The first girl in the trial came in with chronic diarrhea and the immune system of an untreated HIV patient. Born with a rare genetic disease that impeded her ability to make B and T cells, she had once been given a stem cell transplant but it didnt take. Back in the hospital, she was injected with a new experimental antibody and then given a new stem cell transplant. Soon, she gained weight. The diarrhea stopped.

She has normal T cells now, Judith Shizuru, the Stanford scientist who pioneered the antibody, told Endpoints News. Shes in school.

Its the kind of medical story to launch a biotech around, and thats what Shizuruis doing. Today, her company Jasper Therapeutics is emerging out of stealth-mode with $35 million in Series A funding led by Abingworth and Qiming, a molecule from Amgen, and a Phase I trial set for its first readout on Monday at ASH.

Jasper is broadly aimed at making stem cell transplants safer, more accessible and more effective by using antibodies as conditioning agents. Theseagents clear out bone marrow to make room for the new stem cells to graft onto the body.

Their Phase I uses a naked antibody called JSP191 to help patients with severe combined autoimmune deficiency receive stem cell transplants the only possible cure for the life-threatening disease but such transplants are used in a wide variety of conditions and Jasper has broader aims. Those include other autoimmune diseases, acute myeloid leukemia and cell-directed gene therapy.

Theres a significant amount of progress being made in gene therapy, interim CEO William Lis told Endpoints, but no progress being made in a conditioning agent that will help graft gene therapy.

Shizuru path to the new antibody was long and fortuitous. In 1987, Arl Arzst, the legendary ad executive and president of Proctor and Gamble international flew in on a recruiting trip for Stanford business students. There he visited Shizuru, a young biologyPhD candidate, because he knew her roommate. Arzsts daughter had diabetes and as Shizuru explained the work she was doing on pancreatic islet cell transplants, he told her to come to Europe.

Shizuru had never been to Europe, but there Arszt introduced her to Ken Farber and the other founders of the Juvenile Diabetes Foundation (now the JDRF). The founders struck a years-long correspondence and encouraged Shizuru to go to medical school, where she decided that if scientists were ever going to develop transplants that didnt trigger an immune response, it would be through stem cell work. She continued her work at the Irv Weissman Stanford regenerative lab, where eventually a graduate student made a discovery that piqued her interest.

To put new stem cells in, you have to get the old stem cells out. Thats not always easy. The cells sit inthese pockets in the bone marrow, and theyre pretty comfortable there. Doctors have to force them out, often using chemotherapy or radiation, which damage DNA and cause severe side effects. The costs sometimes outweigh the benefits.

There are diseases were not treating because its too dangerous, Shizuru said. And the kids were treating, theyre so, so fragile.

The grad student had shown in mice that antibodies could be used to deplete the stem cells and potentially eliminate the need for chemotherapy or radiation. Shizuru and her team began looking to see if anyone had developed a human version of the antibody, CD117. It turned out Amgen had already developed a version of this antibody for a different use. It also turned out she had a former postdoc and a former advisor who worked there. They began a collaboration.

We set out to cross the valley of death, Shizuru said, using an industry slang term for the jump from animal models to human uses.

After making a variety of tweaks to the treatment, they published a paper inScience Translational Medicine in 2016showing the antibodies created a 10,000 fold reduction in the number of stem cells in mice.

The same year, they began a clinical trial on 90 SCID patients. These patients had received stem cell transplants when they were very young but hadnt been given chemo or radiation for fear the side effects would be too severe. The original transplants boosted their numberof immune cells, but without chemo or radiation, the stem cells dont graft into those pockets and the body wont continue producing T cells. Without those, they are extraordinarily prone to infection. Many pass away before age 2.

The hope is that the antibodies allowed the stem cells to graft, and the preliminary answer to that question will be out on Monday. For the first girl in the trial, life has improved but questions about how long her body will make immune cells remain. Still, for that girl and others, Shizuru is confident.

We see there is stem cell engraftment, Shurizi said. They are actually making new T cells.

Continued here:
Jasper Therapeutics launches out of Stanford with new approach to stem cell treatment - Endpoints News

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.

Consideration

Previous Agreement (2015, 2018)

Amended Agreement (2019)

Focus

Cancer

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.

Read more from the original source:
Celgene Gave This Tech Back to Editas Medicine, but It Could Prove Valuable - The Motley Fool

ORLANDO, Florida Chimeric antigen receptor (CAR) T-cell therapy has been hailed as a major advance and a game changer, but their cost has redefined the meaning of "expensive."

