Shahriar Koochekpour, MD, PhD

Associate Professor of Cancer Genetics, Urology, and Oncology
Department of Cancer Genetics
Center for Genetics and Pharmacology

Roswell Park Cancer Institute

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Dr. Koochekpour joined the staff of Roswell Park Cancer Institute (RPCI) as an Associate Professor of Cancer Genetics, Urology and Oncology in 2011. Dr. Koochekpour graduated from Shiraz Medical School, Shiraz University of Health Sciences Center (Iran), with an MD degree and followed that with a short-term residency in General Pathology. Dr. Koochekpour obtained his PhD in cellular and molecular oncology from Kings College School of Medicine, University of London; London, UK. Dr. Koochekpour has comprehensive training and experience in cellular and molecular biology of cancer, analyzing gene expression and functions, oncogenes and tumor suppressors, genetics, health disparity and translational cancer research.

Phone Number:

(716) 845-3345

Fax:

(716) 845-1698

E-mail Address:

Shahriar.Koochekpour@RoswellPark.org

Research Information

Research Interests:

Identifying soluble, genetic or epigenetic biomarkers of prostate cancer aggressiveness and progression

Elucidating biological mechanisms underlying androgen receptor-dependent signaling and androgen-independent progression of prostate cancer

Developing molecular targeted therapy for metastatic castrate-resistant prostate cancer

Identifying biological factors and molecular mechanisms responsible for disparities at presentation, aggressiveness and progression, treatment, and outcome in African-American men affected by prostate cancer

Defining the clinicohistopathological significance of prosaposin (PSAP) in prostate carcinogenesis and its androgen-independent or metastatic progression

Current Program:

To define the clinical significance of tissue or serum-prosaposin (PSAP) as a marker of prostate cancer (PCa) progression or aggressiveness: Using a large pool of tissue or serum samples from African-American and Caucasian patients with organ-confined, locally-invasive, or metastatic tumors, immunohistochemical staining, a highly sensitive sandwich-ELISA assay established in his laboratory, and biostatistical procedures, Dr. Koochekpour will determine the association between tissue and/or serum-PSAP levels and the progression or aggressiveness of PCa that is based on clinical stage, prognostic, or risk factors (e.g., age, race, PSA, Gleason’s score).

To determine the association between PSAP and invasive and metastatic phenotypes in PSAP-over-expressed or -silenced PCa cells: To study the cause-and-effect relationship between PSAP expression levels and invasive and metastatic phenotypes in PCa progression models, we will use the PCa cell lines established from Caucasians and the two available authentic PCa cell lines derived from African-American patients (the non-metastatic E006AA cell line and the metastatic MDA PCa 2b cell line). We will test how alterations in PSAP expression levels will affect tumor growth rate and invasive and metastatic abilities using subcutaneous and orthotopic xenograft implantation in athymic nude mice and NOD-SCID mice.

To dissect the biology and clinical significance of the “hypermutator” phenotype in African-American men with PCa: Based on his preliminary investigation searching for a higher incidence of somatic or inherited genetic variations/alterations (e.g., mutation, SNPs, polymorphisms, etc.) in androgen receptors (AR) in African-Americans compared with Caucasians, Dr. Koochekpour studies their incidence and clinicohistopathological significance in tissue and other biological specimens in African-Americans with PCa. Using in vitro site-directed mutagenesis, transfections, and reporter gene assays, he will determine the functional characteristics of mutant ARs by analyzing their binding affinity to specific hormones and androgen-response elements and transcriptional activity and transactivation potential in response to androgens, steroid hormones and non-steroidal anti-androgens in AR-negative PCa and other cell types (e.g., PC-3, COS-7).

Dr. Koochekpour is also conducting additional studies to evaluate his hypothesis that both hormonal-deprivation and hormonal-induction increases gene-specific and/or genome-wide genetic instability in normal or malignant prostate cells. He is interested in characterizing the underlying molecular mechanisms behind such genetic instabilities and in identifying specific target(s) affected by this phenomenon.

Selected Publications:

KoochekpourS, Maresh GA, Katner A, Parker-Johnson K, Lee TJ, Hebert FE, Kao YS, Skinner J, Rayford W. Establishment and characterization of a primary androgen-responsive African-American prostate cancer cell line, E006AA. Prostate, 60:141-52, 2004.

