UCSF HELEN DILLER FAMILY COMPREHENSIVE CANCER CENTER

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Presentations MicroRNA-383 located in frequently deleted chromosomal locus 8p22 regulates prostate cancer stem cell marker CD44 Authors*: Nathan Bucay, Kiran Sekhon, Varahram Shahryari, Yozo Mitsui, Guoren Deng, Z. Laura Tabatabai, Shahana Majid, Soichiro Yamamura, Rajvir Dahiya, Yuichiro Tanaka, Sharanjot Saini Pres #: 1934 Section: 6 Presentation Date/Time: Monday, April 18: 1:00-5:00PM Location: Presentation Type: Poster Session Saini Lab Expertise: The Saini lab focuses primarily on understanding the molecular basis of progression and metastasis of prostate cancer, in particular the role of microRNA (miRNA) genes located at frequently deleted genomic regions in prostate cancer epithelial-to mesenchymal transition (EMT), recurrence and metastasis. A role for miRNAs that affects EMT and progression and metastasis of human cancers has begun to emerge and Dr. Saini’s research provided initial evidence that miR-203 regulates EMT by directly targeting ZEB2 and other EMT regulators that in turn regulate PCa invasion and metastasis. Her recent research has identified additional novel miRNAs in prostate cancer that play an important role in prostate cancer EMT, recurrence and metastasis. https://www.ncire.org/research/researchers_by_name/Sharanjot-Saini-PhD/ __________________________________________________________________________ A discovery study to identify clinical and genetic risk factors for bevacizumab (BEV)-related gastrointestinal (GI) hemorrhage (HEM) in metastatic castration-resistant prostate cancer (mCRPC) patients (pts) treated on CALGB 90401 (Alliance) Authors*: Jai N. Patel, Chen Jiang, Kouros Owzar, Daniel L. Hertz, Flora A. Mulkey, William K. Kelly, Susan Halabi, Yoichi Furukawa, Cameron Lassiter, Susan G. Dorsey, Paula N. Friedman, Eric J. Small, Michael A. Carducci, John F. Mahoney, Michael J. Kelley, Yusuke Nakamura, Michiaki Kubo, Mark J. Ratain, Michael J. Morris, Howard L. McLeod Pres #: 2037 Section: 14 Presentation Date/Time: Monday, April 18: 1:00-5:00PM Location: Presentation Type: Poster Session Small Lab Expertise: The Stand Up To Cancer Dream Team led by Dr. Eric Small is exploring the idea that resistance to hormonal therapy occurs as a result of the prostate cancer cells using common cellular responses — what the Dream Team calls “adaptive pathways” — to escape the current prostate cancer therapies. They believe that, by identifying these pathways and inhibiting them, they will be able to overcome treatment resistance and profoundly improve the care of men affected by this fatal disease. This team is a six institution consortium to include UC Los Angeles, UC Davis, UC Santa Cruz, University of British Columbia, Oregon Health and Science University, with UCSF as the lead administrative site. http://cancer.ucsf.edu/people/profiles/small_eric.3671 *UCSF authors in bold 22
Presentations Toxicity, bioavailability, pharmacokinetics, tissue distribution and metabolism of a novel small molecule inhibitor of IL-6-induced STAT3 activation Authors*: Brian F. Kiesel, Robert A. Parise, Jianxia Guo, Donna M. Huryn, Paul A. Johnston, Rafaelle Colombo, Malabika Sen, Jennifer Grandis, Julie L. Eiseman, Jan H. Beumer Pres #: 2083 Section: 16 Presentation Date/Time: Monday, April 18: 1:00-5:00PM Location: Presentation Type: Poster Session Grandis Lab Expertise: We performed a high content screening (HCS) campaign of a 95,000 compound subset of the NIH Molecular Library Screening Center Network (MLSCN) small-molecule library and identified four chemical hit series that selectively inhibited IL-6-induced STAT3 pathway activation in head and neck cancer cell lines that progressed into lead optimization. In the present study we assessed the toxicity, bioavailability, PK , tissue distribution and metabolism of a lead compound (UPCDC10205). Preliminary results indicate that UPCDC10205 was metabolically stable. No gross toxicity was observed in mice administered the maximum soluble dose. UPCDC10205 was widely distributed into tissues and cleared rapidly. Bioavailability was ~5%. In vivo metabolism of UPCDC10205 was by direct glucuronidation, explaining why microsomal stability (reflective of phase I metabolism) did not translate to in vivo metabolic stability. http://ohns.ucsf.edu/jennifer-grandis __________________________________________________________________________ Aurora kinase A (AURKA) dependence underlies the emergence of acquired resistance to 3rd generation EGFR inhibitors in NSCLC Authors*: Khyati Niral Shah, Henry J. Haringsma, Andrew D. Simmons, Sourav Bandyopadhyay Pres #: 2118 Section: 17 Presentation Date/Time: Monday, April 18: 1:00-5:00PM Location: Presentation Type: Poster Session Bandyopadyay Lab Expertise: In the context of cancer, we are mapping genetic interactions systematically in high-throughput using RNAi and small-molecule based screens. Our primary interest is uncovering genes and pathways which modify the activity of major oncogenes including EGFR and KRAS. Our systems-biology approaches can be used to identify alternative, synthetic lethal targets as well as potential routes of resistance to therapies. In previous work we have interrogated the MYC oncogene in triple negative breast cancer and identified new therapies that can be used in a synthetic lethal manner to target MYC-high breast tumors [Martins et al Cancer Discovery 5(2):154-67 2015] http://cancersignaling.net/ *UCSF authors in bold 23
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UCSF HELEN DILLER FAMILY COMPREHENSIVE CANCER CENTER

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