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News Article | May 2, 2017
Site: www.eurekalert.org

Washington, DC - May 2, 2017 - The cells of vertebrates have evolved pathways that act like an internal defense, inhibiting viral infections by preventing replication of the pathogens. Drugs that activate those existing systems suggest a promising novel approach to treating dangerous infections by Zika and other viruses, say researchers from the Vaccine and Gene Therapy Institute at Oregon Health and Science University (OHSU), in Portland. In a new study published this week in mBio, the scientists report on a novel compound that triggers a cell's innate antiviral system, inhibiting replication of Zika, Chikungunya, and Dengue viruses. Recent outbreaks of Zika and Chikungunya infections that began in Latin and South America and spread to other continents -- as well as the ongoing presence of Dengue -- have spurred disease researchers to search for new antiviral medications. No treatments are available for the three infections, and only Dengue has a vaccine, which is licensed in some Asian and South American countries where the disease is endemic. The three viruses spread by way of the same mosquito species and elicit similar symptoms. Chikungunya emerged in the Americas in Caribbean islands in 2013, and since then it has infected more than a million people on five continents. Zika was first identified 70 years ago, but a 2015 outbreak that began in Brazil has spread to 50 countries and, according to estimates from the World Health Organization, will infect three to four million people this year. Zika infection during pregnancy can cause severe birth defects, including microcephaly. More than 350 million people are infected with Dengue annually; the virus is a leading cause of illness and death among children in some countries. Virologist Victor R. DeFilippis, at OHSU, led the work. He predicts that cellular innate immune responses may be pharmacologically harnessed to block infections as a kind of antiviral immunotherapy. "The tools that we need to fight off virus infection are programmed into our cells as a result of evolution," he says. "I think that's a potentially lost opportunity for the identification of novel broad-spectrum antiviral strategies." Interferons are proteins, secreted by cells, that are known to induce protection against a wide variety of infections, including viral. In the new paper, DeFilippis and his colleagues report on a novel small molecule, which they named AV-C, that triggers the built-in cellular defenses by activating the interferon system. In lab experiments, the researchers treated human fibroblasts with AV-C and, six hours later, infected the cells with one of the three viruses. The drug kept the viral presence low, leading them to conclude that AV-C establishes a cellular state antagonistic to replication. AV-C also triggered secretion of other proinflammatory cytokines, suggesting that it may have potential to enhance vaccine efficacy. The researchers also investigated whether the molecule has potential therapeutic effects by administering it to cells after infection with Zika and Chikungunya. For Zika, the results were promising. AV-C did block Zika replication in the cells when administered as late as 16 hours post-infection. For Chikungunya, however, the molecule failed to block replication when given just two hours post-infection. Next, says DeFilippis, the researchers need to evaluate the clinical utility of the drug in animal models. Early experiments in mice suggest AV-C does not inhibit virus replication in those animals, but DeFilippis hopes to test it in other species, such as nonhuman primates. He sees AV-C as the first of a family of compounds worth exploring. He and his team found the drug by using high-throughput screening to examine 51,000 different compounds that might trigger the innate response. After they narrowed down their list to a few promising candidates, AV-C was one of the first they studied in earnest. "There are potential drugs out there we haven't really taken a look at," says DeFilippis. "We're characterizing a number of other agents that are just as promising, and many are even more promising." The American Society for Microbiology is the largest single life science society, composed of over 48,000 scientists and health professionals. ASM's mission is to promote and advance the microbial sciences. ASM advances the microbial sciences through conferences, publications, certifications and educational opportunities. It enhances laboratory capacity around the globe through training and resources. It provides a network for scientists in academia, industry and clinical settings. Additionally, ASM promotes a deeper understanding of the microbial sciences to diverse audiences.