However, new "real-world" data now suggests that CAR-T cell therapy may actually be cost effective, as it may lower other expenses related to the illness.

When used in a population of older adults with non-Hodgkin's lymphoma, these new data show that CAR-T cell therapy cut related expenditures compared with healthcare costs prior to receiving this treatment.

"CAR-T therapy was associated with fewer hospitalizations, shorter time in the hospital, fewer ED visits, and lower total healthcare costs," said lead study author Karl M. Kilgore, PhD, of Avalere Health in Washington, DC.

He presented the findings here at the 2019 annual meeting of the American Society of Hematology (abstract 793).

CAR-T cell therapies were approved in the United States in 2017. First came tisagenlecleucel (Kymriah, Novartis), for the treatment of pediatric and young adult patients with acute lymphoblastic leukemia, with a price tag of $475,000. Closely following it was axicabtagene ciloleucel (Yescarta, Kite/Gliead), indicated for adult patients with relapsed/refractory aggressive B-cell non-Hodgkin's lymphoma who are ineligible for autologous stem cell transplant, with a price tag of $373,000.

The formidable price tags sent shock waves through the blood cancers community, which is struggling to incorporate this novel approach because of the remarkable responses that have been seen.

In the current study, Kilgore and colleagues evaluated the demographic and clinical characteristics of Medicare patients who received CAR-T therapy (axicabtagene ciloleucel or tisagenlecleucel) and then compared healthcare utilization, costs, and outcomes pre- and post-CAR T therapy.

"The goal of this study was to look at the real use of CAR-T cell therapy and real-world data on the use of these therapies," said Kilgore. "And to look at healthcare utilization."

Data was obtained from the Centers for Medicare & Medicaid Services 100% Medicare Fee-for-Service Part A and B claims data, and patients were included in the study if they had been diagnosed with lymphoma and received CAR T therapy between October 1, 2017, and September 30, 2018.

A total of 177 patients met all of the inclusion criteria and were included in the analysis.

The average age was 70 years, more than half (58.8%) were male, and they were primarily white (87.6%). Nearly all patients (91.5%) had a primary diagnosis of diffuse large B-cell lymphoma (DLBCL), as well as multiple co-morbidities with 74.6% having a Charlson Comorbidity Index score 3. Fewer than 5% of patients had undergone a previous autologous stem cell transplant, and 51% had one or more comorbidities that would have disqualified them from participating in CAR-T clinical trials (eg, renal failure, heart failure, recent history of DVT/PE).

Just over half of participants (52%) had been treated with intravenous chemotherapy in the 6 months prior to receiving CAR-T cell therapy, and 60% received outpatient lymphodepletion.

During their index episode of care for CAR-T infusion, the patients spent a median of 16 days (interquartile range, 10) in the hospital during and 45.5% required ICU care after infusion. In the 6-month period prior to CAR-T cell therapy (pre-index), 51.2% had been hospitalized at least once, and almost 20% had three or more periods of hospitalization. Of that group, 27.1% were readmitted during the post-index period.

Among patients who required hospitalization, the median length of stay pre-index was 7 days and 5 days post-index. The number of ED visits was also lower in the post- vs pre-index (15.8% vs 29.9%).

"Patients spent 17% less time in the hospital 6 months after CAR-T cell therapy than before," he said.

While there were no deaths during the post-index period, a small percentage (< 5%) were admitted to hospice care. It is unclear if any patients received chemotherapy during the 100-day post-index period, which would suggest disease progression. However, the authors note that claims for the period might be lagging behind for some patients.

Kilgore pointed out that half of the patients had one or more chronic conditions that, in some cases, would have excluded them from clinical trials. "But 73% remain alive at 6 months," he said. "We have data that goes out to 21 months, and over 50% are still alive at almost 2 years."

As for cost, the median total healthcare costs during the pre-index period were $51,999 (mean, 58,820; standard deviation [SD], 45,701) and $14,014 post-index (mean, 23,738; SD, 29,698). This extrapolates into $9,749 pre- vs $7,121 post-index for each patient per month, which is a 27% decrease in expenditures.

Kilgore explained that the total paid amounts for CAR-T from all sources (Medicare and patient) varied significantly, depending on whether patients were treated in a clinical trial and whether the hospital was reimbursed under standard Medicare prospective payment system (PPS) for inpatient facilities or through the PPS-exempt payment system.

