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Marizomib is a novel brain-penetrant proteasome inhibitor in development for patients with glioblastoma and relapsed and/or refractory multiple myeloma. TORONTO and SAN DIEGO, Nov. 17, 2016 (GLOBE NEWSWIRE) -- Triphase Accelerator Corporation, a private drug development company dedicated to advancing novel compounds through Phase 2 proof-of-concept, today announced that Celgene Corporation, through an affiliate, has acquired the company’s assets related to its proteasome inhibitor, marizomib (MRZ), which is in development for glioblastoma and relapsed and/or refractory multiple myeloma. Under the terms of the agreement, Celgene will make an upfront payment plus additional regulatory, approval and sales milestone payments.  Specific financial terms were not disclosed.  “This acquisition validates the potential of marizomib based on early clinical results.  Our vision is to become a leading early stage oncology drug development company, and this first opt-in by Celgene brings us a step closer to achieving that goal,” said Mohit Trikha, Ph.D., chief scientific officer, Triphase Accelerator Corporation. “Just as importantly, this transaction affords us the opportunity to accelerate our efforts on advancing other assets in our pipeline.” “Consistent with our deep commitment and passion for the patients, glioblastoma is an area of significant unmet medical need, and Celgene is committed to helping these patients.  We are pleased with Triphase Accelerator’s rapid and high quality work to date, and we value the exceptional collaboration we have with them to advance marizomib,” said Celgene’s President of Hematology Oncology, Michael Pehl. Going forward Celgene has full responsibility for the development of marizomib and will pay Triphase to complete the ongoing clinical studies with marizomib, including a Phase 1 study in relapsed refractory multiple myeloma, a Phase 2 study in recurrent glioma and a Phase 1 study in newly diagnosed glioma. About Marizomib Marizomib is a novel, brain-penetrant proteasome inhibitor, which inhibits all three proteasome subunits.  Triphase Accelerator is developing marizomib in both intravenous (IV) and oral formulations as a proteasome inhibitor for hematologic malignancies and solid tumors. The IV formulation has been evaluated in more than 300 patients in multiple clinical studies in patients with solid and hematologic malignancies, either as a single agent or in combination with dexamethasone, a histone deacetylase inhibitor, or an immunomodulatory drug. The company is currently evaluating marizomib in a proof-of-concept clinical study in combination with bevacizumab (Avastin®) in patients with Grade IV malignant glioma (glioblastoma), and has received Orphan Drug designation for marizomib in glioblastoma in the United States from the FDA. In addition, Triphase Accelerator is currently developing marizomib in combination with pomalidomide and dexamethasone in patients with relapsed and refractory multiple myeloma, and has received Orphan Drug designation for marizomib in multiple myeloma in the United States and the European Union. Triphase Accelerator is also evaluating an oral formulation in preclinical studies. Marizomib has not been approved for any use in any country. About Triphase Accelerator Triphase Accelerator is a private drug development company with a primary focus on oncology and with operations in Toronto and San Diego. Triphase Accelerator is dedicated to advancing novel compounds through Phase 2 proof-of-concept clinical studies using a unique, science-based, high-quality model that is faster and more cost-effective than traditional pharmaceutical and biotech industry drug development approaches. Triphase Accelerator was spun out of the Ontario Institute for Cancer Research (OICR), with support from the Fight Against Cancer Innovation Trust (FACIT), MaRS Innovation and MaRS. It has a strategic relationship with Celgene for marizomib. For more information, visit www.triphaseco.com or LinkedIn.


