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Radiation Oncology UCLA

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Research Areas

Four main areas of research exist within the Division

Proteasomes: We were the first to show that the proteasome is a direct redox-sensitive target for radiation and that even very low doses can slow the rate of protein degradation, including that of critically important signaling molecules. Proteasome inhibition using drugs is a useful means of causing radiosensitization in vitro and in vivo. Led by Frank Pajonk and William H. McBride.

Stem Cells:  Thanks to the extensive experience in stem cell research of our faculty, we were the first to describe the radiation resistance of breast cancer stem cells. An intensive area of research in the lab focuses on the relative radioresistance in the intrinsic radiosensitivity of stem cells in normal and tumorous tissues, which is likely a cause of normal tissue and tumor regeneration after radiation exposure. Led by Frank Pajonk

Growth factor and cytokine signaling: These pathways influence the response of normal tissues and tumors to irradiation (the process of being exposed to radiation). We have shown that TNFR signaling dictates the response of normal brain to irradiation. In addition, we have a large research effort in the control of these pathways through SOCS proteins, and how their expression modulates radiation responses. Led by Nick Cacalano and William H. McBride.

Immunity and Radiation: The intercellular "danger" response to radiation would be expected to activate antigen presenting cells resulting in the development of immune responses. In fact, we believe that radiation is a poor signal for this response and indeed switches off antigen presentation by dendritic cells without killing them. We are involved in attempts to prevent this functional immunosuppression and so as to better translate tumor cell killing into the generation of tumor-specific immunity. This would help improve local control and eliminate micrometastatic disease. Led by William H. McBride.

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