Commenting on the study, Sarah Rutherford, MD, a hematologist at Weill Cornell Medicine and New York-Presbyterian in New York City, believes that the key takeaway from this study is that the majority of participants who were older and sicker than many enrolled on CAR T-cell clinical trials did quite well.

"Diffuse large B-cell lymphoma is a disease that usually causes people to die quickly if they are refractory to multiple lines of therapy, so the 6-month survival of 75% in this patient population is impressive," she said. "A large proportion of these patients are likely to have died had they not received CAR T-cell therapy."

Rutherford noted that the study authors analyzed the costs associated with patients in the pre- and post- CAR T-cell setting, finding that healthcare costs were lower following CAR T-cell therapy in this Medicare patient subset compared with costs prior to the therapy.

"I think CAR T-cell use is certainly justified given the lack of efficacious therapies in relapsed and refractory DLBCL patients, and this study indicates that there may be a financial benefit as well, though the actual costs associated with CAR T-cell therapy were not included in the analysis," she told Medscape Medical News.

Kilgore has disclosed research funding from Kite Pharma. Several of the other co-authors have disclosed relationships with industry, which are noted in the abstract.

2019 Annual Meeting of the American Society of Hematology: Abstract 793. Presented December 9, 2019.

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The rest is here:
'Real-World' Data Show CAR-T Therapies Are Cost Effective - Medscape

Syros Pharmaceuticals (NASDAQ:SYRS), a leader in the development of medicines that control the expression of genes, today announced that it has discovered and validated a novel fetal hemoglobin repressor, Nuclear Factor I X (NFIX), using its gene control platform. The finding sheds light on how the gamma-globin gene, which leads to the production of fetal hemoglobin, is controlled and points to new potential targets for therapeutic intervention in sickle cell disease. These data will be presented in an oral presentation tomorrow at the 61st American Society of Hematology (ASH) Annual Meeting and were highlighted today in an ASH press briefing.

"This discovery highlights the power of our platform to elucidate regulatory regions of the genome to control the expression of a single gene for therapeutic benefit," said Eric R. Olson, Ph.D., Syross Chief Scientific Officer. "Based on real-world genetic and clinical data from patients, we believe it is possible to provide a functional cure for sickle cell disease by switching on the gamma-globin gene, which is typically turned off at birth, to make healthy red blood cells. Our discovery of NFIX as a critical player in silencing the gamma-globin gene opens up new potential therapeutic approaches as we advance our effort to discover an oral medicine that addresses the root cause of disease in sickle cell patients."

The focus of Syros drug discovery program in sickle cell disease is to develop an oral medicine to mimic a condition found in a subset of patients, who also inherit a hereditary persistence of fetal hemoglobin (HPFH) mutation, in which the gamma-globin gene remains activated after birth. Despite having the mutated adult beta-globin gene that causes sickled cells, these patients are largely asymptomatic because the activated gamma-globin gene leads to the production of enough fetal hemoglobin for red blood cells to function normally.

Using its gene control platform, Syros scientists analyzed and compared regulatory regions of the genome in red blood cell precursors, known as erythroblasts, at various stages of maturity from fetal and adult sources to identify novel drug targets involved in the switch from fetal to adult hemoglobin expression. The genome-wide analysis pointed to NFIX as a potential fetal hemoglobin repressor. The scientists then validated the role of NFIX in silencing fetal hemoglobin by knocking down the NFIX gene in primary cells and an erythroid cell line that expresses adult hemoglobin. The data showed:

The oral presentation will take place tomorrow during the Thalassemia and Globin Gene Regulation: Hemoglobin Regulation and Beta Thalassemia Research session from 4:30-6:30 p.m. ET in Valencia A (W415A) at the Orange County Convention Center, Valencia A (W415A). The ASH presentation is also now available on the Publications and Abstracts section of the Syros website at http://www.syros.com.

About Syros Pharmaceuticals:

Syros is redefining the power of small molecules to control the expression of genes. Based on its unique ability to elucidate regulatory regions of the genome, Syros aims to develop medicines that provide a profound benefit for patients with diseases that have eluded other genomics-based approaches. Syros is advancing a robust pipeline of development candidates, including SY-1425, a first-in-class oral selective RAR agonist in a Phase 2 trial in a genomically defined subset of acute myeloid leukemia patients, and SY-5609, a highly selective and potent oral CDK7 inhibitor in investigational new drug application-enabling studies in cancer. Syros also has multiple preclinical and discovery programs in oncology and monogenic diseases, including sickle cell disease. For more information, visit http://www.syros.com and follow us on Twitter (@SyrosPharma) and LinkedIn.