TORONTO and SAN DIEGO, Dec. 21, 2016 (GLOBE NEWSWIRE) -- Triphase Accelerator Corporation, a private drug development company dedicated to advancing novel compounds through Phase 2 proof-of-concept, today announced a new strategic collaboration with Celgene Corporation. Under the Agreement, Celgene has an option to acquire all Triphase Accelerator’s assets relating to TRPH-222 (CD22-4AP), an antibody-drug conjugate in development for lymphoma. Pursuant to the Agreement, Triphase Accelerator received an upfront payment from Celgene.  Triphase Accelerator will control development and will retain all commercial rights to TRPH-222 (CD22-4AP). If Celgene exercises its option to acquire TRPH-222 (CD22-4AP), Celgene will become responsible for development and commercialization, and Triphase Accelerator will be eligible to receive development, regulatory and sales milestone payments.  This is the third product option deal between Triphase Accelerator and Celgene. “This collaboration is important to Triphase Accelerator in multiple ways.  First, it continues to solidify the relationship we have developed over time with Celgene.  They have been a valued collaborator to us and we are grateful.  Just as importantly, it continues to validate our business model of acquiring early-stage assets and applying our methodology to accelerate programs through the proof-of-concept phase and into the clinic,” said Mohit Trikha, Ph.D., chief scientific officer, Head of Triphase Accelerator. “As we continue to acquire and develop new assets, we look forward to finding new ways to demonstrate how our approach is uniquely science based, efficient, and cost-effective, with the ultimate goal to help patients.” TRPH-222 is a novel, site-specific antibody-drug conjugate (ADC) targeting CD22, a B-cell-restricted sialogycoprotein that is an important modulator of B-cell signaling and survival, which is expressed on nearly all B-cell malignancies.  CD22 is a validated ADC target for Non-Hodgkin’s lymphoma and acute lymphoid leukemia.  The compound itself combines a site-specific modified humanized antibody conjugated to a toxin payload and a 4AP linker. “We have enjoyed a long-standing relationship with Triphase Accelerator and believe in their approach to drug development,” said Celgene’s President of Hematology Oncology, Michael Pehl. “This latest agreement, which closely follows our acquisition of their marizomib asset, represents our confidence in their approach to drug development, and we look forward to a continued collaboration with the company.” About Triphase Accelerator Triphase Accelerator is a private drug development company with a primary focus on oncology and with operations in Toronto and San Diego. Triphase Accelerator is dedicated to advancing novel compounds through Phase 2 proof-of-concept clinical studies using a unique, science-based, high-quality model that is faster and more cost-effective than traditional pharmaceutical and biotech industry drug development approaches. Triphase Accelerator was spun out of the Ontario Institute for Cancer Research (OICR), with support from the Fight Against Cancer Innovation Trust (FACIT), MaRS Innovation and MaRS. It has a strategic relationship with Celgene for oncology-focused drug development opportunities. For more information, visit www.triphaseco.com or LinkedIn.


CINCINNATI--Researchers at the University of Cincinnati (UC) have found that a cancer stem cell vaccine, engineered to express a pro-inflammatory protein called interleukin-15 (IL-15) and its receptor (IL-15Ralpha), caused T cell production in animal models and enhanced immune responses against tumors. This T cell production showed a cellular immune response that could lead to new immunotherapy treatments for cancer with improved side effects. These findings are being presented via poster abstract at the American Society of Gene and Cell Therapy's annual meeting in Washington, D.C., May 10-13. "IL-15 is a powerful stimulator of the maturation and activation of T cells and natural killer cells that recognize and attack tumor cells. Human IL-15 was first used in Phase I clinical trials to test its efficacy for treatment of a number of cancers, including melanoma and kidney cancer, but caused a number of side effects that made high doses difficult for patients to tolerate," says John Morris, MD, co-author of this study, clinical co-leader of the Molecular Therapeutics and Diagnosis Program for the Cincinnati Cancer Consortium, co-leader of the UC Cancer Institute's Comprehensive Lung Cancer Program, professor in the Division of Hematology Oncology at the UC College of Medicine and UC Health medical oncologist. "In this work, we showed that transferring the genes for both IL-15 with its receptor into cancer cells increased the cell-surface presentation of IL-15 to T cells, and in turn, stopped the tumor cells from reproducing with little evidence of side effects in animal models. "In an effort to enhance antitumor activity and reduce side effects, we studied a vaccine targeting cancer stem cells, the cells in a tumor thought to be resistant that give rise to recurrent tumors after treatment, by genetically altering them to express IL-15 and IL-15Ralpha to see if lung cancers implanted in animal models shrunk." Using animal models and their lung cancer cell lines, researchers introduced the IL-15/IL-15Ralpha-modified lung cancer stem cells as a vaccine and saw dramatically reduced tumor growth. "Animal lung cancer stem cells expressing IL-15 and IL-15Ralpha stimulated proliferation of T cells suggesting the ability to enhance immune responses," he says. "These findings further support evidence of IL-15's ability as a cancer treatment. We are continuing vaccination studies in animal models with hopes of moving this research to a Phase I trial in humans to see if side effects are reduced." Donatien Toukam, PhD, post-doctoral fellow in the Division of Hematology Oncology, is the lead author of this study funded in part by the Lcs Foundation. He cites no conflicts of interest.


