The long-term goal of the Prostate Cancer Program is to address major clinical challenges associated with prostate cancer by applying knowledge of the basic biology of the disease. The goals of the Prostate Cancer Program, reflect the major investigational challenges with this disease: (i) to elucidate mechanisms underlying prostate cancer initiation;(ii) to understand whether and if so how cell types in the prostate contribute to the heterogeneity of the disease;(iii) to discriminate between men who should be treated for cure from those who do not require treatment;(iv) to improve and augment patient care and minimize racial disparities in care;and (v) to understand the relationship between bone biology and bone metastases. The hallmarks of the Prostate Cancer Program are its emphasis on these major clinical challenges and its exceptional integration of outstanding basic research and clinical studies to address these challenges. Thus, the major themes of the Prostate Program are: 1) Mechanisms and treatment of early stage prostate cancer;2) Mechanisms and treatment of advanced prostate cancer;and 3) Biology of bone and metastasis. The number of new prostate cancer patients seen has averaged 409/year. Of these many are low-risk patients that are followed without intervention. Of patients with advanced disease, 24/year (peak 30) have been enrolled on therapeutic clinical trials. 30% of patients accrued were minorities. Currently, the Prostate Cancer (PC) program consists of 21 members (12 full) from six departments within the College of Physicians and Surgeons, Mailman School of Public Health, and Columbia College. The program is enhanced by several multi-investigator grants including a NCI-funded program project grant and an NCI-funded UOl in the mouse models of human cancer consortium. For the last funding period of the grant (July 1, 2012 to June 30, 2013), the program received a total of $6.9M (direct costs) in cancer-relevant grant supporting including $2.2M (direct costs) in NCI funding, $3.4M (direct costs) in other cancer-related peer-reviewed funding, and $1.3M (direct costs) in other cancer-related non peer-reviewed funding. The total number of publications since the previous submission {i.e., 2008 to present) was 339, of which 14% were inter-programmatic, 19% intra-programmatic and 19% were in high impact journals (Impact Factor>10).

National Institute of Health (NIH)
National Cancer Institute (NCI)
Center Core Grants (P30)
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Subcommittee G - Education (NCI)
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Columbia University (N.Y.)
New York
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Sengillo, Jesse D; Lee, Winston; Bilancia, Colleen G et al. (2018) Phenotypic expansion and progression of SPATA7-associated retinitis pigmentosa. Doc Ophthalmol 136:125-133
Moayedi, Yalda; Duenas-Bianchi, Lucia F; Lumpkin, Ellen A (2018) Somatosensory innervation of the oral mucosa of adult and aging mice. Sci Rep 8:9975
Hopkins, Benjamin D; Pauli, Chantal; Du, Xing et al. (2018) Suppression of insulin feedback enhances the efficacy of PI3K inhibitors. Nature 560:499-503
Kroeger, Heike; Grimsey, Neil; Paxman, Ryan et al. (2018) The unfolded protein response regulator ATF6 promotes mesodermal differentiation. Sci Signal 11:
Jauregui, Ruben; Thomas, Amanda L; Liechty, Benjamin et al. (2018) SCAPER-associated nonsyndromic autosomal recessive retinitis pigmentosa. Am J Med Genet A :
Ghorpade, Devram S; Ozcan, Lale; Zheng, Ze et al. (2018) Hepatocyte-secreted DPP4 in obesity promotes adipose inflammation and insulin resistance. Nature 555:673-677
Bianchetti, E; Bates, S J; Carroll, S L et al. (2018) Usp9X Regulates Cell Death in Malignant Peripheral Nerve Sheath Tumors. Sci Rep 8:17390
Jauregui, Ruben; Park, Karen Sophia; Duong, Jimmy K et al. (2018) Quantitative Comparison of Near-infrared Versus Short-wave Autofluorescence Imaging in Monitoring Progression of Retinitis Pigmentosa. Am J Ophthalmol 194:120-125
Proto, Jonathan D; Doran, Amanda C; Subramanian, Manikandan et al. (2018) Hypercholesterolemia induces T cell expansion in humanized immune mice. J Clin Invest 128:2370-2375
Shang, Enyuan; Zhang, Yiru; Shu, Chang et al. (2018) Dual Inhibition of Bcl-2/Bcl-xL and XPO1 is synthetically lethal in glioblastoma model systems. Sci Rep 8:15383

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