Fen Xia, M.D., Ph.D.
- Clinical Trials Information
- Clinical Trials: 1-800-811-8480
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- Other Telephone NumbersVanderbilt-Ingram Cancer Center Radiation Oncology
- FaxesVanderbilt-Ingram Cancer Center Radiation Oncology Fax
The Vanderbilt Clinic (TVC) - Preston Research Building
Department of Radiation Oncology
1301 22nd Ave., South, B1003
Nashville, TN 37232-5671
Vanderbilt-Ingram Cancer Center Radiation Oncology
22nd at Pierce Avenue, B1034
Nashville, TN 37232-5671
Dr. Xia is an Assistant Professor of Radiation Oncology and an established physician scientist at Vanderbilt. Dr. Xia provides comprehensive radiation treatment for patients with brain tumor using the latest technologies, including intensity modulated radiation therapy, imaging guided radiotherapy, Brachytherapy, and stereotactic radiosurgery.
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Dr. Xia is an Assistant Professor of Radiation Oncology and an established physician scientist at Vanderbilt. Dr. Xia provides comprehensive radiation treatment for patients with brain tumor using the latest technologies, including intensity modulated radiation therapy, imaging guided radiotherapy, Brachytherapy, and stereotactic radiosurgery. Dr. Xia's laboratory is pioneering on studying how cancer cells can efficiently repair their damaged DNA and resist to therapy. Her research aims at identifying novel molecular targets to enhance brain tumor response to treatment.
- Ph.D. - Harvard University, 1996
- M.D. - Suzhou Medical College, 1983
- Residency - Vanderbilt University Medical Center, 2006
- Internship - New England Medical Center, 2002
DNA damage response, chromosomal break repair, apoptosis.
Research in the Xia laboratory focuses on elucidating the mechanisms that regulate the repair of chromosomal double-strand breaks (DSB) that arise during physiological DNA metabolism and after radiation therapy or chemotherapy. We aim to understand 1) the impact of deregulated DSB repair on carcinogenesis and the development of tumor resistance to therapy and 2) to explore novel avenues of cancer treatment targeting the DSB repair pathways. We have developed an array of intrachromosomal and extrachromosomal repair substrates that allow analysis of the quantity and quality of DSB repair by different mechanisms in mammalian cells. An understanding of the defects of DNA repair and its interplay with apoptosis in tumors may offer novel avenues for both cancer prevention and tailored therapy.
Project 1: There are several DSB repair subpathways, each with different impacts on mutagenesis and cell viability. Our main interests in this area are 1) understanding how cells determine which subpathway to use and 2) how regulation of these subpathways may be altered during carcinogenesis and cancer and determine tumor response to cancer therapies.
Project 2: Another major goal of our lab is to understand how DNA repair machinery communicates with cell death machinery in order to maintain genomic stability. We have begun these studies by examining BRCA1, a tumor suppressor involved in DSB repair and able to induce apoptosis, and Bid, a proapoptotic protein recently discovered to be involved in the DNA damage response. Brain tumors are among the model systems used for this project.
Project 3: Our research group has made an intriguing finding that indicates genetically wild type BRCA1 function can be disrupted by its mislocalization within the cell. We have also found another important tumor suppressor p53 is involved in regulating BRCA1’s nuclear/cytoplasmic shuttling.
We are currently studying the molecular mechanism that regulates this shuttling and the potential use of BRCA1 mislocalization as a biomarker for tailored cancer therapy.
An opening is available for interested candidates in any of the three areas of research.
- Yang, ES, Wang, H, Jiang, G, Nowsheen, S, Fu, A, Hallahan, DE, Xia, F Lithium-mediated protection of hippocampal cells involves enhancement of DNA-PK-dependent repair in mice. J Clin Invest, 119(5), 1124-35, 2009.
- Li, L, Wang, H, Yang, ES, Arteaga, CL, Xia, F Erlotinib attenuates homologous recombinational repair of chromosomal breaks in human breast cancer cells. Cancer Res, 68(22), 9141-6, 2008.
- Yan J, Kim YS, Yang XP, Li LP, Liao G, Xia F, Jetten AM. The Ubiquitin-Interacting Motif Containing Protein RAP80 Interacts with BRCA1 and Functions in DNA Damage Repair Response.. Cancer Reseach, 67(14), 6647-56, 2007.
- Zhuang, J, Zhang, J, Willers, H, Wang, H, Chung, JH, van Gent, DC, Hallahan, DE, Powell, SN, Xia, F Checkpoint kinase 2-mediated phosphorylation of BRCA1 regulates the fidelity of nonhomologous end-joining. Cancer Res, 66(3), 1401-8, 2006.