PORTLAND, Ore., SAN DIEGO, and TORONTO, May 08, 2017 (GLOBE NEWSWIRE) -- Oregon Health & Science University (OHSU) and  Aptose Biosciences Inc. (NASDAQ:APTO) (TSX:APS) announced the presentation of preclinical data demonstrating that CG’806, a highly potent pan-FLT3/BTK inhibitor, kills malignant cells in samples from patients with various hematologic malignancies. The data were presented in a poster on Sunday, May 7 at the 2017 American Association for Cancer Research (AACR) Conference Hematologic Malignancies: Translating Discoveries to Novel Therapies, held May 6-9 in Boston, MA. The poster, entitled CG’806, a First-in-Class FLT3/BTK Inhibitor, Exhibits Potent Activity against AML Patient Samples with Mutant or Wild-Type FLT3, as well as Other Hematologic Malignancy Subtypes, demonstrated the broad potency of CG’806 against various hematologic malignancy cell lines and patient primary bone marrow specimens. In addition, data for CG’806 indicated greater potency of CG’806 when compared to other non-proprietary competitive agents in acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL), including the bromodomain inhibitors OTX-015 and JQ-1, and the FLT3 inhibitor quizartinib. “The analyses of CG’806 against primary hematologic malignancy patient samples and cultured cell lines show evidence of potent and broad drug activity in AML and other disease subtypes and support further development of this agent for hematologic malignancies,” said Stephen E. Kurtz, Ph.D., lead author and Research Assistant Professor at the OHSU Knight Cancer Institute. "These findings further strengthen our commitment to develop CG’806 as a targeted treatment for AML and other hematologic malignancies," commented William G. Rice, Ph.D., Chairman and Chief Executive Officer of Aptose. “We are actively preparing ’806 for clinical studies and look forward to filing an IND and taking the molecule into patients as soon as possible.” Through the Beat AML Initiative, primary patient mononuclear cells were derived from 82 patients diagnosed with AML. Primary samples were also collected from patients with myelodysplastic syndrome/myeloproliferative neoplasms (MDS/MPN, n=15), acute lymphoblastic leukemia (ALL, n=17), and chronic lymphocytic leukemia (CLL, n=58). Sensitivity to CG’806 was evaluated across a range of concentrations after a 72-hour treatment. IC values were calculated as a measure of drug sensitivity and compared to other agents. Across the four general subtypes of hematologic malignancies in the dataset, there was broad sensitivity to CG’806, with 59% (48/82) of AML, 29% (5/17) of ALL, 53% (8/15) of MDS/MPN, and 40% (23/58) of CLL cases exhibiting an IC of less than 100 nM. Primary AML and CLL cells were sensitive to CG’806 with median IC values of 70 nM and 220 nM, respectively. Among the 38 tested AML samples with known FLT3 mutational status, the FLT3-ITD+ AML samples tended to have enhanced sensitivity to CG’806 (median IC = 20 nM, n=8) relative to the FLT3-WT samples (median IC = 120 nM, n=30). CG’806 also exerted potent anti-proliferative activity against human AML, B-ALL, mantle cell lymphoma, Burkitt’s lymphoma, and diffuse large B-cell lymphoma cell lines. In comparison to the FLT3 inhibitor quizartinib, CG’806 completely inhibited phosphorylation of FLT3 and STAT5 in MV4-11 cells, whereas quizartinib only partially inhibited their phosphorylation. The presentation will be published in the AACR Hematologic Malignancies Conference Proceedings. The poster can also be accessed here or at the Publications & Presentations section of the Aptose website, www.aptose.com. CG’806 is a once-daily, oral, first-in-class pan-FLT3/BTK inhibitor. This small molecule demonstrates potent inhibition of mutant forms of FLT3 (including internal tandem duplication, or ITD, and mutations of the receptor tyrosine kinase domain and gatekeeper region), eliminates AML tumors in the absence of toxicity in murine xenograft models, and represents a potential best-in-class therapeutic for patients with FLT3-driven AML. Likewise, CG’806 demonstrates potent, non-covalent inhibition of the Cys481Ser mutant of the BTK enzyme, as well as other oncogenic kinases operative in B cell malignancies, suggesting CG’806 may be developed for CLL and MCL patients that are resistant/refractory/intolerant to covalent BTK inhibitors. The Leukemia & Lymphoma Society and the Knight Cancer Institute at Oregon Health & Science University (OHSU) — joined by partnering medical institutions and industry collaborators — are performing groundbreaking research to better understand acute myeloid leukemia (AML).  Led by researchers at the Knight Cancer Institute, Beat AML collects samples from participating AML patients treated at 11 academic medical centers across the U.S. Knight Cancer Institute researchers conduct deep genomic sequencing analyses on those samples to create a profile of the possible genetic drivers of AML.  Researchers also test the sensitivity of patients' leukemic cells to a diverse panel of targeted therapies and novel combination regimens. The goal is to eventually match patients with treatments that precisely target their leukemia for durable remissions in AML. Aptose Biosciences is a clinical-stage biotechnology company committed to developing personalized therapies addressing unmet medical needs in oncology. Aptose is advancing new therapeutics focused on novel cellular targets on the leading edge of cancer. The company's small molecule cancer therapeutics pipeline includes products designed to provide single agent efficacy and to enhance the efficacy of other anti-cancer therapies and regimens without overlapping toxicities. For further information, please visit www.aptose.com. This press release may contain forward-looking statements within the meaning of Canadian and U.S. securities laws, including, but not limited to, statements relating to the therapeutic potential of CG’806 and its clinical development as well as statements relating to Aptose’s plans, objectives, expectations and intentions and other statements including words such as “continue”, “expect”, “intend”, “will”, “should”, “would”, “may”, and other similar expressions. Such statements reflect our current views with respect to future events and are subject to risks and uncertainties and are necessarily based upon a number of estimates and assumptions that, while considered reasonable by us are inherently subject to significant business, economic, competitive, political and social uncertainties and contingencies. Many factors could cause our actual results, performance or achievements to be materially different from any future results, performance or achievements described in this press release. Such factors could include, among others: our ability to obtain the capital required for research and operations and to continue as a going concern; the inherent risks in early stage drug development including demonstrating efficacy; development time/cost and the regulatory approval process; the progress of our clinical trials; our ability to find and enter into agreements with potential partners; our ability to attract and retain key personnel; changing market conditions; inability of new manufacturers to produce acceptable batches of GMP in sufficient quantities; unexpected manufacturing defects; and other risks detailed from time-to-time in our ongoing quarterly filings, annual information forms, annual reports and annual filings with Canadian securities regulators and the United States Securities and Exchange Commission. Should one or more of these risks or uncertainties materialize, or should the assumptions set out in the section entitled "Risk Factors" in our filings with Canadian securities regulators and the United States Securities and Exchange Commission underlying those forward-looking statements prove incorrect, actual results may vary materially from those described herein. These forward-looking statements are made as of the date of this press release and we do not intend, and do not assume any obligation, to update these forward-looking statements, except as required by law. We cannot assure you that such statements will prove to be accurate as actual results and future events could differ materially from those anticipated in such statements. Investors are cautioned that forward-looking statements are not guarantees of future performance and accordingly investors are cautioned not to put undue reliance on forward-looking statements due to the inherent uncertainty therein.

