Abstract

The postdoctoral training program of the Science Park - Research Division (SPRD) of the University of Texas M.D. Anderson Cancer Center has as its main objective to prepare trainees to carry out independent, productive research in carcinogenesis and mutagenesis. Trainees who are accepted into the program will have the opportunity to work in the laboratory most closely aligned with their research interests. Collaboration occurs at every level in the research programs at SPRD and will continue to be stressed in the research training of postdoctoral fellows. Postdoctoral fellows will he encouraged to develop their areas of expertise beyond those established during pre doctoral training. Although scientific research in carcinogenesis and mutagenesis will be the major effort of postdoctoral trainees, they also will have the opportunity to expand their understanding of various aspects of carcinogenesis by auditing the graduate school courses taught at SPRD as well as by attending various seminar series and journal clubs.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Institutional National Research Service Award (T32)
Project #
5T32CA009480-15
Application #
6172464
Study Section
Cancer Research Manpower and Education Review Committee (CRME)
Program Officer
Gorelic, Lester S
Project Start
1984-09-01
Project End
2001-06-30
Budget Start
2000-07-01
Budget End
2001-06-30
Support Year
15
Fiscal Year
2000
Total Cost
$181,231
Indirect Cost

  Institution

Name
University of Texas MD Anderson Cancer Center
Department
Type
Organized Research Units
DUNS #
001910777
City
Houston
State
TX
Country
United States
Zip Code
77030

  Publications

Rycaj, Kiera; Cho, Eun Jeong; Liu, Xin et al. (2016) Longitudinal tracking of subpopulation dynamics and molecular changes during LNCaP cell castration and identification of inhibitors that could target the PSA-/lo castration-resistant cells. Oncotarget 7:14220-40
Liu, Ruifang; Liu, Can; Zhang, Dingxiao et al. (2016) miR-199a-3p targets stemness-related and mitogenic signaling pathways to suppress the expansion and tumorigenic capabilities of prostate cancer stem cells. Oncotarget 7:56628-56642
Wyatt, David W; Feng, Wanjuan; Conlin, Michael P et al. (2016) Essential Roles for Polymerase ?-Mediated End Joining in the Repair of Chromosome Breaks. Mol Cell 63:662-673
Mitchell, David; Paniker, Lakshmi; Lin, Kevin et al. (2015) Interspecific variation in the repair of UV damaged DNA in the genus Xiphophorus as a factor in the decline of the Rio Grande Platyfish. Photochem Photobiol 91:486-92
Tomida, Junya; Takata, Kei-ichi; Lange, Sabine S et al. (2015) REV7 is essential for DNA damage tolerance via two REV3L binding sites in mammalian DNA polymerase ?. Nucleic Acids Res 43:1000-11
Yousefzadeh, Matthew J; Wyatt, David W; Takata, Kei-Ichi et al. (2014) Mechanism of suppression of chromosomal instability by DNA polymerase POLQ. PLoS Genet 10:e1004654
Aldaz, C Marcelo; Ferguson, Brent W; Abba, Martin C (2014) WWOX at the crossroads of cancer, metabolic syndrome related traits and CNS pathologies. Biochim Biophys Acta 1846:188-200
Reeh, Kaitlin A G; Cardenas, Kim T; Bain, Virginia E et al. (2014) Ectopic TBX1 suppresses thymic epithelial cell differentiation and proliferation during thymus organogenesis. Development 141:2950-8
Angel, Joe M; Abel, Erika L; Riggs, Penny K et al. (2014) Fine mapping reveals that promotion susceptibility locus 1 (Psl1) is a compound locus with multiple genes that modify susceptibility to skin tumor development. G3 (Bethesda) 4:1071-9
Lin, Yi-Chen; Richburg, John H (2014) Characterization of the role of tumor necrosis factor apoptosis inducing ligand (TRAIL) in spermatogenesis through the evaluation of trail gene-deficient mice. PLoS One 9:e93926

Showing the most recent 10 out of 66 publications