Patients with double hit lymphoma (DHL) who undergo autologous stem-cell transplantation (autoSCT) after achieving remission are not more likely to remain in remission or live longer than patients who do not undergo autoSCT, according to a new analysis from the Perelman School of Medicine and the Abramson Cancer Center of the University of Pennsylvania. The study looked at long term outcomes for patients who achieved remission and, in most cases, found no clear benefit to the transplant, except potentially in patients who received standard front-line chemotherapy, who were less likely to remain in remission than those patients receiving intensive front-line chemotherapy. The findings are published this month in the Journal of Clinical Oncology. DHL is a form of aggressive B cell non-Hodgkin lymphoma characterized by genetic alterations that drive the lymphoma's growth. This variant is associated with a poor prognosis as compared to other forms of aggressive B cell lymphomas, as patients with this disease survive only an average of two years after diagnosis. Relapses of this disease are almost always fatal, meaning that keeping patients in remission is crucial. "A major dilemma for oncologists who treat this disease was whether or not to recommend the potentially harmful therapy of autoSCT to patients with this disease a strategy to help keep them in remission," said Daniel J. Landsburg, MD, an assistant professor of Hematology Oncology at Penn and the study's lead author. Landsburg and his team looked at data on 159 patients from 19 different academic medical centers across the United States. Patients were diagnosed between 2006 and 2015, and all achieved remission following intensive front-line chemotherapy or the standard chemotherapy regimen containing rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP). Of the total patients, 62 underwent an autoSCT, while 97 did not. Landsburg noted that there were no significant differences between the patient groups at baseline. "Our result is not explained by differences in patients' overall health or disease features," Landsburg said. "The transplant and non-transplant arms of this study were very well-matched." Overall, 80 percent of the patients were still in remission three years later, and 87 percent were still alive. When researchers broke the patients into two groups, autoSCT and no autoSCT, they found 89 percent of autoSCT patients were still in remission at three years, as were 75 percent of patients who did not receive an autoSCT. Also at three years, 91 percent of autoSCT patients were still alive, compared to 85 percent of non-autoSCT patients. None of these differences were found to be statistically significant. "Once these patients achieve remission, the data show they are likely to stay in remission," Landsburg said. "In the absence of a large randomized controlled trial, which would be very challenging to carry out in this case, this is the best evidence we have, and it shows there's no clear benefit to these patients undergoing autoSCT." Landsburg did point to one exception in the data, and that was in patients who underwent RCHOP, the standard front-line chemotherapy regimen. Just 56 percent of them were still in remission at three years, far lower than patients who received the more intensive front-line therapies. "Even if patients do go into remission with RCHOP, it appears to be less durable, so in these cases, going forward with autoSCT may still make sense," Landsburg said. Landsburg says the next step will be to study features of patients who don't go into remission in order to understand why their disease is resistant to therapy and if that can be overcome with different treatment strategies. He says it's also important to try to find more effective therapies for DHL patients who relapse.


