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Jonathan Said, M.D.  
   
 
Affiliations
Member, JCCC Hematopoietic Malignancies Program Area

Education:
Medical Degree: M.D., University of the Witwatersrand Medical School, 1971
Certifications:
Medical Board Certification: Clinical Pathology, American Board of Pathology, 1979
Anatomic Pathology, American Board of Pathology, 1976
Education:
Fellowship: Hematopathology, Brigham & Women's Hospital, 1976 - 1977
Residency: Pathology & Laboratory Med., Brigham & Women's Hospital, 1974 - 1976
Internship: Pathology & Laboratory Med., Boston Medical Center, 1973 - 1974
Rotating (Internship), Johannesburg General Hospital, 1972 - 1972


Contact Information:
Work Email Address: jsaid@mednet.ucla.edu
Translational Pathology Core Laboratory: 310-794-9311 (Sarah Dry)
Mailing Address: BOX 951732, 13-226 CHS
Los Angeles, CA 90095
UNITED STATES
Work Address: 13-226 CHS
CAMPUS - 173216
CA
UNITED STATES


Direct Contact Information:

Research Interest:
Pathologic Basis of Neoplastic Disease

The laboratory has a number of ongoing projects related to: Use of tumor markers to characterize neoplastic proliferations. These include use of immunohistochemistry and in-situ hybridization to identify tumor antigens and gene products associated with neoplastic transformation and tumor progression. Mechanisms of lymphomagenesis including the role of dendritic cells in the pathogenesis of lymphomas derived for grminal center lymphocytes and interfollicular proliferations. Pathogenesis of HIV related lymphoid proliferations. The laboratory in association with the NIH sponsored AIDS malignancy tumor bank as accumulated a large bank of neoplastic tissue for evaluation of HIV-related neoplasia. Cell cycle regulation in neoplastic proliferations. The laboratory is evaluating a number of cyclins including cyclin A, cEBP, p15, p16, p21, p27. Prostate and breast cancer cell lines are being evaluated for expression of cyclin genes and the effect of vitamin D and Vitamin D analogs on cellular proliferation, apoptosis, and differentiation. Viral pathogenesis - The laboratory is actively evaluating the roles of viruses including the newly identified Kaposi’s sarcoma associated herpesvirus in the pathogenesis of neoplastic disease including Kaposi’s sarcoma, lymphoma, and plasma cell dyscrazias.


Technical Research Interest:
Pathologic Basis of Neoplastic Disease

The laboratory has a number of ongoing projects related to: Use of tumor markers to characterize neoplastic proliferations. These include use of immunohistochemistry and in-situ hybridization to identify tumor antigens and gene products associated with neoplastic transformation and tumor progression. Mechanisms of lymphomagenesis including the role of dendritic cells in the pathogenesis of lymphomas derived for grminal center lymphocytes and interfollicular proliferations. Pathogenesis of HIV related lymphoid proliferations. The laboratory in association with the NIH sponsored AIDS malignancy tumor bank as accumulated a large bank of neoplastic tissue for evaluation of HIV-related neoplasia. Cell cycle regulation in neoplastic proliferations. The laboratory is evaluating a number of cyclins including cyclin A, cEBP, p15, p16, p21, p27. Prostate and breast cancer cell lines are being evaluated for expression of cyclin genes and the effect of vitamin D and Vitamin D analogs on cellular proliferation, apoptosis, and differentiation. Viral pathogenesis - The laboratory is actively evaluating the roles of viruses including the newly identified Kaposi’s sarcoma associated herpesvirus in the pathogenesis of neoplastic disease including Kaposi’s sarcoma, lymphoma, and plasma cell dyscrazias.


Publications:
Kawabata H, Fleming RE, Gui D, Moon SY, Saitoh T, O'Kelly J, Umehara Y, Wano Y, Said JW, Koeffler HP Expression of hepcidin is down-regulated in TfR2 mutant mice manifesting a phenotype of hereditary hemochromatosis.. Blood. . 2005; 105(1): 376-81.
Sakajiri S, Kumagai T, Kawamata N, Saitoh T, Said JW, Koeffler HP Histone deacetylase inhibitors profoundly decrease proliferation of human lymphoid cancer cell lines.. Experimental hematology. . 2005; 33(1): 53-61.
Takeuchi S, de Vos S, Takeuchi N, Fermin AC, Grogan TM, Seo H, Said JW, Koeffler HP Allelic loss during progression of follicular lymphoma.. Leukemia research. . 2004; 28(6): 567-9.
Tsukasaki K, Tanosaki S, DeVos S, Hofmann WK, Wachsman W, Gombart AF, Krebs J, Jauch A, Bartram, CR, Nagai K, Tomonaga M, Said JW, Koeffler HP Identifying progression-associated genes in adult T-cell leukemia/lymphoma by using oligonucleotide microarrays.. International journal of cancer. Journal international du cancer. . 2004; 109(6): 875-81.
Xie D, Yin D, Tong X, O'Kelly J, Mori A, Miller C, Black K, Gui D, Said JW, Koeffler HP Cyr61 is overexpressed in gliomas and involved in integrin-linked kinase-mediated Akt and beta-catenin-TCF/Lef signaling pathways.. Cancer research. . 2004; 64(6): 1987-96.
Kumagai, T Ikezoe, T Gui, D O'Kelly, J Tong, XJ Cohen, FJ Said, JW Koeffler, HP RWJ-241947 (MCC-555), a unique peroxisome proliferator-activated receptor-gamma ligand with antitumor activity against human prostate cancer in vitro and in beige/nude/ X-linked immunodeficient mice and enhancement of apoptosis in myeloma cells induced by arsenic trioxide.. Clinical cancer research : an official journal of the American Association for Cancer Research. . 2004; 10(4): 1508-20.


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