CAMBRIDGE, Mass.--(BUSINESS WIRE)--InVivo Therapeutics Holdings Corp. (NVIV) today announced that a new patient has been enrolled into The INSPIRE Study (InVivo Study of Probable Benefit of the Neuro-Spinal Scaffold™ for Safety and Neurologic Recovery in Subjects with Complete Thoracic AIS A Spinal Cord Injury) at Oregon Health & Science University (OHSU) in Portland, Oregon. Jason J. Chang, M.D., Assistant Professor of Neurological Surgery and co-study investigator, performed the surgery and implantation approximately 77 hours after the injury occurred. Mark Perrin, InVivo’s Chief Executive Officer and Chairman, said, “We were pleased to hear that the procedure was a success and that the patient is doing well. We now have 15 patients enrolled and in follow up, and we look forward to completing enrollment in the INSPIRE study.” For more information on the INSPIRE study, please visit the company’s ClinicalTrials.gov registration site: http://clinicaltrials.gov/ct2/show/study/NCT02138110 Following acute spinal cord injury, surgical implantation of the biodegradable Neuro-Spinal Scaffold within the decompressed and debrided injury epicenter is intended to support appositional healing, thereby reducing post-traumatic cavity formation, sparing white matter, and allowing neural regeneration across the healed wound epicenter. The Neuro-Spinal Scaffold, an investigational device, has received a Humanitarian Use Device (HUD) designation and currently is being evaluated in The INSPIRE Study for the treatment of patients with acute, complete (AIS A), thoracic traumatic spinal cord injury and a pilot study for acute, complete (AIS A), cervical (C5-T1) traumatic spinal cord injury. For more information on the cervical study, refer to https://clinicaltrials.gov/ct2/show/study/NCT03105882. InVivo Therapeutics Holdings Corp. is a research and clinical-stage biomaterials and biotechnology company with a focus on treatment of spinal cord injuries. The company was founded in 2005 with proprietary technology co-invented by Robert Langer, Sc.D., Professor at Massachusetts Institute of Technology, and Joseph P. Vacanti, M.D., who then was at Boston Children’s Hospital and who now is affiliated with Massachusetts General Hospital. In 2011, the company earned the David S. Apple Award from the American Spinal Injury Association for its outstanding contribution to spinal cord injury medicine. In 2015, the company’s investigational Neuro-Spinal Scaffold received the 2015 Becker’s Healthcare Spine Device Award. The publicly-traded company is headquartered in Cambridge, MA. For more details, visit www.invivotherapeutics.com. Any statements contained in this press release that do not describe historical facts may constitute forward-looking statements within the meaning of the federal securities laws. These statements can be identified by words such as "believe," "anticipate," "intend," "estimate," "will," "may," "should," "expect," “designed to,” “potentially,” and similar expressions, and include statements regarding the safety and effectiveness of the Neuro-Spinal Scaffold and the progress of the clinical program. Any forward-looking statements contained herein are based on current expectations, and are subject to a number of risks and uncertainties. Factors that could cause actual future results to differ materially from current expectations include, but are not limited to, risks and uncertainties relating to the company’s ability to successfully open additional clinical sites for enrollment and to enroll additional patients; the timing of the Institutional Review Board process; the company’s ability to commercialize its products; the company’s ability to develop, market and sell products based on its technology; the expected benefits and efficacy of the company’s products and technology in connection with the treatment of spinal cord injuries; the availability of substantial additional funding for the company to continue its operations and to conduct research and development, clinical studies and future product commercialization; and other risks associated with the company’s business, research, product development, regulatory approval, marketing and distribution plans and strategies identified and described in more detail in the company’s Quarterly Report of the three months ended March 31, 2017, and its other filings with the SEC, including the company’s Form 10-Qs and current reports on Form 8-K. The company does not undertake to update these forward-looking statements.

