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Department of Radiation Oncology

Andrew Vaughan, Ph.D.

Andrew Vaughan

Clinical/Research Interests

Dr. Vaughan's research interests are focused on the mechanism(s) whereby both solid tumors and leukemias are formed. He has proposed that the process through which cells normally die, called apoptosis, may sometimes be corrupted and fail to operate normally. Such cells are at higher risk of developing into tumors. In his research, Dr. Vaughan will try to identify such cells and eliminate them.

Title:

 Professor

Specialty:

 Radiation Oncology

Center/Program Affiliation:

 UC Davis Cancer Center

Education:

 Birmingham University
Birmingham, UK
UK
Ph.D. 1978

Education:

 Portsmouth Polytechnic
Portsmouth, UK
UK
B.Sc. 1974

Professional Memberships:

 American Association for Cancer Research
American Society for Therapeutic Radiology and Oncology
Radiation Research Society of North America

Select Recent Publications:

Betti CJ, Villalobos MJ, Diaz MO, Vaughan, ATM Apoptotic stimuli initiate MLL-AF9 translocations that are transcribed in cells capable of division: Cancer Research. 63 1377-81 2003.

Vaughan ATM, Betti CJ, Villalobos MJ. Surviving Apoptosis. Apoptosis 7 173-177 2002.

Betti CJ, Villalobos MJ, Diaz MO, Vaughan, ATM Apoptotic triggers initiate translocations within the MLL gene involving the non homologous end joining repair system Cancer Research 61 4550-4555 2001.

Kamradt MC, Walter S, Shafer L, Weijzen S, Velders MP and Vaughan ATM Steroid-mediated inhibition of radiation-induced apoptosis in C4-1 cervical carcinoma cells is p53 dependent. European Journal of Cancer 37 2240-2246, 2001.

Narayana A, Vaughan ATM, Kathuria S, Fisher SG, Walter SA and Reddy SP. P53 overexpression is associated with bulky tumor and poor local control in T1 glottic cancer. International Journal of Radiation Oncology and related studies in Biology and Physics 46(1), 1-26, 2000.

Kamradt M, Mohideen N, Kreuger E, Scott W and Vaughan ATM. Inhibition of radiation-induced apoptosis by dexamethasone in cervical carcinoma depends upon increased HPV E6/E7. British Journal of Cancer 82, 1709-1716, 2000.

Kamradt M, Mohideen N and Vaughan ATM. RU486 increases radiosensitivity and restores apoptosis through modulation of HPV E6/E7 in dexamethasone-treated cervical carcinoma cells. Gynecologic Oncology 77, 177-82, 2000.

Khodarev NN, Bennett T, Shearing N, Sokolova I, Walter S, Koudelik J and Vaughan ATM. LINE L1 retrotransposable element is targeted during the initial stages of apoptotic DNA fragmentation. Journal of Cell Biochem. 79 486-495 2000.

Khodarev NN, Sokolova I, and Vaughan ATM. Abortive apoptosis as an initiator of chromosomal translocations. Medical Hypothesis 52, 373-376, 1999.