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News Article | February 15, 2017

WINNIPEG, Manitoba, Feb. 15, 2017 (GLOBE NEWSWIRE) -- 3D Signatures Inc. (TSX-V:DXD) (OTCQB:TDSGF) (FSE:3D0) (the "Company" or "3DS"), is pleased to announce that Harry Glorikian has joined its Business Advisory Board. Mr. Glorikian has over 30 years of private and public company success in the biomedical and life sciences industries. He is recognized as a global innovator with high-profile consulting, executive and board experience and a passion for data driven medical diagnostics. Mr. Glorikian’s notable recent experience includes roles as Entrepreneur in Residence to GE Ventures – New Business Creation Group and as a member of the board of directors of GeneNews Ltd. (a molecular diagnostic company). He also serves on the advisory board of Nucelis (a gene-editing industrial biotech company) and Evidation Health (a digital health startup launched with support from GE Ventures). He is also a co-founder and an advisory board member of DrawBridge Health (a diagnostics startup launched with support from GE Ventures). Previously Mr. Glorikian co-founded and held the position of managing director and head of consulting services for Scientia Advisors, a company that became the go-to provider of strategic advice and implementation services for next-generation healthcare and life science innovators and Global 25 market leaders. Scientia Advisors was acquired by Precision for Medicine in November of 2012. Among his other professional roles, Mr. Glorikian served as senior manager for global business development at PE Applied Biosystems, founded X-Cell Laboratories, managed global sales at Signet Laboratories and held various roles at BioGenex Laboratories. “With the addition of Harry Glorikian to the Business Advisory Board, 3DS has gained tremendous insight into the development and commercialization of cutting-edge medical diagnostics,” noted Jason Flowerday, CEO of 3DS. “Mr. Glorikian has a track record of innovation and commercial success. His addition to the team is a very positive step forward for 3DS.” Mr. Glorikian holds an MBA from Boston University and a bachelor's degree from San Francisco State University. He has addressed the National Institutes of Health, Molecular Medicine Tri-Conference, World Theranostics Congress and other audiences, worldwide. He has authored numerous articles for industry publications, appeared on CBS Evening News and been quoted regularly by Dow Jones, The Boston Globe, BioWorld Today, Los Angeles Times, London Independent, Medical Device Daily, Science Magazine, Genetic Engineering News and many other media outlets. Mr. Glorikian is also author of the recently published and highly-relevant book, “Commercializing Novel IVDs: A Comprehensive Manual for Success.” An IVD is an in-vitro diagnostic device which is the type of diagnostic tool that 3DS is currently developing. Mr. Glorikian’s unique manual provides an overview of the major components to IVD development, from product conception through commercialization. His understanding of the diagnostic commercialization process in the context of clinical utility and cost effectiveness is an enormous asset to 3DS. 3DS (TSXV:DXD) (OTCQB:TDSGF) (FSE:3D0) is a personalized medicine company with a proprietary software platform based on the three-dimensional analysis of chromosomal signatures. The technology is well developed and supported by 20 clinical studies on over 2,000 patients on 13 different cancers and Alzheimer’s disease. Depending on the desired application, this platform technology can measure the stage of disease, rate of progression of disease, drug efficacy, and drug toxicity. The technology is designed to predict the course of disease and to personalize treatment for the individual patient. For more information, visit the Company’s new website at This news release includes forward-looking statements that are subject to risks and uncertainties. Forward-looking statements involve known and unknown risks, uncertainties, and other factors that could cause the actual results of the Company to be materially different from the historical results or from any future results expressed or implied by such forward-looking statements. All statements within, other than statements of historical fact, are to be considered forward looking. Although 3DS believes the expectations expressed in such forward-looking statements are based on reasonable assumptions, such statements are not guarantees of future performance and actual results or developments may differ materially from those in forward-looking statements. Risk factors that could cause actual results or outcomes to differ materially from the results expressed or implied by forward-looking information include, among other things: market demand; technological changes that could impact the Company’s existing products or the Company’s ability to develop and commercialize future products; competition; existing governmental legislation and regulations and changes in, or the failure to comply with, governmental legislation and regulations; the ability to manage operating expenses, which may adversely affect the Company’s financial condition; the Company’s ability to successfully maintain and enforce its intellectual property rights and defend third-party claims of infringement of their intellectual property rights; adverse results or unexpected delays in clinical trials; changes in laws, general economic and business conditions; and changes in the regulatory regime. There can be no assurances that such statements will prove accurate and, therefore, readers are advised to rely on their own evaluation of such uncertainties. We do not assume any obligation to update any forward-looking statements. Neither the TSX Venture Exchange nor its Regulation Service Provider (as that term is defined in the policies of the TSX Venture Exchange) accepts responsibility for the adequacy or accuracy of this release.

Rubin M.A.,Precision for Medicine | Rubin M.A.,New York Medical College
Cancer Discovery | Year: 2014

Lucas and colleagues nominate transmembrane serine protease type II (TMPRSS2) as an important player in the initiation of epithelial-mesenchymal transition (EMT) in prostate cancer. Cancer cells maintain androgen receptor-regulated cytoplasmic TMPRSS2 expression, which facilitates EMT invasion and metastasis in model systems through hepatocyte growth factor and c-MET signaling. In addition to providing a rationale for potentially targeting this organ-specific enabler of metastatic disease progression, this study also highlights the importance of understanding how organ/tissue-specifi c genes are co-opted in the context of cancer. © 2014 American Association for Cancer Research.