The new technique uses the gene-editing tool CRISPR to target a mutation in nuclear DNA that causes hypertrophic cardiomyopathy, a common genetic heart disease that can cause sudden cardiac death and heart failure. The research, published Aug. 2 in the journal Nature, demonstrates a new method for repairing a disease-causing mutation and preventing it from being inherited by succeeding generations. This is the first time scientists have successfully tested the method on donated clinical-quality human eggs. "Every generation on would carry this repair because we've removed the disease-causing gene variant from that family's lineage," said senior author Shoukhrat Mitalipov, Ph.D., who directs the Center for Embryonic Cell and Gene Therapy at OHSU. "By using this technique, it's possible to reduce the burden of this heritable disease on the family and eventually the human population." The study provides new insight into a technique that could apply to thousands of inherited genetic disorders affecting millions of people worldwide. The gene-editing technique described in this study, done in concert with in vitro fertilization, could provide a new avenue for people with known heritable disease-causing genetic mutations to eliminate the risk of passing the disease to their children. It could also increase the success of IVF by increasing the number of healthy embryos. "If proven safe, this technique could potentially decrease the number of cycles needed for people trying to have children free of genetic disease," said co-author Paula Amato, M.D., associate professor of obstetrics and gynecology in the OHSU School of Medicine. The new study focused on the genetic mutation that causes hypertrophic cardiomyopathy. The disease affects an estimated 1 in 500 people and can lead to heart failure and sudden death. "Although it affects men and women of all ages, it's a common cause of sudden cardiac arrest in young people, and it could be eliminated in one generation in a particular family," said co-author Sanjiv Kaul, M.D., a professor of medicine (cardiovascular medicine) in the OHSU School of Medicine and director of the OHSU Knight Cardiovascular Institute. Researchers worked with healthy donated human oocytes and sperm carrying the genetic mutation that causes cardiomyopathy. Embryos created in this study were used to answer pre-clinical questions about safety and effectiveness. The study noted that "genome editing approaches must be further optimized" before moving to clinical trials. "This research significantly advances scientific understanding of the procedures that would be necessary to ensure the safety and efficacy of germline gene correction," said Daniel Dorsa, Ph.D., senior vice president for research at OHSU. "The ethical considerations of moving this technology to clinical trials are complex and deserve significant public engagement before we can answer the broader question of whether it's in humanity's interest to alter human genes for future generations." Research conducted in this study adhered to guidelines established by OHSU's Institutional Review Board and additional ad-hoc committees established for scientific and ethical review. Further, the work is consistent with recommendations issued this year by the National Academy of Sciences and the National Academy of Medicine joint panel on human genome editing. CRISPR, which stands for clustered regularly interspaced short palindromic repeats, holds promise for correcting mutations in the human genome to prevent genetic disease. Using an enzyme called Cas9, it's possible to snip a specific target sequence on a mutant gene. The new study found that human embryos effectively repair these breaks in the mutant gene using the normal copy of this gene from a second parent as a template. The resulting embryos contain now repaired, mutation-free copies of this gene. The technique already has been used in animals for generating mutant models; however, the new study is the first to demonstrate that technique can be used in human embryos to convert mutant genes back to normal. The study also demonstrated a way for overcoming a crucial problem in genome editing in embryos known as mosaicism. Mosaicism refers to an outcome when not all cells in a multicellular embryo get repaired and some cells still carry a mutation. Mosaicism could undermine the very purpose of the gene-correction, rendering the repair moot if the developing embryo still carries a few cells with the disease-causing mutation that could ultimately find its way into the child's DNA. Researchers overcame this challenge in the new study by co-injecting the repair enzyme and the mutation-carrying sperm into the donor oocyte. As a result of initiating the repair process at the time of fertilization, every cell in a multicellular embryo had the mutation-free DNA exclusively. In addition to OHSU, co-authors on the study represented the Center for Genome Engineering, within the Institute for Basic Science, and Seoul National University in South Korea; the Salk Institute for Biological Studies in La Jolla, California; and BGI-Qingdao and Shenzhen Engineering Laboratory for Innovative Molecular Diagnostics in China. Studies conducted at OHSU were supported by OHSU institutional funds, including the Knight Cardiovascular Institute. Work in the laboratory of co-author Jin-Soo Kim of Seoul National University was supported by the Institute for Basic Science. Work in the laboratory of co-author Juan Carlos Izpisua Belmonte of the Salk Institute was supported by the G. Harold and Leila Y. Mathers Charitable Foundation, the Moxie Foundation and The Leona M. and Harry B. Helmsley Charitable Trust. Work at BGI was supported by the Shenzhen Municipal Government. Oregon Health & Science University is a nationally prominent research university and Oregon's only public academic health center. It serves patients throughout the region with a Level 1 trauma center and nationally recognized Doernbecher Children's Hospital. OHSU operates dental, medical, nursing and pharmacy schools that rank high both in research funding and in meeting the university's social mission. OHSU's Knight Cancer Institute helped pioneer personalized medicine through a discovery that identified how to shut down cells that enable cancer to grow without harming healthy ones. OHSU Brain Institute scientists are nationally recognized for discoveries that have led to a better understanding of Alzheimer's disease and new treatments for Parkinson's disease, multiple sclerosis and stroke. OHSU's Casey Eye Institute is a global leader in ophthalmic imaging, and in clinical trials related to eye disease. Staff biographies at Center for Embryonic Cell and Gene Therapy

