growing up in Cambridge, Massachusetts, Tovar became interested in science at a young age. She frequently read science books and encyclopedias and watched countless hours of the Discovery Channel. She also spent some of her childhood in Haiti, where she became fascinated by the way microscopic organisms could cause diseases that devastate entire countries.

Tovar earned a BS in microbiology from the University of Massachusetts, Amherst, where she was awarded the universitys 21st Century Leader Award. She joined Stanford Medicine in 2015.

Erin Smith, a first-year student and native of Kansas, is the founder ofFacePrint, an AI tool to detect and monitor Parkinsons disease and commonly misidentified neurological disorders using video technology and early-stage facial expression indicators. She is currently off campus pursuing a Thiel Internship.

Smiths research interest was spurred when she watched a video by the Michael J. Fox Foundation and noticed that Parkinsons patients smiles and laughter often appeared emotionally distant years before diagnosis. She talked to clinicians and caretakers, who reported similar observations. As she read through past medical papers. she found that the often-overlooked parts of the brain that experience some of the earliest changes in Parkinsons patients are the same parts involved in the formation of facial expressions. Smith became captivated by the idea of using facial expressions to monitor changes in the brain like Parkinsons and objectively detect its onset.

Mentors have had a pivotal impact on my life, said Smith. I am looking forward to the opportunity to engage with young students and help shape their futures.

Read more in the Roundabout.

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Stanford postdoc and students cited as example to girls interested in STEM fields | The Dish - Stanford University News

Goodbye, Celgene. Hello, Bristol-Myers Squibb (NYSE:BMY).

With Bristol-Myers Squibb's acquisition of Celgene closing on Wednesday, one of my favorite biotech stocks is now gone. Celgene became a subsidiary of BMS and is no longer a publicly traded company on its own. Like many former Celgene shareholders, I now own Bristol-Myers Squibb stock.

I've thought quite a bit about what I would do when the buyout deal concluded. My final conclusion: Do nothing. Here's why I plan to hold on to my new Bristol-Myers Squibb shares.

Image source: Getty Images.

I agree with market researcher EvaluatePharma that BMS's cancer immunotherapy Opdivo and its blood-thinning drug Eliquis are likely torank among the world's top-selling drugs over the next few years. But to be honest, the growth prospects for Opdivo and Eliquis alone wouldn't be enough to make me want to keep my newfound BMS shares. However, now that the big drugmaker owns Celgene's pipeline, it's a different story altogether.

Ozanimod appears to have very good chances of winning FDA approval for treating relapsed multiple sclerosis early next year. I expect the drug will generate peak annual sales in the ballpark of $5 billion if approved.

Celgene's cancer cell therapies liso-cel and ide-cel should also be in a pretty good position to secure regulatory approvals. These two drugs could tack on another $4 billion or so in combined peak annual sales. There could also be additional indications for recently approved Reblozyl (luspatercept) on the way that could help the drug achieve peak sales of close to $2 billion.

Looking farther down the road, I have high hopes for Celgene's CelMOD therapies that are currently in early stage clinical studies targeting blood cancers. I also think bb21217, a cell therapy that Celgene is developing with bluebird bio, could be a big winner.

These pipeline candidates make me excited about BMS's growth prospects. Yes, the company will have to offset the inevitable sales declines for Revlimid as generic rivals enter the market beginning in 2022. However, sales of those generics will be volume-limited at first. I think that the combination of Celgene's pipeline and already-approved drugs such as Pomalyst and Inrebic along with BMS's drugs should give the "new" company a solid growth runway.

In addition to its impressive blockbusters already mentioned, Bristol-Myers Squibb claims something remarkable of its own -- its dividend. The drugmaker's dividend currently yields 2.9%. That's a level that most investors would find quite attractive.

BMS has also been consistent at increasing its dividend payout through the years. Granted, those dividend hikes haven't been awe-inspiring. Still, a growing dividend is a good dividend in my book, especially with the already great yield.

I'm not worried at all about Bristol-Myers Squibb's ability to keep the dividends flowing and growing in the future. CFO Charles Bancroft noted in the company's third-quarter conference call that BMS will be able to increase its dividend, along with paying down its debt. He added that the company has "modeled annual increases" to its dividend in its pro forma financial projections.

It also helps that BMS just received $13.4 billion from the sale of Celgene's immunology drug Otezla to Amgen. While I would have preferred that BMS have Otezla in its lineup, the divestiture was necessary to make regulators happy and ended up being a good deal for all involved parties.

Celgene shareholders didn't just receive BMS stock with the closing of the acquisition. We also received $50 in cash per share plus a contingent value right (CVR) that will pay $9 if specified regulatory milestones are achieved.