Feng F.Y.,University of Michigan | de Bono J.S.,Prostate Cancer Targeted Therapy Group | Rubin M.A.,Precision for Medicine | Rubin M.A.,New York Medical College | Knudsen K.E.,Thomas Jefferson University
Molecular Cell | Year: 2015

Poly(ADP-ribose) polymerase 1 (PARP1) inhibitors were recently shown to have potential clinical impact in a number of disease settings, particularly as related to cancer therapy, treatment for cardiovascular dysfunction, and suppression of inflammation. The molecular basis for PARP1 inhibitor function is complex, and appears to depend on the dual roles of PARP1 in DNA damage repair and transcriptional regulation. Here, the mechanisms by which PARP-1 inhibitors elicit clinical response are discussed, and strategies for translating the preclinical elucidation of PARP-1 function into advances in disease management are reviewed. Poly(ADP-ribose) polymerase 1 (PARP1) inhibitors were recently shown to have clinical impact in a number of disease settings. In this Perspective, the mechanisms by which PARP1 inhibitors elicit clinical response are discussed, and strategies for translating the preclinical elucidation of PARP1 function into advances in disease management are reviewed. © 2015 Elsevier Inc.

Agency: GTR | Branch: Innovate UK | Program: | Phase: Centre | Award Amount: 9.00M | Year: 2015

Awaiting Public Project Summary

Rosell R.,Precision for Medicine | Karachaliou N.,University of Barcelona
Nature Reviews Gastroenterology and Hepatology | Year: 2015

In 2014, developments in our understanding of escape signaling circuits implicated in resistance to targeted agents in patients with lung cancer have led to improvements in tackling such resistance. The potential role for PET in the management of erlotinib therapy, novel combination therapies and pharmacogenomic-driven individualization of platinum-based chemotherapy represent other key advances. © 2015 Macmillan Publishers Limited.

Pancreatitis occurs in approximately 4% of patients treated with the thiopurines azathioprine or mercaptopurine. Its development is unpredictable and almost always leads to drug withdrawal. We identified patients with inflammatory bowel disease (IBD) who had developed pancreatitis within 3 months of starting these drugs from 168 sites around the world. After detailed case adjudication, we performed a genome-wide association study on 172 cases and 2,035 controls with IBD. We identified strong evidence of association within the class II HLA region, with the most significant association identified at rs2647087 (odds ratio 2.59, 95% confidence interval 2.07–3.26, P = 2 × 10-16). We replicated these findings in an independent set of 78 cases and 472 controls with IBD matched for drug exposure. Fine mapping of the HLA region identified association with the HLA-DQA1*02:01–HLA-DRB1*07:01 haplotype. Patients heterozygous at rs2647087 have a 9% risk of developing pancreatitis after administration of a thiopurine, whereas homozygotes have a 17% risk. © 2014 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.

Ci W.M.,Precision for Medicine | Liu J.,Chinese Academy of Sciences
Physiology | Year: 2015

5-Methylcytosine (5mC) is a major epigenetic modification in animals. The programming and inheritance of parental DNA methylomes ensures the compatibility for totipotency and embryonic development. In vertebrates, the DNA methylomes of sperm and oocyte are significantly different. During early embryogenesis, the paternal and maternal methylomes will reset to the same state. Herein, we focus on recent advances in how offspring obtain the DNA methylation information from parents in vertebrates. ©2015 Int. Union Physiol. Sci./Am. Physiol. Soc.

Du W.,Precision for Medicine | Elemento O.,Precision for Medicine
Oncogene | Year: 2015

The transformation of normal cells into cancer cells and maintenance of the malignant state and phenotypes are associated with genetic and epigenetic deregulations, altered cellular signaling responses and aberrant interactions with the microenvironment. These alterations are constantly evolving as tumor cells face changing selective pressures induced by the cells themselves, the microenvironment and drug treatments. Tumors are also complex ecosystems where different, sometime heterogeneous, subclonal tumor populations and a variety of nontumor cells coexist in a constantly evolving manner. The interactions between molecules and between cells that arise as a result of these alterations and ecosystems are even more complex. The cancer research community is increasingly embracing this complexity and adopting a combination of systems biology methods and integrated analyses to understand and predictively model the activity of cancer cells. Systems biology approaches are helping to understand the mechanisms of tumor progression and design more effective cancer therapies. These approaches work in tandem with rapid technological advancements that enable data acquisition on a broader scale, with finer accuracy, higher dimensionality and higher throughput than ever. Using such data, computational and mathematical models help identify key deregulated functions and processes, establish predictive biomarkers and optimize therapeutic strategies. Moving forward, implementing patient-specific computational and mathematical models of cancer will significantly improve the specificity and efficacy of targeted therapy, and will accelerate the adoption of personalized and precision cancer medicine. © 2015 Macmillan Publishers Limited.

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