Benjamin E. Bonavida, Ph.D.


Work Titles
UCLA Professor, Microbiology, Immunology & Molecular Genetics
Education:
Degrees:
Ph.D.

Contact Information:

Work Email Address:

bbonavida@mednet.ucla.edu


Work Phone Number:

(310) 825-2233

Laboratory Address:

Laboratory
CHS
Los Angeles, CA 90095


Office Address:

Office
CHS
Los Angeles, CA 90095


Detailed Biography:

Research Interest: Various functions within the Immune System The laboratory is currently involved in research investigations that deal with tumor cell induction of apoptosis in cytotoxic anti-tumor effector cells, and on the mechanism of resistance of tumor cells to immunotherapy. In the first project, we have demonstrated that interaction of tumor target cells with natural killer (NK) cells resulted in the induction of apoptosis in the sensitive target cells and thereafter the induction of apoptosis in the cytotoxic effector cells. This project investigates the underlying biochemical and molecular mechanisms by which the tumor target cells trigger programmed cell death in the cytotoxic cells. The role of MHC-killer inhibitory receptors (KIR) and killer activating receptors (KAR) as well as the role of the FC-receptor in intracellular signaling pathways that result in NK apoptosis are being investigated. The second project examines the resistance of tumor cells to cytotoxicity and apoptosis by cytotoxic lymphocytes. The mechanism of resistance to Fas-ligand, TRAIL and TNF-a (effector pathways in cytotoxic lymphocytes) are being examined. In addition, we have demonstrated that resistant tumor cells can be sensitized by various agents to killing by these cytotoxic effector mechanisms. The underlying mechanisms of immunosensitization are being examined. Aside form the in vitro studies, translational in vivo studies to enhance gene/immunotherapy strategies against resistant tumor cells are also being evaluated.

Publications:

A selected list of publications:

Hongo F, Garban H, Huerta-Yepez S, Vega M, Jazirehi AR, Mizutani Y, Miki T, Bonavida B   Inhibition of the transcription factor Yin Yang 1 activity by S-nitrosation Biochemical and biophysical research communications. , 2005; 336(2): 692-701.
Vega MI, Jazirehi AR, Huerta-Yepez S, Bonavida B   Rituximab-induced inhibition of YY1 and Bcl-xL expression in Ramos non-Hodgkin's lymphoma cell line via inhibition of NF-kappa B activity: role of YY1 and Bcl-xL in Fas resistance and chemoresistance, respectively Journal of immunology (Baltimore, Md. : 1950) , 2005; 175(4): 2174-83.
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Jazirehi AR, and Bonavida B   Cellular and Molecular Signal Transduction Pathways Modulated by Rituximab (Rituxan, anti-CD20 mAb) in Non-Hodgkin's Lymphoma: Implications in Chemo-sensitization, Oncogene, 2005; 24: 2121-2143.
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  Rituximab (chimeric anti-CD20 mAb) inhibits the constitutive NIK/IKK/IkB/NF-kB signaling pathway in non-Hodgkin's lymphoma (NHL) B-cell lines: role in sensitization to chemotherapeutic drug-induced apoptosis, Cancer Research, 2005; 65: 264-275.
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Huerta-Yepez S, Vega M, Jazirehi A, Garban H, Hongo F, Cheng G, Bonavida B   Nitric oxide sensitizes prostate carcinoma cell lines to TRAIL-mediated apoptosis via inactivation of NF-kappa B and inhibition of Bcl-xl expression Oncogene. , 2004; 23(29): 4993-5003.
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Odabaei G, Chatterjee D, Jazirehi AR, Goodglick L, Yeung K, Bonavida B   Raf-1 kinase inhibitor protein: structure, function, regulation of cell signaling, and pivotal role in apoptosis Advances in cancer research. , 2004; 91: 169-200.
Vega MI, Huerta-Yepaz S, Garban H, Jazirehi A, Emmanouilides C, Bonavida B   Rituximab inhibits p38 MAPK activity in 2F7 B NHL and decreases IL-10 transcription: pivotal role of p38 MAPK in drug resistance Oncogene. , 2004; 23(20): 3530-40.
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Vega MI, Huerta-Yepaz S, Garban H, Jazirehi A, Emmanouilides C, Bonavida B   Rituximab inhibits p38 MAPK activity in 2F7 B NHL and decreases IL-10 transcription: pivotal role of p38 MAPK in drug resistance Oncogene. , 2004; 23(20): 3530-40.
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Jazirehi AR, Gan XH, De Vos S, Emmanouilides C, and Bonavida B   Rituximab (anti-CD20) Selectively Down-Regulates Bcl-xl and Up-Regulates Apaf-1 in Non-Hodgkin's Lymphoma (NHL) B-Cells: Complementation with Paclitaxel Results in Synergy in Apoptosis, Molecular Cancer Therapeutics, 2003; 2: 1183-1193.
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Alas S, Bonavida B   Inhibition of constitutive STAT3 activity sensitizes resistant non-Hodgkin's lymphoma and multiple myeloma to chemotherapeutic drug-mediated apoptosis Clinical cancer research : an official journal of the American Association for Cancer Research. , 2003; 9(1): 316-26.
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Ng CP, Bonavida B   A new challenge for successful immunotherapy by tumors that are resistant to apoptosis: two complementary signals to overcome cross-resistance Advances in cancer research. , 2002; 85: 145-74.

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