- Zhang, J, Willers, H, Feng, Z, Ghosh, JC, Kim, S, Weaver, DT, Chung, JH, Powell, SN, Xia, F Chk2 phosphorylation of BRCA1 regulates DNA double-strand break repair. Mol Cell Biol, 24(2), 708-18, 2004.
- Feng, Z, Kachnic, L, Zhang, J, Powell, SN, Xia, F DNA damage induces p53-dependent BRCA1 nuclear export. J Biol Chem, 279(27), 28574-84, 2004.
- Powell, SN, Willers, H, Xia, F BRCA2 keeps Rad51 in line. High-fidelity homologous recombination prevents breast and ovarian cancer. Mol Cell, 10(6), 1262-3, 2002.
- Weng, Q, Xia, F, Jin, W Measurement of histamine in individual rat peritoneal mast cells by capillary zone electrophoresis with electrochemical detection. J Chromatogr B Analyt Technol Biomed Life Sci, 779(2), 347-52, 2002.
- Willers, H, Xia, F, Powell, SN Recombinational DNA Repair in Cancer and Normal Cells: The Challenge of Functional Analysis. J Biomed Biotechnol, 2(2), 86-93, 2002.
- Xia, F, Powell, SN The molecular basis of radiosensitivity and chemosensitivity in the treatment of breast cancer. Semin Radiat Oncol, 12(4), 296-304, 2002.
- Xia, F, Taghian, DG, DeFrank, JS, Zeng, ZC, Willers, H, Iliakis, G, Powell, SN Deficiency of human BRCA2 leads to impaired homologous recombination but maintains normal nonhomologous end joining. Proc Natl Acad Sci U S A, 98(15), 8644-9, 2001.
- Wang, H, Zeng, ZC, Bui, TA, DiBiase, SJ, Qin, W, Xia, F, Powell, SN, Iliakis, G Nonhomologous end-joining of ionizing radiation-induced DNA double-stranded breaks in human tumor cells deficient in BRCA1 or BRCA2. Cancer Res, 61(1), 270-7, 2001.
- Willers, H, McCarthy, EE, Wu, B, Wunsch, H, Tang, W, Taghian, DG, Xia, F, Powell, SN Dissociation of p53-mediated suppression of homologous recombination from G1/S cell cycle checkpoint control. Oncogene, 19(5), 632-9, 2000.
- Mao, Z, Bonni, A, Xia, F, Nadal-Vicens, M, Greenberg, ME Neuronal activity-dependent cell survival mediated by transcription factor MEF2. Science, 286(5440), 785-90, 1999.
- Turner, NA, Xia, F, Azhar, G, Zhang, X, Liu, L, Wei, JY Oxidative stress induces DNA fragmentation and caspase activation via the c-Jun NH2-terminal kinase pathway in H9c2 cardiac muscle cells. J Mol Cell Cardiol, 30(9), 1789-801, 1998.
- Xia, F, Liber, HL The tumor suppressor p53 modifies mutational processes in a human lymphoblastoid cell line. Mutat Res, 373(1), 87-97, 1997.
- Xia, F, Wang, X, Wang, YH, Tsang, NM, Yandell, DW, Kelsey, KT, Liber, HL Altered p53 status correlates with differences in sensitivity to radiation-induced mutation and apoptosis in two closely related human lymphoblast lines. Cancer Res, 55(1), 12-5, 1995.
- Xia, F, Liber, HL Electroporation of human lymphoblastoid cells. Methods Mol Biol, 48151-60, 1995.
- Phillips, EN, Xia, F, Kelsey, KT, Liber, HL Spectra of spontaneous and X-ray-induced mutations at the hprt locus in related human lymphoblast cell lines that express wild-type or mutant p53. Radiat Res, 143(3), 255-62, 1995.
- Xia, F, Amundson, SA, Nickoloff, JA, Liber, HL Different capacities for recombination in closely related human lymphoblastoid cell lines with different mutational responses to X-irradiation. Mol Cell Biol, 14(9), 5850-7, 1994.
- Kelsey, KT, Xia, F, Bodell, WJ, Spengler, JD, Christiani, DC, Dockery, DW, Liber, HL Genotoxicity to human cells induced by air particulates isolated during the Kuwait oil fires. Environ Res, 64(1), 18-25, 1994.
- Amundson, SA, Xia, F, Wolfson, K, Liber, HL Different cytotoxic and mutagenic responses induced by X-rays in two human lymphoblastoid cell lines derived from a single donor. Mutat Res, 286(2), 233-41, 1993.