The Molecular and Cellular Oncogenesis Program (MCO) is comprised of eleven investigators who work collaboratively in broad areas of cancer biology. Over the last budget period, the MCO Program has undergone an extensive realignment in research focus, thematic areas of collaboration and Program membership. In line with the strategic reorganization ofthe Cancer Center, the MCO Program appointed a new Program Leader (Dr. Murphy), recruited four new investigators at all academic ranks, and received one faculty member (Dr. Janicki) from the Gene Expression and Regulation (GER) Program. Concomitantly, three MCO members transferred to the newly created Program in Tumor Microenvironment and Metastasis (TMM). As a result, the MCO Program is now a more focused and highly collaborative research initiative, bringing together multidisciplinary expertise around three general flagship themes: Mechanisms of growth control (i);Cancer biomarkers and bio-signatures (ii);and Targeted cancer therapeutics (iii). The overarching goal of the Program is to combine a mechanistic understanding of cancer signaling networks with novel molecular approaches to disease diagnosis and treatment, along the continuum of basic, translational and patient-oriented cancer research. Synergy among the scientists is facilitated by a strong programmatic foundation in computational and integrative biology, a broad utilization of Cancer Center Shared Resources, and productive inter-programmatic and inter-institutional collaborations. Over the last budget period, MCO investigators made impressive gains on a broad portfolio of scientific discoveries in line with Program goals. The National Cancer Institute (NCI) funding base of the Program has grown by 27% compared to the last budget period, from $2.05 million in 2008 to $2.79 million in 2013 (direct costs), and the rate of collaborative publications has increased by more than five-fold, from 6.9% in 2008 to 36% in 2013 (total of intra- and inter-programmatic publications), with a total of 187 peer-reviewed cancer-relevant publications. MCO investigators continue to lead large programmatic and disease-relevant collaborations (Program Project grants, SPORE), contribute substantially to the translational mission of the Cancer Center in the Melanoma and Ovarian Cancer Research Continuum Signatures, and actively participate in education, mentoring and career development of faculty and trainees. The MCO Program will continue to build on these strengths during the next budget period, further expanding its unifying role as a multidisciplinary hub for basic and translational cancer research.
The MCO Program supports an integrated and multidisciplinary team effort to elucidate the cellular and molecular requirements of tumor maintenance, identify pathways of resistant disease and devise novel, molecularly-grounded approaches for cancer diagnosis and treatment.
|Seo, Jae Ho; Rivadeneira, Dayana B; Caino, M Cecilia et al. (2016) The Mitochondrial Unfoldase-Peptidase Complex ClpXP Controls Bioenergetics Stress and Metastasis. PLoS Biol 14:e1002507|
|Haut, Larissa H; Gill, Amanda L; Kurupati, Raj K et al. (2016) A Partial E3 Deletion in Replication-Defective Adenoviral Vectors Allows for Stable Expression of Potentially Toxic Transgene Products. Hum Gene Ther Methods :|
|Peck, Barrie; Schug, Zachary T; Zhang, Qifeng et al. (2016) Inhibition of fatty acid desaturation is detrimental to cancer cell survival in metabolically compromised environments. Cancer Metab 4:6|
|Tempera, Italo; De Leo, Alessandra; Kossenkov, Andrew V et al. (2016) Identification of MEF2B, EBF1, and IL6R as Direct Gene Targets of Epstein-Barr Virus (EBV) Nuclear Antigen 1 Critical for EBV-Infected B-Lymphocyte Survival. J Virol 90:345-55|
|Nelson, David M; Jaber-Hijazi, Farah; Cole, John J et al. (2016) Mapping H4K20me3 onto the chromatin landscape of senescent cells indicates a function in control of cell senescence and tumor suppression through preservation of genetic and epigenetic stability. Genome Biol 17:158|
|Kumar, Vinit; Patel, Sima; Tcyganov, Evgenii et al. (2016) The Nature of Myeloid-Derived Suppressor Cells in the Tumor Microenvironment. Trends Immunol 37:208-20|
|Kung, Che-Pei; Murphy, Maureen E (2016) The role of the p53 tumor suppressor in metabolism and diabetes. J Endocrinol 231:R61-R75|
|Patro, Sean C; Azzoni, Livio; Joseph, Jocelin et al. (2016) Antiretroviral therapy in HIV-1-infected individuals with CD4 count below 100 cells/mm3 results in differential recovery of monocyte activation. J Leukoc Biol 100:223-31|
|Chae, Young Chan; Vaira, Valentina; Caino, M Cecilia et al. (2016) Mitochondrial Akt Regulation of Hypoxic Tumor Reprogramming. Cancer Cell 30:257-72|
|Vazquez, Alexei; Kamphorst, Jurre J; Markert, Elke K et al. (2016) Cancer metabolism at a glance. J Cell Sci 129:3367-73|
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