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Thomson j hudson3/1/2024 ![]() ‘TGF-beta3 protects normal human hematopoietic progenitor cells treated with 4-hydroperoxycyclophosphamide in vitro’. Lemoli, R.M., Strife, A., Clarkson, B.D., Haley, J.D. ‘The effects of TGF-beta3 on the growth of highly enriched hematopoietic progenitor cells derived from normal human bone marrow and peripheral blood’. Strife, A., Lambek, C., Perez, A., Darzynkiewicz, Z., Skierski, J., Gulati, S., Haley, J.D., ten Dijke, P., Iwata, K. ‘Contributory effects of de novo transcription and premature transcript termination in the regulation of human epidermal growth factor receptor proto-oncogene RNA synthesis’. ‘Analysis of mammalian fibroblast transformation by normal and mutated human EGF receptors’. (1987) ‘Porcine relaxin: Gene structure and expression’. Haley, J., Crawford, W., Hudson, P., Scanlon, D., Tregear, G., Shine, J. (1983) ‘Structure of a genomic clone encoding biologically active human relaxin’ Nature 30l, 628-631. Hudson, P., Haley, J., John, M., Cronk, M., Crawford, R., Haralambidis, J., Tregear, G., Shine, J., and Niall, H. (1982) ‘Porcine relaxin: Molecular cloning and cDNA structure’ DNA 1, 155-162. Haley, J., Hudson, H., Scanlon, D., John, M., Cronk, M., Shine, J., Tregear, G., and Niall, H. (1981) ‘Molecular cloning and characterization of cDNA sequences coding for rat relaxin’ Nature 291, 127-131. Hudson, P., Haley, J., Cronk, M., Shine, J. Through his experience in the Pharmaceutical industry, he is seeking to foster partnerships with peer institutions and with biotechnology and pharmaceutical companies, with the vision of developing novel approaches to cancer therapies at Stony Brook Medicine. He has presented numerous research seminars at national meetings, and he has served on a number of NCI grant review study sections. Haley holds numerous patents and has authored over 60 manuscripts related to the development of novel cancer therapeutics. He has published on the exploration of cancer drug resistance and cancer biomarkers, and has organized and chaired several AACR symposia and mini-symposia on the subject. He has a strong interest in drug discovery and development, most recently in Translational Medicine and Pharmacogenomics at OSI Pharmaceuticals, using biological mass spectrometry as a research tool for the quantitation of signaling networks. Haley served as Senior Director for Exploratory Cancer Research, Senior Research Director for Translational and EMT Research, and Senior Research Director for Discovery Research. as Program Manager for Cancer Therapeutics and was subsequently recruited to OSI Pharmaceutical Inc. in Molecular Endocrinology from the Howard Florey Institute for Experimental Physiology and the University of Melbourne and completed postdoctoral research fellowships at the Howard Florey Institute in Melbourne and at the Imperial Cancer Research Fund and the Ludwig Institute for Cancer Research in London. Haley earned a BA in Chemistry from Tufts University and a Ph.D. Current research interests include defining and exploiting mechanisms for overcoming anti-cancer drug resistance and cancer metastasis.ĭr. Through the generation and molecular characterization of EMT models, through RNAi-based target validation studies and follow-on pharmacology studies, new targets and compounds which promote death of metastatic cells can be identified and validated in panels of cell lines. New therapeutics are needed to target the new spectrum of tumor survival signals now present within EMT-derived cells and within related cancer-stem cells. EMT is an important cellular change which allows for metastasis and is associated with poor prognosis and resistance to chemo and targeted therapies in cancer patients. Several forms of plasticity have been documented, including epithelial mesenchymal transition (EMT), endothelial-mesenchymal transition and epithelial-neuroendocrine transition. Cellular plasticity plays a major role in the progression of cancer and the acquisition of mesenchymal cancer stem cell-like phenotypes has been correlated with poor prognosis. It is clear that metastatic cancers are increasingly heterogeneous, that is many different cell types and states are present within cancer tissues, and importantly metastatic cancers show increased resistance to radiation, chemotherapies and targeted therapies. Over 90% of cancer patient deaths are attributable to metastasis and the majority of patients treated in Phase I and Phase II clinical trials have metastatic cancers. ![]() Associate Professor of Research, Department of Pathologyĭirector, Developmental Therapeutics, SBU Cancer Center
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