): The renewal of this ongoing postdoctoral training program for Years 17-21 will support six (6) postdoctoral fellows. The training program provides research training essential to the academic and research base of DNA damage response. The goal is the training of independent investigators on the molecular basis of DNA damage response and on the ways this knowledge can be translated to new cancer therapies. It emphasizes direct research experience in the laboratory and is supplemented by formal courses, seminars and conferences, as well as by exposure in the clinical environment. The revised program offers training adapted to the emerging requirements of Cancer Research and takes full advantage of the available resources within the Jefferson Campus. It includes training on the essential aspects of DNA damage response such as signal transduction, DNA repair, checkpoint activation, apoptosis, and response modifiers. A unique feature of the program is the exposure of trainees to the clinical environment and their assignment to clinician scientists working at the forefront of clinical cancer research. Applicants must have a Ph.D. in the biological, chemical or physical sciences or an M.D., D.O., D.V.M., or comparable degree. Candidates with a Ph.D. degree must be graduates of outstanding programs, have a proven record of research accomplishments during their predoctoral work and have a clear interest in a research career. The training program consists of 2-3 years of direct laboratory experience under the supervision of one of the preceptors. The training emphasizes hypothesis oriented research, the development of an appropriate experimental design and the use of modern techniques to address pertinent issues of cancer research. Trainees publish their results in peer-reviewed scientific journals. The specific areas of research represented by the program faculty are emphasized. Following completion of the program trainees will be prepared to enter independent research careers in modern aspects of cancer research in a university, government laboratory or industrial research setting.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Institutional National Research Service Award (T32)
Project #
5T32CA009137-19
Application #
6172526
Study Section
Subcommittee G - Education (NCI)
Program Officer
Gorelic, Lester S
Project Start
1978-07-01
Project End
2003-05-31
Budget Start
2000-06-01
Budget End
2001-05-31
Support Year
19
Fiscal Year
2000
Total Cost
$184,243
Indirect Cost
Name
Thomas Jefferson University
Department
Radiation-Diagnostic/Oncology
Type
Schools of Medicine
DUNS #
061197161
City
Philadelphia
State
PA
Country
United States
Zip Code
19107
Wang, Huichen; Rosidi, Bustanur; Perrault, Ronel et al. (2005) DNA ligase III as a candidate component of backup pathways of nonhomologous end joining. Cancer Res 65:4020-30
Perrault, Ronel; Wang, Huichen; Wang, Minli et al. (2004) Backup pathways of NHEJ are suppressed by DNA-PK. J Cell Biochem 92:781-94
Hargis, M T; Storck, C W; Wickstrom, E et al. (2004) Hsp27 anti-sense oligonucleotides sensitize the microtubular cytoskeleton of Chinese hamster ovary cells grown at low pH to 42 degrees C-induced reorganization. Int J Hyperthermia 20:491-502
Wang, Hongyan; Wang, Huichen; Powell, Simon N et al. (2004) ATR affecting cell radiosensitivity is dependent on homologous recombination repair but independent of nonhomologous end joining. Cancer Res 64:7139-43
Masciullo, Valeria; Susini, Tommaso; Zamparelli, Alessandra et al. (2003) Frequent loss of expression of the cyclin-dependent kinase inhibitor p27(Kip1) in estrogen-related Endometrial adenocarcinomas. Clin Cancer Res 9:5332-8
Burd, Randy; Lavorgna, Stephanie N; Daskalakis, Constantine et al. (2003) Tumor oxygenation and acidification are increased in melanoma xenografts after exposure to hyperglycemia and meta-iodo-benzylguanidine. Radiat Res 159:328-35
Wang, Xiang; Wang, Huichen; Iliakis, George et al. (2003) Caffeine-induced radiosensitization is independent of nonhomologous end joining of DNA double-strand breaks. Radiat Res 159:426-32
Wang, Huichen; Wang, Xiang; Iliakis, George et al. (2003) Caffeine could not efficiently sensitize homologous recombination repair-deficient cells to ionizing radiation-induced killing. Radiat Res 159:420-5
Masciullo, Valeria; Baldassarre, Gustavo; Pentimalli, Francesca et al. (2003) HMGA1 protein over-expression is a frequent feature of epithelial ovarian carcinomas. Carcinogenesis 24:1191-8
Wang, Hongyan; Wang, Xiang; Zhou, Xiang-Yang et al. (2002) Ku affects the ataxia and Rad 3-related/CHK1-dependent S phase checkpoint response after camptothecin treatment. Cancer Res 62:2483-7

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