News Article | May 11, 2017
Site: www.prnewswire.com

"Among our recent achievements, we are pleased to have been selected to participate in the Addario Lung Cancer Medical Institute's (ALCMI) landmark 400-patient clinical trial, ALCMI-009, which seeks to demonstrate the utility of liquid biopsy in patients with advanced non-small cell lung cancer (NSCLC).  Importantly, clinical results from this trial will be used to create a large, well-controlled, uniformly collected biorepository of patient blood samples for liquid biopsy profiling, response to treatment, and monitoring of disease," he added. "Additionally, we entered into a commercial collaboration for liquid biopsy testing with Oregon Health and Sciences University (OHSU), a leading cancer treatment center.  In this multi-phase agreement, OHSU's Knight Diagnostic Laboratory will utilize Biocept testing to aid in patient treatment decisions, participate in the development of enhancements to our liquid biopsy platform, and will play a role in beta testing our molecular pathology partnership model, which we expect to roll out later this year. "One of our 2017 strategic initiatives is to partner with leading cancer treatment centers in the United States, such as OHSU, aimed at increasing the commercial adoption of our proprietary Target Selector™ liquid biopsy platform.  In addition to OHSU, we signed a laboratory supply agreement for liquid biopsy testing with a national multi-center cancer treatment institution that is using our services for cancer profiling and therapeutic monitoring – the key areas for growth in liquid biopsy. "We also are capitalizing on the growing awareness of liquid biopsy by adding new sales executives to the team, bringing our field force to 12 representatives and three managers. I am enthusiastic about the high caliber of our new hires, and we believe that we are on track to grow our sales team to 15 to 20 representatives by the end of this year," Mr. Nall concluded. Review of First Quarter 2017 and Recent Accomplishments We accessioned 1,107 billable samples during the first quarter of 2017, a 38% increase from 801 billable samples accessioned during the first quarter of 2016.  Total sample accessions, which also include samples from research, assay validations, and other non-billable sources, were 1,246 for the first quarter of 2017, also up 38% from 902 total samples for the first quarter of 2016. Revenues for the first quarter of 2017 of $1.68 million increased from $221,000 reported in the first quarter of 2016.  First quarter 2017 revenues included $897,000 in commercial test revenues recognized on a cash basis and $61,000 in development services test revenues.  During the first quarter of 2017, we converted from cash-based revenue recognition for our commercial revenues, to accrual-based revenue recognition.  As a result, revenues for the three months ended March 31, 2017 included the recognition of $726,000 in commercial accounts receivable, net of reserves taken for third-party health plan and patient payments totaling $420,000, as well as reserves for contractual and payer-specific adjustments. Given the timing of the change to accrual accounting, we recognized a total of nonrecurring revenue of $877,000, which relates to revenue recognized in the first quarter of 2017 for commercial tests completed during 2016. Under this method of reporting, we believe that our revenues in future quarters will more accurately align with billable test volumes and operating expenses for the corresponding quarters. Cost of revenues for the first quarter of 2017 of $2.1 million compared with $1.5 million for the first quarter of 2016, with the increase primarily attributable to higher commercial test volumes. As test volumes continue to increase, we expect to leverage our fixed and semi-variable costs, reducing costs per patient sample and improving margins. Research and development expenses for the first quarter of 2017 of $757,000 increased slightly from $728,000 for the prior-year period, due to greater consumption of materials and higher costs associated with research and development activities. General and administrative expenses for the first quarter of 2017 were $1.9 million compared with $1.5 million for the first quarter of 2016, primarily due to higher personnel costs associated with the expansion of our in-house billing and investor relation functions, as well as higher consulting and third-party service provider fees associated with increased commercial activities. Sales and marketing expenses for the first quarters of 2017 and 2016 were unchanged at $1.3 million, notwithstanding higher accession volumes in the first quarter of 2017. The net loss for the first quarter of 2017 was $4.4 million, or 21 cents per share. This compares to a net loss for the first quarter of 2016 of $4.9 million, or 74 cents per share. Cash and cash equivalents were $14.0 million as of March 31, 2017, compared with $4.6 million as of December 31, 2016. On March 31, 2017, we completed an equity offering raising gross proceeds of $9.3 million. Additionally, we benefitted from $5.3 million in cash proceeds from the exercise of warrants in the first quarter of 2017. Biocept will hold a conference call today at 4:30 pm Eastern time to discuss these results and answer questions. The conference call can be accessed by dialing (855) 656-0927 for domestic callers, (855) 669-9657 for Canadian callers or (412) 902-4109 for other international callers. A live webcast of the conference call will be available on the investor relations page of the company's website at http://ir.biocept.com/events.cfm. A replay of the webcast will be available for 90 days. A replay of the call will be available for 48 hours following the conclusion of the call and can be accessed by dialing (877) 344-7529 for domestic callers, (855) 669-9658 for Canadian callers or (412) 317-0088 for other international callers. Please use event passcode 10101325. Biocept, Inc. is a molecular diagnostics company with commercialized assays for lung, breast, gastric, colorectal and prostate cancers, and melanoma.  The Company leverages its proprietary liquid biopsy technology to provide physicians with clinically actionable information for treating and monitoring patients diagnosed with cancer.  