PHILADELPHIA - Patients with double hit lymphoma (DHL) who undergo autologous stem-cell transplantation (autoSCT) after achieving remission are not more likely to remain in remission or live longer than patients who do not undergo autoSCT, according to a new analysis from the Perelman School of Medicine and the Abramson Cancer Center of the University of Pennsylvania. The study looked at long term outcomes for patients who achieved remission and, in most cases, found no clear benefit to the transplant, except potentially in patients who received standard front-line chemotherapy, who were less likely to remain in remission than those patients receiving intensive front-line chemotherapy. The findings are published this month in the Journal of Clinical Oncology. DHL is a form of aggressive B cell non-Hodgkin lymphoma characterized by genetic alterations that drive the lymphoma's growth. This variant is associated with a poor prognosis as compared to other forms of aggressive B cell lymphomas, as patients with this disease survive only an average of two years after diagnosis. Relapses of this disease are almost always fatal, meaning that keeping patients in remission is crucial. "A major dilemma for oncologists who treat this disease was whether or not to recommend the potentially harmful therapy of autoSCT to patients with this disease a strategy to help keep them in remission," said Daniel J. Landsburg, MD, an assistant professor of Hematology Oncology at Penn and the study's lead author. Landsburg and his team looked at data on 159 patients from 19 different academic medical centers across the United States. Patients were diagnosed between 2006 and 2015, and all achieved remission following intensive front-line chemotherapy or the standard chemotherapy regimen containing rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP). Of the total patients, 62 underwent an autoSCT, while 97 did not. Landsburg noted that there were no significant differences between the patient groups at baseline. "Our result is not explained by differences in patients' overall health or disease features," Landsburg said. "The transplant and non-transplant arms of this study were very well-matched." Overall, 80 percent of the patients were still in remission three years later, and 87 percent were still alive. When researchers broke the patients into two groups, autoSCT and no autoSCT, they found 89 percent of autoSCT patients were still in remission at three years, as were 75 percent of patients who did not receive an autoSCT. Also at three years, 91 percent of autoSCT patients were still alive, compared to 85 percent of non-autoSCT patients. None of these differences were found to be statistically significant. "Once these patients achieve remission, the data show they are likely to stay in remission," Landsburg said. "In the absence of a large randomized controlled trial, which would be very challenging to carry out in this case, this is the best evidence we have, and it shows there's no clear benefit to these patients undergoing autoSCT." Landsburg did point to one exception in the data, and that was in patients who underwent RCHOP, the standard front-line chemotherapy regimen. Just 56 percent of them were still in remission at three years, far lower than patients who received the more intensive front-line therapies. "Even if patients do go into remission with RCHOP, it appears to be less durable, so in these cases, going forward with autoSCT may still make sense," Landsburg said. Landsburg says the next step will be to study features of patients who don't go into remission in order to understand why their disease is resistant to therapy and if that can be overcome with different treatment strategies. He says it's also important to try to find more effective therapies for DHL patients who relapse. Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $6.7 billion enterprise. The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 20 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $392 million awarded in the 2016 fiscal year. The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania and Penn Presbyterian Medical Center -- which are recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report -- Chester County Hospital; Lancaster General Health; Penn Wissahickon Hospice; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine. Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2016, Penn Medicine provided $393 million to benefit our community.


News Article | February 14, 2017
Site: www.cemag.us

A team of investigators from Cedars-Sinai and UCLA is using a new blood-analysis technique and tiny experimental device to help physicians predict which cancers are likely to spread by identifying and characterizing tumor cells circulating through the blood. The investigators are conducting "liquid biopsies" by running blood through a postage-stamp-sized chip with nanowires 1,000 times thinner than a human hair and coated with antibodies, or proteins, that recognize circulating tumor cells. The device, the NanoVelcro Chip, works by "grabbing" circulating tumor cells, which break away from tumors and travel through the bloodstream, looking for places in the body to spread. Use of the chip in liquid biopsies could allow doctors to regularly and easily monitor cancer-related changes in patients, such as how well they're responding to treatment. The research earned the lead investigators a place in the U.S. Cancer Moonshot program, an initiative led by former Vice President Joe Biden to make more therapies available to more patients and to prevent cancer. "It's far better to draw a tube of blood once a month to monitor cancer than to make patients undergo repeated surgical procedures," says Edwin Posadas, MD, medical director of the Urologic Oncology Program at the Cedars-Sinai Samuel Oschin Comprehensive Cancer Institute and one of the lead investigators. "The power of this technology lies in its capacity to provide information that is equal to or even superior to traditional tumor sampling by invasive procedures." Although some forms of prostate cancer grow so slowly that they pose little risk to patients, other forms of the disease are lethal. Identifying which patients have which type of disease has become a crucial area of study because prostate cancer is one of the leading causes of cancer death among men in the U.S. Nearly 27,000 U.S. men are expected to die from the disease in 2017, according to the American Cancer Society. The research team has determined that in certain cancer cells, the nucleus is smaller than in other, more typical, cancer cells. Patients with the most advanced cases of aggressive prostate cancer have cells with these very small nuclei. The investigators' teamwork also revealed that very small nuclei are associated with metastasis, or cancer spread, to the liver and lung in patients with advanced cases of prostate cancer. Those nuclei developed before the metastases were detected. Identifying very small nuclei early in the disease progression may help pinpoint which patients have high risk of developing cancer that can spread and be fatal. Hsian-Rong Tseng, PhD, professor, Department of Molecular and Medical Pharmacology in the David Geffen School of Medicine at UCLA and the other lead investigator, says his work with Posadas is focused on improving the quality of life for cancer patients. "We're on a mission to dramatically change patients' everyday lives and their long-term outcomes," Tseng says. "We now have powerful new tools to accomplish that." Posadas and Tseng join an elite cadre of academicians, technology leaders and pharmaceutical experts as partners in the Blood Profiling Atlas in Cancer (BloodPAC) Project, a Moonshot program. Participants will collect and share data gathered from circulating tumor cells. Posadas and Tseng expect to contribute microscopic images from 1,000 circulating tumor cells that have not yet been analyzed, as well as additional data and cells they have cataloged. For the past five years, Posadas and Tseng have collected blood samples from cancer patients to profile and analyze the circulating tumor cells and other components. That process has helped them understand how prostate and other cancers evolve. The two investigators and their teams hope their findings will contribute to developing effective, targeted treatments for many types of cancer. "Minimally invasive methods to both diagnose and follow cancer, through simple blood tests, offer a unique and novel approach that can lead to earlier diagnosis and treatment, leading to more cures," says Robert A. Figlin, MD, director of the Division of Hematology Oncology and deputy director of the Samuel Oschin Comprehensive Cancer Institute.