I plan on holding on to my CVR. My expectation is that these CVR shares will eventually pay out the full $9 as BMS wins FDA approvals for ozanimod, liso-cel, and ide-cel.

As for the cash that I received with the acquisition of Celgene, I plan to invest in stocks, of course. Bristol-Myers Squibb won't be one of them, though, because I want to diversify more outside healthcare. The good news is that there are plenty of great stocks to choose from.

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Why I'm Holding On to My Bristol-Myers Squibb Shares Now That the Celgene Acquisition Has Closed - The Motley Fool

BOSTON--(BUSINESS WIRE)--Immunitas Therapeutics (Immunitas), a single cell genomics-based drug discovery company founded by Longwood Fund, today announced a $39 million Series A financing led by Leaps by Bayer and Novartis Venture Fund and joined by additional investors including Evotec, M Ventures, Alexandria Venture Investments, and other institutional investors. The company plans to use this funding to advance its first programs, monoclonal antibody therapeutics with single agent activity in preclinical models of oncology, to clinical studies.

Underlying the companys programs is the unique drug development platform crafted by the Immunitas team along with Aviv Regev (Professor of Biology and Core Member of the Broad Institute and Investigator at the Howard Hughes Medical Institute) that dissects the microenvironment of human tumors using single cell genomics-based approaches to identify novel immune targets. The Immunitas platform has generated fully humanized antibodies that act on these targets, advancing to human efficacy studies driven by specific clinical biomarkers, and a breadth of promising druggable cancer targets.

The scientific founders of Immunitas are pioneers in studying the immunobiology of human tumors, including the use of single cell genomics-based techniques and antibody-development techniques:

Single cell genomic sequencing has tremendous promise to help unravel the interactions between immune cells and cancer cells in tumors to advance cancer drug development but focusing it appropriately to discover meaningful new targets based on human biology has been challenging, said Dr. Wucherpfennig. The Immunitas platform is designed to reveal novel and important adaptive and innate immune interactions with tumor cells, which may open up new possibilities in cancer therapy. My scientific co-founders and I look forward to continuing to work with the Immunitas team as they advance this powerful science.

Our scientific founders are pioneers in the field of single cell sequencing and analysis. They have extensive expertise in deep computational biology, which has enabled us to discover novel therapeutic targets directly from human immunology, said Lea Hachigian, Ph.D., co-founder, director and President of Immunitas Therapeutics. The data from this platform have also provided us with biomarkers for patient selection, which has potential to accelerate our development plans and provides improved chances for efficacy for individual patients.

Immunitas was founded to directly address the challenge of translating findings from laboratory research in model organisms to meaningful clinical advances in humans. Immunitas focuses on human samples, allowing the company to start with and stay closer to the most relevant and translatable biology for patients.

One of todays biggest challenges in oncology is how to efficiently and effectively move preclinical research into human therapies while avoiding the false signals often seen in animal models, said Dr. Jrgen Eckhardt, Head of Leaps by Bayer, Bayer AGs strategic venture capital unit. The scientific founders of Immunitas have elegantly solved this problem by dissecting the biology of immune cells in human tumors directly. We are excited to support this approach which has the potential to significantly improve cancer drug development.

Longwood-founded Immunitas also announced key senior management appointments as well as the Board of Directors of the company. Dr. Lea Hachigian is co-founder, director and President of Immunitas as well as a Principal at Longwood Fund. She is also a co-founder and director of TScan Therapeutics. Tarek Samad, Ph.D. is the Chief Scientific Officer at Immunitas Therapeutics. He has over two decades of experience in academia and industry leading small molecule and antibody biologic programs into the clinic. Amanda Wagner joins the company as Vice President of Strategy and Operations with over ten years of biotech experience in similar roles. The Board of Directors includes Dr. Laura Brass, Dr. Jrgen Eckhardt, Dr. Lea Hachigian, Dr. Lucio Iannone, Dr. Christoph Westphal, and Dr. Vincent Xiang.

About Immunitas Therapeutics

Immunitas Therapeutics, founded by Longwood Fund, employs a single cell genomics platform to dissect the biology of immune cells in human tumors, thereby advancing discoveries directly from the bench into meaningful clinical improvements. Our focus on human data allows us to start with and stay closer to the biology that is most relevant in patients and greatly accelerates the pace of our research. The Immunitas team of scientific pioneers innovates around each step of the drug development process, first identifying novel targets, then designing therapeutic strategies, and developing key biomarkers to guide the selection of patients who may benefit from our new drugs. http://www.ImmunitasTx.com.

Immunitas the human approach to oncology

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Immunitas Therapeutics Launches with $39 Million to Advance Lead Programs to Human Efficacy Studies Based on a Unique Immunology-Focused Drug...