Biocept's patented Target Selector™ liquid biopsy technology platform captures and analyzes tumor-associated molecular markers in both circulating tumor cells (CTCs) and in circulating tumor DNA (ctDNA). With thousands of tests performed, the platform has demonstrated the ability to identify cancer mutations and alterations to inform physicians about a patient's disease and therapeutic options. For additional information, please visit www.biocept.com. This news release contains forward-looking statements that are based upon current expectations or beliefs, as well as a number of assumptions about future events. Although we believe that the expectations reflected in the forward-looking statements and the assumptions upon which they are based are reasonable, we can give no assurance that such expectations and assumptions will prove to be correct. Forward-looking statements are generally identifiable by the use of words like "may," "will," "should," "could," "expect," "anticipate," "estimate," "believe," "intend" or "project," or the negative of these words or other variations on these words or comparable terminology. To the extent that statements in this news release are not strictly historical, including, without limitation, statements as to our ability to provide physicians with clinically actionable information to improve the outcomes of cancer patients, our ability to roll out our molecular pathology partnership model, our ability to increase the commercial adoption of our proprietary Target Selector™ liquid biopsy platform, our ability to grow our sales team, and our ability to make investments to accelerate our growth, such statements are forward-looking, and are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. The reader is cautioned not to put undue reliance on these forward-looking statements, as these statements are subject to numerous risk factors as set forth in our Securities and Exchange Commission (SEC) filings. The effects of such risks and uncertainties could cause actual results to differ materially from the forward-looking statements contained in this news release. We do not plan to update any such forward-looking statements and expressly disclaim any duty to update the information contained in this press release except as required by law. Readers are advised to review our filings with the SEC at www.sec.gov. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/biocept-reports-first-quarter-2017-financial-results-300456420.html

The OHSU Knight Cancer Institute's project aims to develop strategies for improving treatment-resistant triple negative breast cancer, an aggressive form of breast cancer that lacks key receptors known to fuel most breast cancers: estrogen receptors, progesterone receptors and human epidermal growth factor receptor 2 (HER2). Using advanced microscopy, the team will leverage tools for quantitative analysis and visualization of images generated, together with computational approaches for integrating diverse molecular data types. Through analysis of core cell lines, patient-derived cultures and primary tumors, the team aims to uncover molecular networks that underlie disease progression and therapeutic response. Joe Gray, Ph.D., director of the OHSU Center for Spatial Systems Biomedicine (OCSSB) and the OHSU Knight Cancer Institute associate director for biophysical oncology will lead the investigative team as a principal investigator. "Triple negative breast cancer is a particularly difficult form of the disease to treat," said Gray. "Our goals in the CSBC Research Center are to identify the mechanisms by which these cancers evolve and adapt to become resistant to treatment, and to develop new strategies to counter these mechanisms. Our multidisciplinary approach treats these cancers as adaptive systems that can be controlled using multiple drug combinations." Co-principal investigators on the project include: Rosalie Sears, Ph.D., professor of molecular and medical genetics in the OHSU School of Medicine and a senior member of the Knight Cancer Institute; Claire Tomlin, Ph.D., the Charles A. Desoer Professor of Engineering in the Department of Electrical Engineering and Computer Sciences at the University of California, Berkeley; Adam Margolin, Ph.D., associate professor of biomedical engineering and director of computational biology in the OHSU School of Medicine and the Knight Cancer Institute. Overall research themes of the consortium's Research Centers address important questions in basic cancer research, including the emergence of drug resistance, the mechanisms underlying cancer metastasis, and the role of the immune system in cancer progression and treatment. The interdisciplinary investigators of the CSBC will integrate experimental biology with mathematical and computational modeling to gain insight into processes relevant to cancer initiation, progression and treatment options. The consortium brings together clinical and basic science cancer researchers with physician-scientists, engineers, mathematicians and computer scientists to tackle key questions in cancer biology from a novel point of view. "Cancer is a complex disease and it challenges our traditional approaches, making it hard to predict tumor growth and drug response," said Daniel Gallahan, Ph.D., deputy director of NCI's Division of Cancer Biology. "Cancer systems biologists embrace that complexity and use many different types of data to build mathematical models that allow us to make predictions about whether a tumor will metastasize or what drug combinations will be effective." In addition to applying systems biology approaches to gain important insight into cancer, each consortium Research Center supports an outreach program to promote training in interdisciplinary science, disseminate important research findings to the community, and to engage the public in cancer systems biology research. Sage Bionetworks in Seattle serves as the consortium's Coordinating Center, facilitating data and resource sharing and collaborative scientific activities across the nine Research Centers as well as two new Research Projects. More information can be found on the project website. The Knight Cancer Institute at Oregon Health & Science University is a pioneer in the field of precision cancer medicine. The institute's director, Brian Druker, M.D., helped prove it was possible to shut down just the cells that enable cancer to grow. This breakthrough has made once-fatal forms of the disease manageable and transformed how cancer is treated. The OHSU Knight Cancer Institute is the only National Cancer Institute-designated Cancer Center between Sacramento and Seattle – an honor earned only by the nation's top cancer centers. It is headquarters for one of the National Cancer Institute's largest research collaboratives, SWOG, in addition to offering the latest treatments and technologies as well as hundreds of research studies and clinical trials. For additional information on the OHSU Knight Cancer Institute visit www.ohsu.edu/xd/health/services/cancer or follow us on Facebook and Twitter. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/ohsu-knight-cancer-institute-selected-to-join-prestigious-national-consortium-receive-92-million-300464180.html