Cautionary Note Regarding Forward-Looking Statements

This press release contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995, including without limitation statements regarding the power of the Companys gene control platform and the Companys ability to discover an oral medicine that can restore healthy blood function in sickle cell patients and provide a functional cure for sickle cell disease. The words anticipate, believe, continue, could, estimate, expect, "hope," intend, may, plan, potential, predict, project, target, should, would, and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Actual results or events could differ materially from the plans, intentions and expectations disclosed in these forward-looking statements as a result of various important factors, including Syros ability to: successfully advance the development of its programs; demonstrate in any current and future clinical trials the requisite safety, efficacy and combinability of its drug candidates; replicate scientific and non-clinical data in clinical trials; obtain and maintain patent protection for its drug candidates and the freedom to operate under third party intellectual property; obtain and maintain necessary regulatory approvals; identify, enter into and maintain collaboration agreements with third parties; manage competition; manage expenses; raise the substantial additional capital needed to achieve its business objectives; attract and retain qualified personnel; and successfully execute on its business strategies; risks described under the caption "Risk Factors" in Syros Annual Report on Form 10-K for the year ended December 31, 2018 and Quarterly Report on Form 10-Q for the quarter ended September 30, 2019, each of which is on file with the Securities and Exchange Commission; and risks described in other filings that Syros makes with the Securities and Exchange Commission in the future. Any forward-looking statements contained in this press release speak only as of the date hereof, and Syros expressly disclaims any obligation to update any forward-looking statements, whether because of new information, future events or otherwise.

View source version on businesswire.com: https://www.businesswire.com/news/home/20191208005032/en/

Contacts

Media: Naomi AokiSyros Pharmaceuticals, Inc.617-283-4298naoki@syros.com

Investors: Hannah DeresiewiczStern Investor Relations, Inc.212-362-1200hannah.deresiewicz@sternir.com

Link:
Syros Presents on Identification of Novel Fetal Hemoglobin Repressor as Part of Broader Drug Discovery Program in Sickle Cell Disease at 61st Annual...

DetailsCategory: AntibodiesPublished on Sunday, 08 December 2019 13:21Hits: 143

Mosunetuzumab data to be presented at the American Society of Hematology 2019 Annual Meeting Plenary Scientific Session demonstrate durable complete responses in people with relapsed or refractory non-Hodgkins lymphoma

Preliminary safety and efficacy data for CD20-TCB support potential of combination approaches with anti-CD20 therapies

SOUTH SAN FRANCISCO, CA, USA I December 07, 2019 I Genentech, a member of the Roche Group (SIX: RO, ROG; OTCQX: RHHBY), today announced new data on two investigational CD20-CD3 T-cell engaging bispecific antibodies, mosunetuzumab and CD20-TCB, in people with relapsed or refractory (R/R) B-cell non-Hodgkins lymphoma (NHL). Results from the Phase I/Ib GO29781 study of mosunetuzumab, including data from people previously treated with chimeric antigen receptor (CAR) T-cell therapy, will be presented at the 61st American Society of Hematology (ASH) 2019 Annual Meeting during the Plenary Scientific Session. The Plenary Scientific Session highlights the top six abstracts submitted to the meeting, as determined by the ASH Program Committee. Additionally, results from the Phase I/Ib NP30179 study evaluating CD20-TCB as a combination therapy with Gazyva (obinutuzumab) for people with R/R NHL, will be presented.

Despite recent treatment advancements, slow-growing and aggressive non-Hodgkins lymphomas present increasingly difficult management challenges with each subsequent relapse, said Levi Garraway, M.D., Ph.D., chief medical officer and head of Global Product Development. Were encouraged by these early results, which suggest that our novel bispecific cancer immunotherapies may help people with relapsed or treatment-refractory disease who need more options.