News Article | February 28, 2017
Site: www.eurekalert.org

CINCINNATI--Researchers at the University of Cincinnati (UC) College of Medicine have discovered a new potential strategy to personalize therapy for brain and blood cancers. These findings are reported in the Feb. 28 edition of Cell Reports. "We found a new combination of therapeutics that could treat cancers that lack a protein called PTEN. PTEN is an important tumor suppressor, which means that it stops cell growth and division according to the needs of the body," says David Plas, PhD, Anna and Harold W. Huffman Endowed Chair for Glioblastoma Experimental Therapeutics. Plas is an associate professor in the Department of Cancer Biology, a member of the University of Cincinnati Cancer Institute and a researcher in the Brain Tumor Center of the UC Gardner Neuroscience Institute. Atsuo Sasaki, PhD, and Hala Elnakat Thomas, PhD, both in the Division of Hematology Oncology at the UC College of Medicine, were collaborators on the study. In early work using experimental therapeutics in human cancer cells and in tumor models, the Plas laboratory showed that stopping the production and function of the protein S6K1 could eliminate PTEN-deficient glioblastoma cells. Glioblastoma, the most aggressive form of brain cancer, is difficult to treat with targeted therapeutics. "We used support from the Huffman Foundation to conduct a sophisticated biochemical analysis of how cells respond to S6K1 targeting," Plas says. "Combining the biochemical results with computational analysis gave us the insight that we needed--there are targets in addition to S6K1 that can be hit to trigger the elimination of PTEN-deficient cancer cells." With the new information, the research team tested pharmaceutical-grade drug combinations for the ability to eliminate PTEN-deficient cancer cells. Results showed that the drugs LY-2779964 and BMS-777607 work together to specifically eliminate PTEN-deficient cells. "This is a completely new combination of targets in oncology," Plas says. "We have great hope that our new data will lead academic and industry researchers to investigate S6K1 as the center of new combination strategies for cancers of the brain, blood and other tissues." Future work in the project will test the safety and efficacy of the new combination using tumor models, with the goal of preparing the combination strategy for clinical trial. Ronald Warnick, MD, medical director of the UC Brain Tumor Center and a professor in the Department of Neurosurgery within the UC College of Medicine, adds that this kind of project is necessary in finding new and beneficial therapies for brain tumors. "There is a desperate need for novel therapeutic agents for patients with glioblastoma," he says. "This combination of drugs has the potential to become a game-changer." This study was funded by the American Cancer Society, the National Institutes of Health (R01 CA133164, R01 CA168815, R21NS100077, R01NS089815), the UC Brain Tumor Center, the Anna and Harold W. Huffman Endowed Chair for Glioblastoma Experimental Therapeutics and the UC Medical Scientist Training Program. Plas cites no conflict of interest.