Genta R.M.,Miraca Life science Research Institute | Sonnenberg A.,OHSU
Alimentary Pharmacology and Therapeutics | Year: 2015

Results Of 895 323 patients, 10.6% had Hp-gastritis and 1.5% Helicobacter-negative gastritis. Hp-gastritis, but not Helicobacter-negative gastritis, was more common in males than females (OR 1.17, 95% CI: 1.16-1.19). While Hp-gastritis was more prevalent in high than in low-prevalence areas (OR 3.65, 95% CI: 3.57-3.74), Helicobacter-negative gastritis was only minimally affected by the underlying H. pylori prevalence (1.7% vs. 1.5%). The age-specific prevalence of Hp-gastritis peaked in the 4th to 5th decades; Helicobacter-negative gastritis exhibited a low and relatively flat pattern. The geographic distribution of H. pylori-positive and -negative gastritis showed no significant correlation. Intestinal metaplasia was found in 13.0% of patients with Hp-gastritis and in 6.1% of those with Helicobacter-negative gastritis (OR 0.43, 95% CI: 0.40-0.47). Conclusion These data suggest that Helicobacter-negative gastritis is, in the vast majority of cases, a nosologically and epidemiologically distinct entity that deserves further investigation.Background Helicobacter-negative gastritis is diagnosed when no organisms are detected in a gastric mucosa with typical features of Helicobacter gastritis (Hp-gastritis). If Helicobacter-negative gastritis consisted mostly of 'missed' Helicobacter infections, its prevalence should represent a constant percentage of these infections in a population, and their clinico-epidemiological features would overlap.Aim To compare the epidemiologic patterns of Hp-positive and Hp-negative gastritis.Methods From a pathology database, we extracted demographic, clinical and histopathological data from patients with gastric biopsies (1.2008-12.2013). We allocated patients to high (≥12%) and low (≤6%) H. pylori prevalence regions defined by ZIP code-based data. The prevalence of H. pylori-positive and -negative gastritis by sex, age and state were expressed as a per cent of the total study population stratified accordingly. © 2014 John Wiley & Sons Ltd.

SEATTLE--(BUSINESS WIRE)--In the second paragraph, second sentence, the URL embedded in "publication" should read: https://doi.org/10.1038/sdata.2017.5 (instead of https://www.doi.org/10.1038/sdata.2017.5) Mole photos, measurements, and melanoma risk factor data contributed by over 2,500 participants are made available by Sage Bionetworks and OHSU to accelerate skin cancer research. Sage Bionetworks and Oregon Health & Science University (OHSU) today publicly released data contributed by 2,798 participants in the Mole Mapper melanoma study. The app-based research study uses Apple’s ResearchKit to enroll participants who use the phone camera to map and measure their moles over time. Abnormal or changing moles can be an indicator of the skin cancer melanoma, so remote monitoring with the possibility of early detection holds great promise for cancer prevention. Whereas most research data are generated in a clinical or laboratory setting, Mole Mapper is crowd-sourced by individuals contributing data to the study from their own phones. Curated Mole Mapper data, consisting of mole photos and measurements together with melanoma risk factors, have been made available to qualified researchers on Sage Bionetworks’ collaborative science platform Synapse and accompanied by a publication in Nature Scientific Data. This is the second such mobile health study that has been made broadly available to qualified researchers around the world. “In designing the study, we first wanted to know if research run remotely and entirely through an app could find the same melanoma risks as years of rigorous epidemiology and genetics research,” said lead author Dan Webster, Research Fellow at the National Cancer Institute. “We show, for instance, that Mole Mapper participants with red hair were significantly more likely to be diagnosed with melanoma. This is in alignment with previously published data showing that people with red hair caused by mutations in the MC1R gene have a higher risk for melanoma.” The study data also touches on a frequently asked question about moles: “Is this normal?” Stanford University researchers recently demonstrated that algorithms can accurately diagnose skin conditions by training on a large database of high-quality medical skin images. The Mole Mapper team aims to create a similarly foundational database from participant-contributed data. While clinical resources will undoubtedly be important in answering this question, most moles that are measured and monitored in a clinical setting are already suspect and may already be abnormal. “With Mole Mapper, we have a unique ability to collect thousands of measurements from ‘pre-clinical’ moles that people measure themselves at home,” said Webster. “Over time, this can provide a basis for mole size and shape distributions to serve as a new benchmark for future studies.” The release of the Mole Mapper study data is a part of the larger mobile health ecosystem that Sage Bionetworks is cultivating. Developing open-source modules for integration into mobile applications and enabling the broad sharing of the resulting data are cornerstones of this effort. “In the promising space of mobile health, too often data is controlled by private interests,” said study coauthor Brian Bot, Principal Scientist, Sage Bionetworks. “Shared data resources such as these will help enable the scientific community to more quickly determine what can and cannot be gleaned from these types of remote measurements.” Sage Bionetworks is a 501(c) (3) nonprofit biomedical research organization, founded in 2009, with a vision to promote innovations in personalized medicine by enabling a community-based approach to scientific inquiries and discoveries. Sage Bionetworks strives to activate patients and to incentivize scientists, funders and researchers to work in fundamentally new ways in order to shape research, accelerate access to knowledge and transform human health. It is located on the campus of the Fred Hutchinson Cancer Research Center in Seattle, Washington and is supported through a portfolio of philanthropic donations, competitive research grants, and commercial partnerships. More information is available at http://www.sagebase.org.