Koochekpour, S, Zhuang, Yu-Jun, Beroukhim, R, Hssieh C-L, Hofer, M. D, Zhau, HE,Hiraiwa, M, Pattan, D, Ware, J. L, Luftig, R, Sandhoff, K, Sawyers, C. L, Pienta K.J, Rubin MA, Vessella RL, Sellers WR, and Sartor, O. Amplification and Overexpression of Prosaposin in Prostate Cancer and Other Malignant Cells. Genes, Chromosomes & Cancer, 44:351-364, 2005.

Koochekpour S. Prosaposin (PSAP). Atlas Genet Cytogenet Oncol Haematol, 10: 370-384, 2006.

Koochekpour, S., Lee, T-J., Wang, R., Sun, Y., Delorme, N., Caffey, S., Grabowski, GA., Culig, Z., Minokadeh, A. Prosaposin is a novel androgen-target gene. J. Cell. Biochem, 2007. J Cell Biochem. 101:631-641, 2007.

Koochekpour, S., Lee, T-J., Wang, R., Vadlamudi, R. K., Zoran Culig., Delorme, N., Caffey, S., Marrero, L., Aguirre, J., Garcia, M.Z. Prosaposin Upregulates Androgen Receptor Expression and Activity In Prostate Cancer Cells (LNCaP), Prostate, 67:178-189, 2007.

Sujit S. Nair, Mueller, J. M., Koochekpour, S., Qiu, Y., Tekmal, R. R., Schüle, R., Kung, H-J., Kumar, R., and Vadlamudi, R. K. PELP1/MNAR modulates transactivation of LIM-only coactivator FHL2. Mol. Endocrinol, 21:613-624, 2007.

Koochekpour S, Lee TJ, Sun Y, Hu S, Grabowski GA, Liu Z, Garay J. Prosaposin is an AR-target gene and its neurotrophic domain upregulates AR expression and activity in prostate stromal cells. J Cell Biochem, 104:2272-2285, 2008.

Singh G, Aras S, Zea AH, Koochekpour S, Aiyar A. Optimal transactivation by Epstein-Barr nuclear antigen 1 requires the UR1 and ATH1 domains. J Virol, 83:4227-4235, 2009.

S, Hu, N, Delorme, Z, Liu,T, Liu,C, Velasco-Gonzalez, J, Garai., A, Pullikuth., and Koochekpour, S. Prosaposin down-modulation decreases metastatic prostate cancer cell adhesion, migration, and invasion. Molecular Cancer. 9:30, 2010.

S. Hu, T. Liu, Z. Liu,E. Ledet, C. Velasco-Gonzalez, D. M. Mandal, S.Koochekpour.Identification of a Novel Germline Missense Mutation of the Androgen Receptor in African American Men with Familial Prostate Cancer. Asian J Andrology, 12:336-343, 2010.

D’Antonio, J., Antony, Vander Griend, D. J., L., Dalrymple, S.L., Koochekpour, S., Isaacs, JT. Loss of growth suppression is necessary but not sufficient for prostate cancer cells acquiring oncogen addition to androgen receptor signaling. PLoS One. 5 (7):e11475, 2010.

Koochekpour, S. Androgen receptor signaling and mutations in prostate cancer. Asian J. Andrology, 12:639-57. Invited Review Article.

Koochekpour S. DNA methylome and the complexity of prostate cancer biomarkers. Asian J Androl. 2011 Jul 4. doi: 10.1038/aja.2011.90. [Epub ahead of print]; PMID: 21725333

Koochekpour S, Hu S, Vellasco-Gonzalez C, Bernardo R, Azabdaftari G, Zhu G, Zhau HE, Chung LW, Vessella RL. Serum prosaposin levels are increased in patients with advanced prostate cancer. Prostate. 2011 May 31. doi: 10.1002/pros.21427. [Epub ahead of print]; PMID: 21630292

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Shahriar Koochekpour, MD, PhD

Shahriar Koochekpour, MD, PhD

Roswell Park

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Roswell Park

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Shahriar Koochekpour, MD, PhD

Shahriar Koochekpour, MD, PhD

Roswell Park

Research Departments

Education

Roswell Park