Home > Press > Cedars-Sinai, UCLA Scientists Use New ‘Blood Biopsies’ With Experimental Device to Speed Cancer Diagnosis and Predict Disease Spread: Leading-Edge Research Is Part of National Cancer Moonshot Initiative Abstract: A team of investigators from Cedars-Sinai and UCLA is using a new blood-analysis technique and tiny experimental device to help physicians predict which cancers are likely to spread by identifying and characterizing tumor cells circulating through the blood. The investigators are conducting “liquid biopsies” by running blood through a postage-stamp-sized chip with nanowires 1,000 times thinner than a human hair and coated with antibodies, or proteins, that recognize circulating tumor cells. The device, the NanoVelcro Chip, works by “grabbing” circulating tumor cells, which break away from tumors and travel through the bloodstream, looking for places in the body to spread. Use of the chip in liquid biopsies could allow doctors to regularly and easily monitor cancer-related changes in patients, such as how well they’re responding to treatment. The research earned the lead investigators a place on the U.S. Cancer Moonshot program, an initiative led by former Vice President Joe Biden to make available more therapies to more patients and to prevent cancer. “It’s far better to draw a tube of blood once a month to monitor cancer than to make patients undergo repeated surgical procedures,” said Edwin Posadas, MD, medical director of the Urologic Oncology Program at Cedars-Sinai’s Samuel Oschin Comprehensive Cancer Institute and one of the lead investigators. “The power of this technology lies in its capacity to provide information that is equal to or even superior to traditional tumor sampling by invasive procedures.” Although some forms of prostate cancer are so slow-growing that they pose little risk to patients, other forms of the disease are lethal. Identifying which patients have which type of disease has become a crucial area of study because prostate cancer is one of the leading causes of cancer death among men in the U.S. Nearly 27,000 U.S. men are expected to die from the disease in 2017, according to the American Cancer Society. The research team has determined that in certain cancer cells, the nucleus is smaller than in other, more typical, cancer cells. Patients with the most advanced cases of aggressive prostate cancer have cells with these very small nuclei. The investigators’ teamwork also revealed that very small nuclei are associated with metastasis, or cancer spread, to the liver and lung in patients with advanced cases of prostate cancer. Those nuclei developed before the metastases were detected. Identifying very small nuclei early in the disease progression may help pinpoint which patients have high risk of developing cancer that can spread and be fatal. Hsian-Rong Tseng, PhD, professor, Department of Molecular and Medical Pharmacology in the David Geffen School of Medicine at UCLA and the other lead investigator, said that his work with Posadas is focused on improving the quality of life for cancer patients. “We’re on a mission to dramatically change patients’ everyday lives and their long-term outcomes,” Tseng said. “We now have powerful new tools to accomplish that.” Posadas and Tseng join an elite cadre of academicians, technology leaders and pharmaceutical experts as partners in the Blood Profiling Atlas in Cancer (BloodPAC) Project, a Moonshot program. Participants will collect and share data gathered from circulating tumor cells. Posadas and Tseng expect to contribute microscopic images from 1,000 circulating tumor cells that have not yet been analyzed, as well as additional data and cells they have cataloged. For the past five years, Posadas and Tseng have collected blood samples from cancer patients to profile and analyze the circulating tumor cells and other components. That process has helped them understand how prostate and other cancers evolve. The two investigators and their teams hope their findings will contribute to developing effective, targeted treatments for many types of cancer. “Minimally invasive methods to both diagnose and follow cancer, through simple blood tests, offer a unique and novel approach that can lead to earlier diagnosis and treatment, leading to more cures,” said Robert A. Figlin, MD, director of the Division of Hematology Oncology and deputy director of the Samuel Oschin Comprehensive Cancer Institute at Cedars- Sinai. About Cedars-Sinai Cedars-Sinai is a leader in providing high-quality healthcare encompassing primary care, specialized medicine and research. Since 1902, Cedars-Sinai has evolved to meet the needs of one of the most diverse regions in the nation, setting standards in quality and innovative patient care, research, teaching and community service. Today, Cedars-Sinai is known for its national leadership in transforming healthcare for the benefit of patients. Cedars-Sinai impacts the future of healthcare by developing new approaches to treatment and educating tomorrow’s health professionals. Additionally, Cedars-Sinai demonstrates a commitment to the community through programs that improve the health of its most vulnerable residents. About the David Geffen School of Medicine at UCLA Since opening in 1951, the David Geffen School of Medicine at UCLA has grown into an internationally recognized leader in research, medical education, patient care and public service. It has almost 2,000 full-time faculty members, including recipients of the Nobel Prize, the Pulitzer Prize and the National Medal of Science. More than 1,400 residents and fellows pursue advanced training at UCLA and its affiliated hospitals, which include Ronald Reagan UCLA Medical Center. For more information, please click If you have a comment, please us. Issuers of news releases, not 7th Wave, Inc. or Nanotechnology Now, are solely responsible for the accuracy of the content.