The GO29781 study evaluated mosunetuzumab in patients with R/R NHL, including patients who have relapsed following, or are resistant to, CAR T-cell therapy a patient population with limited treatment options. Results from this dose-escalation study showed encouraging efficacy with an objective response rate (ORR) of 62.7 percent (n=42/67) in slow-growing NHL and 37.1 percent (n=46/124) in aggressive NHL. Additionally, data demonstrated a complete response (CR) rate of 43.3 percent (n=29/67) in slow-growing NHL and 19.4 percent (n=24/124) in aggressive NHL. CRs showed durability, with 82.8 percent (n=24/29) of patients with slow-growing NHL remaining in remission up to 26 months off initial treatment and 70.8 percent (n=17/24) of patients with aggressive NHL, remaining in remission up to 16 months off initial treatment. Of the participants who received prior CAR T-cell therapy, the ORR was 38.9 percent (n=7/18), and 22.2 percent (n=4/18) achieved a CR. Adverse reactions included cytokine release syndrome (CRS) in 28.9 percent of patients with 20.0 percent at Grade 1 and 1.1 percent at Grade 3. Grade 3 neurological adverse events occurred in 3.7 percent of patients.

Results from the Phase I/Ib dose-escalation NP30179 study, evaluating CD20-TCB at doses ranging from 0.6 mg to 16 mg plus Gazyva in people with R/R B-cell NHL, showed an ORR of 54 percent (n=15/28) and a CR rate of 46 percent (n=13/28). This included an ORR and CR of 66.7 percent (n=4/6) in people with follicular lymphoma and an ORR of 50.0 percent (n=11/22) and a CR of 40.9 percent (n=9/22) in aggressive NHL. The most frequently observed adverse event across all treatment doses was CRS, occurring in 67.9 percent of patients (n=19/28), with the majority of events being low grade (Grade 1-2).

Both mosunetuzumab and CD20-TCB continue to be evaluated in a robust clinical development program, investigating the treatments as monotherapies and in combination with other therapies, in people with slow-growing and aggressive forms of NHL.

About Genentechs Investigational Bispecifics

Genentech is currently developing two T-cell engaging bispecific antibodies, mosunetuzumab and CD20-TCB, designed to target CD20 on the surface of B-cells and CD3 on the surface of T-cells. This dual targeting activates and redirects a patients existing T-cells to engage and eliminate target B-cells by releasing cytotoxic proteins into the B-cells. Mosunetuzumab and CD20-TCB differ in their structures, and both are being developed by Genentech as part of our ongoing strategy to explore multiple bispecific formats, to identify those that maximize potential clinical benefits for patients. The clinical development programs for mosunetuzumab and CD20-TCB include ongoing investigations of these molecules as monotherapies and in combination with other medicines, for the treatment of people with CD20-positive B-cell non-Hodgkins lymphomas, including diffuse large B-cell lymphoma and follicular lymphoma.

About the GO29781 study

The GO29781 study [NCT02500407] is a Phase I/Ib, multicenter, open-label, dose-escalation study evaluating the safety and pharmacokinetics of mosunetuzumab in people with relapsed or refractory B-cell non-Hodgkins lymphoma. Outcome measures include best objective response rate by revised International Working Group criteria, maximum tolerated dose, and tolerability.

About the NP30179 study

The NP30179 study [NCT03075696] is a Phase I/Ib, multicenter, open-label, dose-escalation study, evaluating the efficacy, safety, tolerability and pharmacokinetics of CD20-TCB. In this study, CD20-TCB is assessed as a single agent and in combination with Gazyva, following pre-treatment with a one-time, fixed dose of Gazyva, in people with relapsed or refractory B-cell non-Hodgkins lymphoma. Outcome measures include overall response rate, complete response rate per Lugano 2014 criteria, maximum tolerated dose, and tolerability.

About Non-Hodgkins Lymphoma

There are two main types of lymphoma: Hodgkins lymphoma and non-Hodgkins lymphoma (NHL). NHL has two subsets, aggressive and indolent (slow-growing).

NHL represents approximately 85 percent of all lymphomas diagnosed. According to the American Cancer Society, it is expected that nearly 74,000 people will be diagnosed with NHL in the United States in 2019, and nearly 20,000 will die from the disease.

Most cases of NHL start in B-lymphocytes, cells that are part of the bodys immune system and help to defend the body against infections. B-cell lymphoma develops when these cells become cancerous and begin to multiply and collect in the lymph nodes or lymphatic tissues such as the spleen.

Gazyva Indications

Gazyva (obinutuzumab) is a prescription medicine used:

About Genentech in Hematology

For more than 20 years, Genentech has been developing medicines with the goal to redefine treatment in hematology. Today, were investing more than ever in our effort to bring innovative treatment options to people with diseases of the blood. For more information visit http://www.gene.com/hematology.