News Article | February 23, 2017
Site: www.eurekalert.org

"Mutations are part of life. They are mistakes in a gene like typos in a text message," said Watanabe-Smith, a postdoctoral fellow with the OHSU Knight Cancer Institute. "But which mutations cause cancer? That's the real question. And this problem is impossible to understand without a strong model system to test those mutations." Watanabe-Smith's research, published today in the journal Oncotarget, sought to better understand one "typo" in a standard leukemia assay, or test. While studying cancer biology and completing his doctorate in the lab of Brian Druker, M.D., at the OHSU Knight Cancer Institute, Watanabe-Smith encountered a new problem: an issue with the model system itself. "When I was sequencing the patient's DNA to make sure the original, known mutation is there, I was finding additional, unexpected mutations in the gene that I didn't put there. And I was getting different mutations every time," said Watanabe-Smith. He decided to formally study this phenomenon with his lab advisers, who included Druker; Cristina Tognon, Ph.D., scientific director, Druker lab; and Anupriya Agarwal, Ph.D., assistant professor of hematology & medical oncology, OHSU School of Medicine; researcher with the OHSU Knight Cancer Institute, all co-authors on the paper. "Kevin and team would sequence the DNA, just to make sure the mutation's still there, and in that process they would pick up additional mutations that we didn't put there in the gene we were looking at," said Tognon. "After we saw this in several cases we knew it was worth further study." His initial research, identifying and characterizing a growth-activating mutation in a patient with T-cell leukemia, was first published last April in the journal Leukemia. The research published today was focused on better understanding the lab's model system, to ensure that future researchers trying to identify cancer-causing mutations are using accurate and reproducible methods. Their research investigates a common cell line assay, used since the 1980's, to detect which mutations are important in driving leukemia and other cancers. They found this assay is prone to a previously unreported flaw, where the cells, called Ba/F3 cells, can acquire additional mutations. "The potential impact is that a non-functional mutation could appear functional, and a researcher could publish results that would not be reproducible," Watanabe-Smith said. "Then we had the question: 'Did the cells transform because of a mutation the patient had, or did they transform because these new mutations they managed to pick up somewhere?'" Ultimately, he says, the research team recommends an additional step in the Ba/F3 assay (sequencing outgrown cell lines) to improve reproducibility of future results. While the results urge further research, the message to scientific community is clear: There seems to be more potential for problems than previously anticipated in this standard assay. "We're using this method to advance our understanding of patients' cancers. I now have a better idea of what may be contributing to this patient's leukemia and potentially what drugs could be used to control it. It will hopefully help the next person with the same mutation," Watanabe-Smith said. Particulars: Watanabe-Smith is an Achievement Rewards for College Scientists (ARCS) scholar. Druker is a Howard Hughes Medical Institute Investigator.

A research conducted by scientists at the Oregon Health and Science University (OHSU) has led to a shocking discovery. The research has conclusively proven that antibiotics which are prescribed to patients diagnosed with Cystic Fibrosis (CF), can eventually cause kidney infections and even permanent hearing loss. CF is a disease which affects both the lungs and the digestive systems. It is known to afflict more than 30,000 people in the U.S. alone while another 70,000 suffer from it worldwide. The latest study was led by Angela Garinis and co-authored by Peter Steyger. The research posits that rather than prescribing the antibiotics for CF, doctors should instead find an alternate solution for respiratory issues. If the patient is responsive to the other classes of antibiotics, then it is better to prescribe those and not the CF antibiotics. The study conclusively proves that patients treated with other drugs show less toxins in the body which affect the kidney and the ear compared to those who are on the aminoglycoside antibiotics. "Preventing or ameliorating the effects of permanent [hearing loss] is crucial for patients with CF who already have a significantly compromised quality of life due to the disease," surmisedthe authors. To reach these conclusions, scientists had to first conduct a study consisting of 81 CF patients who were within 15 to 63 years old. These patients were then divided into four groups depending on the cumulative dosage of the aminoglycoside antibiotics that were administered intravenously. After some research it was found that the two groups taking the highest dosage of the antibiotics were 4.79 percent more likely to suffer from hearing loss than the other two groups. Previous research such as this had also established the harmful effects of the aminoglycoside antibiotic, but this is the only study where the cumulative exposure throughout the patient's life has also been taken into account. Furthermore, these findings indicate that it is essential for physicians to constantly monitor hearing in a CF patient who is being treated with antibiotics. The results may be a cause for worry for patients suffering from CF. It is advisable that the next time you visit the physician, make sure he also checks your ears and kidneys for any signs of damage. The results of the study have been published in the Feb. 23 issue of Journal of Cystic Fibrosis. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.

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