News Article | February 15, 2017
Site: www.eurekalert.org

LOS ANGELES (Feb. 13, 2017) - A team of investigators from Cedars-Sinai and UCLA is using a new blood-analysis technique and tiny experimental device to help physicians predict which cancers are likely to spread by identifying and characterizing tumor cells circulating through the blood. The investigators are conducting "liquid biopsies" by running blood through a postage-stamp-sized chip with nanowires 1,000 times thinner than a human hair and coated with antibodies, or proteins, that recognize circulating tumor cells. The device, the NanoVelcro Chip, works by "grabbing" circulating tumor cells, which break away from tumors and travel through the bloodstream, looking for places in the body to spread. Use of the chip in liquid biopsies could allow doctors to regularly and easily monitor cancer-related changes in patients, such as how well they're responding to treatment. The research earned the lead investigators a place on the U.S. Cancer Moonshot program, an initiative led by former Vice President Joe Biden to make available more therapies to more patients and to prevent cancer. "It's far better to draw a tube of blood once a month to monitor cancer than to make patients undergo repeated surgical procedures," said Edwin Posadas, MD, medical director of the Urologic Oncology Program at Cedars-Sinai's Samuel Oschin Comprehensive Cancer Institute and one of the lead investigators. "The power of this technology lies in its capacity to provide information that is equal to or even superior to traditional tumor sampling by invasive procedures." Although some forms of prostate cancer are so slow-growing that they pose little risk to patients, other forms of the disease are lethal. Identifying which patients have which type of disease has become a crucial area of study because prostate cancer is one of the leading causes of cancer death among men in the U.S. Nearly 27,000 U.S. men are expected to die from the disease in 2017, according to the American Cancer Society. The research team has determined that in certain cancer cells, the nucleus is smaller than in other, more typical, cancer cells. Patients with the most advanced cases of aggressive prostate cancer have cells with these very small nuclei. The investigators' teamwork also revealed that very small nuclei are associated with metastasis, or cancer spread, to the liver and lung in patients with advanced cases of prostate cancer. Those nuclei developed before the metastases were detected. Identifying very small nuclei early in the disease progression may help pinpoint which patients have high risk of developing cancer that can spread and be fatal. Hsian-Rong Tseng, PhD, professor, Department of Molecular and Medical Pharmacology in the David Geffen School of Medicine at UCLA and the other lead investigator, said that his work with Posadas is focused on improving the quality of life for cancer patients. "We're on a mission to dramatically change patients' everyday lives and their long-term outcomes," Tseng said. "We now have powerful new tools to accomplish that." Posadas and Tseng join an elite cadre of academicians, technology leaders and pharmaceutical experts as partners in the Blood Profiling Atlas in Cancer (BloodPAC) Project, a Moonshot program. Participants will collect and share data gathered from circulating tumor cells. Posadas and Tseng expect to contribute microscopic images from 1,000 circulating tumor cells that have not yet been analyzed, as well as additional data and cells they have cataloged. For the past five years, Posadas and Tseng have collected blood samples from cancer patients to profile and analyze the circulating tumor cells and other components. That process has helped them understand how prostate and other cancers evolve. The two investigators and their teams hope their findings will contribute to developing effective, targeted treatments for many types of cancer. "Minimally invasive methods to both diagnose and follow cancer, through simple blood tests, offer a unique and novel approach that can lead to earlier diagnosis and treatment, leading to more cures," said Robert A. Figlin, MD, director of the Division of Hematology Oncology and deputy director of the Samuel Oschin Comprehensive Cancer Institute at Cedars- Sinai. Cedars-Sinai is a leader in providing high-quality healthcare encompassing primary care, specialized medicine and research. Since 1902, Cedars-Sinai has evolved to meet the needs of one of the most diverse regions in the nation, setting standards in quality and innovative patient care, research, teaching and community service. Today, Cedars-Sinai is known for its national leadership in transforming healthcare for the benefit of patients. Cedars-Sinai impacts the future of healthcare by developing new approaches to treatment and educating tomorrow's health professionals. Additionally, Cedars-Sinai demonstrates a commitment to the community through programs that improve the health of its most vulnerable residents. Since opening in 1951, the David Geffen School of Medicine at UCLA has grown into an internationally recognized leader in research, medical education, patient care and public service. It has almost 2,000 full-time faculty members, including recipients of the Nobel Prize, the Pulitzer Prize and the National Medal of Science. More than 1,400 residents and fellows pursue advanced training at UCLA and its affiliated hospitals, which include Ronald Reagan UCLA Medical Center.