About Genentech

Founded more than 40 years ago, Genentech is a leading biotechnology company that discovers, develops, manufactures and commercializes medicines to treat patients with serious and life-threatening medical conditions. The company, a member of the Roche Group, has headquarters in South San Francisco, California. For additional information about the company, please visit http://www.gene.com.

SOURCE: Genentech

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Genentech Announces New Data on Novel Cd20-cd3 Bispecific Cancer Immunotherapies in People With Difficult-to-Treat Lymphomas | Antibodies | News...

Long Islanders who live the salt life probably have packed their sunscreen away with the summer beach towels and chairs.

But health experts warn that sun protection is key even when its too cold to catch rays while lounging on the sand or on a boat.

Applying sunscreen before skiing, winter surfing and shoveling snow can go a long way toward helping ward off skin cancer.

Theres this misconception that because its colder that the sun is less strong its really not true, said Dr. Adam C. Berger, chief of Melanoma and Soft Tissue Oncology at Rutgers Cancer Institute of New Jersey. We dont feel the direct heat as much, but we are still getting the direct sunlight.

The sun is actually closer to the Earth during the winter months, but its rays hit at a steeper angle in the summer.

Ultraviolet A (UVA) and Ultraviolet B (UVB) rays, which damage the skin, are present throughout the year. Most skin cancers are caused by overexposure to UV light.

The risk of sun exposure is just as great in the wintertime as it is in the summertime, Berger said.

The U.S. Centers for Disease Control and Prevention lists skin cancer as the most common form of cancer in the nation.

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The majority of those cases are basal cell and squamous cell carcinomas, described by the CDC as highly curable, but can be disfiguring.

However, one type of skin cancer, known as melanoma, can be fatal. In 2016, more than8,000 people died from melanomas of the skin in the United States, according to the CDC, and 82,000 new cases were reported.

People should be aware of the cumulative impact of sun exposure, said Dr. Raman Madan, director of cosmetic dermatology and assistant clinical professor at Northwell Health/Hofstra School of Medicine.

One of the things people dont realize is its not one particular sunburn or one particular sun exposure, Madan said. Its like adding sand to a box, and at some point that box fills up and you get skin cancer. If you are not wearing sunscreen, the box is still filling up. You dont get a break in the winter.

The strength of ultraviolet rays intensify as they reflect off snow and water.

A lot of people dont think about how the sun is reflected off the snow, Berger said. I see people come back from ski trips all the time with horrible sunburn on their face.

Winter surfers, covered head to toe in wet suits, are a common sight along Long Islands shoreline. Skudin Surf, a school in Long Beach, even holds a class called Winter Warriors focused on cold weather surfing, and students are encouraged to use sunscreen.

Sunscreen is something we promote with all our campers, said Nancy Dennehy, office manager for Skudin Surf, which runs programs on Long Beach, Nickerson Beach and Rockaway, as well as in Puerto Rico.

When I go paddleboarding in the winter, I make sure I put sunscreen on my face, she said.

Madan, who is also a dermatologist at Huntington Hospital, recommends that everyone see a board-certified dermatologist physician for a skin check once a year.

He urges patients to be proactive and mindful of any skin changes that could signal a problem. Asymmetrical spots or moles, jagged borders and uneven colors are some of the warning signs of melanoma.

We want to catch that because it can spread and lead to death quickly, Madan said. Basal cell and squamous cell are much more common. With these types of skin cancers, you are looking for pink scaly plaques scabby areas that just dont seem to heal.

Avid outdoorsman Ed Moran of Smithtown said he keeps sunscreen in his backpack during the warm summer months, but takes it out after October.

Hes active year-round, leading people on cross-country skiing, snowshoe and hiking trips through his guide business Eastern Outdoor Experiences.

I know there are certain activities later in the winter where I am more prone to getting a sunburn like skiing, Moran said.

He admitted his own record of wearing sunscreen while skiing is a spotty one.

[I wear it]when Im good and I dont want my wife to yell at me, he said with a laugh.

HOW TO PROTECT YOURSELF IN WINTER MONTHS

SOURCE: U.S. Centers for Disease Control and Prevention

Lisa joined Newsday as a staff writer in 2019. She previously worked at amNewYork, the New York Daily News and the Asbury Park Press covering politics, government and general assignment.

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Medical warning: Sun protection needed even in winter - Newsday