Scientific Interest(s):
Dr. Jonathan Said's research focuses on the pathologic basis of neoplastic disease.
Said's laboratory has a number of ongoing projects related to the use of tumor markers to characterize neoplastic proliferations. These include the use of immunohistochemistry and in situ hybridization to identify tumor antigens and gene products associated with neoplastic transformation and tumor progression.
Also under examination are mechanisms of lymphomagenesis, including the role of dendritic cells in the pathogenesis of lymphomas derived for germinal center lymphocytes and interfollicular proliferations.
Said and his colleagues are studying pathogenesis of HIV-related lymphoid proliferations. The laboratory, in association with the National Institute of Health-sponsored AIDS malignancy tumor bank, has accumulated a large bank of neoplastic tissue for evaluation of HIV-related neoplasia.
Cell cycle regulation in neoplastic proliferations is another focus for the researchers. The laboratory is evaluating a number of cyclins including cyclin A, cEBP, p15, p16, p21 and 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.
Finally, the laboratory is actively evaluating the roles of viruses, including the identified Kaposi's sarcoma associated herpesvirus, in the pathogenesis of neoplastic disease, including Kaposi's sarcoma, lymphoma and plasma cell dyscrasias.
Selected Cancer-Related Publications:
Rao DS, Said JW. Small lymphoid proliferations in extranodal locations. Arch Pathol Lab Med. 2007; 131(3): 383-96.
Chen H, Gordon MS, Campbell RA, Li M, Wang CS, Lee HJ, Sanchez E, Manyak SJ, Gui D, Shalitin D, Said J, Chang Y, Deuel TF, Baritaki S, Bonavida B, Berenson JR. Pleiotrophin is highly expressed by myeloma cells and promotes myeloma tumor growth. Blood. 2007; 110(1): 287-95.
Rao DS, Gui D, Koski ME, Popoviciu LM, Wang H, Reiter RE, Said JW. An inverse relation between COX-2 and E-cadherin expression correlates with aggressive histologic features in prostate cancer. Appl Immunohistochem Mol Morphol. 2006; 14(4): 375-83.
Chien W, Yin D, Gui D, Mori A, Frank JM, Said J, Kusuanco D, Marchevsky A, McKenna R, Koeffler HP. Suppression of cell proliferation and signaling transduction by connective tissue growth factor in non-small cell lung cancer cells. Mol Cancer Res. 2006; 4(8): 591-8.