News Article | December 5, 2016
Site: www.eurekalert.org

Researchers from the UCLA Department of Medicine, Division of Hematology Oncology and the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA have published two studies that define how key genetic factors affect blood-forming stem cells by either accelerating or hindering the cells' regenerative properties. The findings could one day lead to improved treatments for people undergoing common therapies for cancer such as chemotherapy and radiation. Blood-forming stem cells, or hematopoietic stem cells, are found in the bone marrow. These cells have two unique properties: They can self-renew and, through a process called differentiation, they can form any type of blood cell. A healthy immune system depends on the regenerative abilities of hematopoietic stem cells. Common cancer therapies such as chemotherapy and radiation can eliminate cancer by killing cancer cells. But these treatments also damage hematopoietic stem cells, which can impede the cells' ability to regenerate blood, slowing the immune system and resulting in a longer, more complicated recovery for people with cancer. Previous research indicated that certain genes may alter hematopoietic stem cells' regenerative capacity by either accelerating or hindering the cells' ability to restore the immune system, but more research was needed to pinpoint the specific genetic activity and effects. One of the new studies focused on a gene called Grb10 that is expressed by hematopoietic stem cells. Grb10's function was previously not known, so to better understand its role, the scientists deleted Grb10 from hematopoietic stem cells in lab dishes and in mice that had received radiation. They found that deleting Grb10 strongly promotes hematopoietic stem cell self-renewal and differentiation. In the other study, researchers analyzed a protein called DKK1. DKK1 is produced by a gene expressed by a specific "bone progenitor" cell that is present in the "niche," or cellular environment, that surrounds the hematopoietic stem cell. Typically, bone progenitor cells regenerate bone, but scientists had previously hypothesized that these cells also play an important role in regulating hematopoietic stem cells' ability to self-renew and differentiate into other blood cells. "The cellular niche is like the soil that surrounds the stem cell 'seed' and helps it grow and proliferate," said Dr. John Chute, professor of medicine in the Division of Hematology Oncology in the UCLA David Geffen School of Medicine and the study's senior author. "Our hypothesis was that the bone progenitor cell in the niche may promote hematopoietic stem cell regeneration after injury." The researchers showed that adding DKK1 to hematopoietic stem cells in lab dishes and mice that had received radiation produced a cascade effect within the cell niche that greatly enhanced hematopoietic stem cells' ability to self-renew and differentiate into other blood cells. Taken together, the studies uncover two molecular mechanisms that could potentially be manipulated to increase the regenerative properties of hematopoietic stem cells and improve cancer therapy. Scientists can now test drugs that inhibit Grb10 or test the effectiveness of administering DKK1 intravenously to promote immune regeneration in people who have received chemotherapy and radiation or those undergoing bone marrow transplants. Chute, who also is a member of the UCLA Jonsson Comprehensive Cancer Center, is the senior author of both papers. The first author of the Nature Medicine study is Heather Himburg and other authors are Mamle Quarmyne, Xiao Yan, Joshua Sasine, Liman Zhao, Grace Hancock, Jenny Kan, Katie Pohl and Evelyn Tran of UCLA; and Phuong Doan, Nelson Chao and Jeffrey Harris of Duke University. Other authors of the Cell Reports study are Yan, Himburg, Pohl, Quarmyne, Tran, Yurun Zhang, Tianchang Fang, Kan and Zhao of UCLA; and Doan and Chao of Duke University. The studies were published in the journals Nature Medicine (embargo lifts at 11:00 a.m. US Eastern time on Monday, December 5, 2016) and Cell Reports (published on November 1, 2016). The studies were funded by grants from the National Heart, Lung, and Blood Institute (HL-086998-05), the National Institute of Allergy and Infectious Diseases (AI-067798), a California Institute for Regenerative Medicine Leadership Award (LA1-08014), a National Institute of Allergy and Infectious Diseases' Centers for Medical Countermeasures Against Radiation Pilot Award (2U19AI067773-11), and by the UCLA Broad Stem Cell Research Center.

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