The Molecular Mechanisms of Cancer Program (MMC) brings together basic and translational investigators dedicated to the study of cancer through research in cell signaling, molecular biology, systems biology, developmental biology, and chemistry/drug discovery. The Program has refined its membership from 46 to 36 to reflect increased cancer focus. Peer-reviewed funding of $14,681,074 (annual DC), with $5,863,767 from the NCI, has remained steady despite fewer members. Program members are highly-productive, with 416 peer-reviewed publications, including 12% that were intraprogrammatic, and 26% interprogrammatic publications during the past funding period. Moreover, 38% of these articles were published in high impact (impact factor >10) journals. Although our members'interests are varied, several common themes have emerged. Overall, the basic research objectives of our scientists can be divided into the following five themes: 1) to elucidate the molecular mechanisms of tissue-specific and cell type-specific gene expression;2) to elucidate the cellular mechanisms underlying cell growth/division and cell survival/death;3) to understand the multi-faceted mechanisms leading to cancer metastases;4) to use large-scale, high-throughput systems biology approaches and genetic evolutionary approaches to understand cancer biology;and 5) to discover novel developmental pathways relevant to cancer cell signaling. MMC members'fundamental scientific discoveries in these areas are further encouraged by Program 1 leadership to fuel hypothesis-driven clinical and translational cancer research and to contribute to the broader UCCCC initiative of personalized cancer treatment. Significantly, our membership has developed numerous collaborations with clinician-scientists both within the MMC Program and interprogramatically, reflecting the cross-disciplinary and translational nature of our research program. The MMC Program provides support and the structure for these collaborations among the Program's basic cancer biologists, while primarily representing the broad cancer relevant basic science strengths of the University of Chicago (UChicago). Through pilot funding, quarterly membership meetings, a seminar series, an annual retreat, and a strong basic science training program in cancer biology, the MMC Program is poised to continue its successful in-depth and basic research focus on cancer biology, while nurturing collaborative science that will enhance the clinical care of patients at risk or with cancer.
The Molecular Mechanisms of Cancer Program (MMC) of the University of Chicago Comprehensive Cancer Center brings together cancer biologists studying basic mechanisms of cancer into a focused program where faculty interact in research seminars, program meetings, and in educational and mentoring activities. The basic research performed by MMC investigators plays a key role in uncovering novel mechanisms of cancer biology, thereby leading to improved therapeutic approaches and better patient outcomes.
|Feng, Christine H; Gerry, Emily; Chmura, Steven J et al. (2015) An image-guided study of setup reproducibility of postmastectomy breast cancer patients treated with inverse-planned intensity modulated radiation therapy. Int J Radiat Oncol Biol Phys 91:58-64|
|Ming, Mei; Zhao, Baozhong; Shea, Christopher R et al. (2015) Loss of sirtuin 1 (SIRT1) disrupts skin barrier integrity and sensitizes mice to epicutaneous allergen challenge. J Allergy Clin Immunol 135:936-45.e4|
|Ming, Mei; Zhao, Baozhong; Qiang, Lei et al. (2015) Effect of immunosuppressants tacrolimus and mycophenolate mofetil on the keratinocyte UVB response. Photochem Photobiol 91:242-7|
|Shah, Palak; He, Yu-Ying (2015) Molecular regulation of UV-induced DNA repair. Photochem Photobiol 91:254-64|
|Ming, Mei; Han, Weinong; Zhao, Baozhong et al. (2014) SIRT6 promotes COX-2 expression and acts as an oncogene in skin cancer. Cancer Res 74:5925-33|
|Ramírez, Jacqueline; Kim, Tae Won; Liu, Wanqing et al. (2014) A pharmacogenetic study of aldehyde oxidase I in patients treated with XK469. Pharmacogenet Genomics 24:129-32|
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|Weng, Liming; Ziliak, Dana; Lacroix, Bonnie et al. (2014) Integrative "omic" analysis for tamoxifen sensitivity through cell based models. PLoS One 9:e93420|
|Stumpf, Melanie; Zhou, Xuyu; Chikuma, Shunsuke et al. (2014) Tyrosine 201 of the cytoplasmic tail of CTLA-4 critically affects T regulatory cell suppressive function. Eur J Immunol 44:1737-46|
|Geeleher, Paul; Cox, Nancy J; Huang, R Stephanie (2014) Clinical drug response can be predicted using baseline gene expression levels and in vitro drug sensitivity in cell lines. Genome Biol 15:R47|
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