? CANCER EPIGENETICS PROGRAM The Cancer Epigenetics (CE) Program, led by Issa and Studitsky is a new Program at Fox Chase Cancer Center (FCCC). The CE Program is designed to integrate basic and applied research in the field of epigenetics. It is comprised of 19 Primary Members. Program funding is $5M (project direct costs) annually, including $2.4M in peer-reviewed funding of which $1M is from the NCI. CE members have been highly productive since Program initiation in 2012, generating 232 publications, with 9% representing intra- programmatic and 27% representing inter-programmatic collaborations. The CE Program takes advantage of the breadth and depth of faculty expertise in cancer epigenetics arising from the 2012 affiliation between FCCC and Temple University, to advance the overall goal of improving cancer outcomes through new approaches in detection, prognosis and therapy. The CE Program has four overarching themes: 1) Epigenomics: To decipher normal and cancer epigenomes, with the translational goal of discovering biomarkers of cancer risk, prognosis and response to therapy; 2) Readers, Writers and Erasers: To study the proteins that establish, read, modulate and perpetuate epigenetic marks, with the translational goal of discovering potential targets of therapy; 3) Development and Disease: To study epigenetics in normal and abnormal development and relate this information to what is known about cancer epigenetics and biology. The translational goal of this theme is in understanding cancer etiology, and discovering ways to reprogram the epigenome for therapeutic purposes; 4) Epigenetic Therapy: To develop epigenetically-targeted therapeutic approaches and test them in pre-clinical and clinical studies. These themes are developed by investigators working in multidisciplinary teams to identify and address the complex factors that contribute to cancer risk, cancer development and cancer treatment. This new Program was made possible by the recruitment of multiple faculty members at all career stages (junior and senior) and with diverse interests (basic to clinical), and has resulted in a strongly integrated program with both R01 funded basic research and rapidly accruing investigator-initiated clinical trials. These collaborative efforts have created a productive research environment that fosters the identification of new biomarkers of cancer risk, novel molecular targets for preventive intervention, and the successful development and implementation of novel approaches to cancer therapy. CE Program members have successfully accrued 394 research participants into interventional and non-interventional studies during the last funding cycle, and have benefited from the use of 11 of the 12 CCSG-supported Shared Resources at FCCC.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA006927-55
Application #
9996584
Study Section
Subcommittee I - Transistion to Independence (NCI)
Project Start
1997-07-01
Project End
2021-07-31
Budget Start
2020-08-01
Budget End
2021-07-31
Support Year
55
Fiscal Year
2020
Total Cost
Indirect Cost
Name
Research Institute of Fox Chase Cancer Center
Department
Type
DUNS #
064367329
City
Philadelphia
State
PA
Country
United States
Zip Code
19111
Shaikh, Talha; Wang, Lora S; Egleston, Brian et al. (2018) Predictors of Hematologic Toxicity and Chemotherapy Dose Intensity in Patients Undergoing Chemoradiation for Pancreatic Cancer. Am J Clin Oncol 41:59-64
Campbell, Kerry S; Cohen, Adam D; Pazina, Tatiana (2018) Mechanisms of NK Cell Activation and Clinical Activity of the Therapeutic SLAMF7 Antibody, Elotuzumab in Multiple Myeloma. Front Immunol 9:2551
Blackman, Elizabeth; Ashing, Kimlin; Gibbs, Denise et al. (2018) The Cancer Prevention Project of Philadelphia: preliminary findings examining diversity among the African diaspora. Ethn Health :1-17
Fatkhullina, Aliia R; Peshkova, Iuliia O; Dzutsev, Amiran et al. (2018) An Interleukin-23-Interleukin-22 Axis Regulates Intestinal Microbial Homeostasis to Protect from Diet-Induced Atherosclerosis. Immunity 49:943-957.e9
Gupta, Sapna; Kelow, Simon; Wang, Liqun et al. (2018) Mouse modeling and structural analysis of the p.G307S mutation in human cystathionine ?-synthase (CBS) reveal effects on CBS activity but not stability. J Biol Chem 293:13921-13931
Sementino, Eleonora; Menges, Craig W; Kadariya, Yuwaraj et al. (2018) Inactivation of Tp53 and Pten drives rapid development of pleural and peritoneal malignant mesotheliomas. J Cell Physiol 233:8952-8961
Araiza-Olivera, Daniela; Chernoff, Jonathan (2018) Hras helps hippo heterodimerize to evade tumor suppression. Small GTPases 9:327-331
Peng, Hongzhuang; Prokop, Jeremy; Karar, Jayashree et al. (2018) Familial and Somatic BAP1 Mutations Inactivate ASXL1/2-Mediated Allosteric Regulation of BAP1 Deubiquitinase by Targeting Multiple Independent Domains. Cancer Res 78:1200-1213
Reese, Jennifer Barsky; Smith, Katherine Clegg; Handorf, Elizabeth et al. (2018) A randomized pilot trial of a couple-based intervention addressing sexual concerns for breast cancer survivors. J Psychosoc Oncol :1-22
Shaikh, Talha; Handorf, Elizabeth A; Meyer, Joshua E et al. (2018) Mismatch Repair Deficiency Testing in Patients With Colorectal Cancer and Nonadherence to Testing Guidelines in Young Adults. JAMA Oncol 4:e173580

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