The main objective of this training program in The Molecular Genetics of Cancer is to prepare predoctoral (4) and postdoctoral (5) trainees for careers in cancer research. The training program is based at the world renowned M. D. Anderson Cancer Center. Faculty are collegial and interactive, and belong to five departments, one clinical, with cross appointments in other clinical departments. The interests of the faculty include the study of tumor suppressors (p53, PTEN, WT1, Brca1), genetic modifiers of the cancer phenotype, inherited cancer syndromes, the DNA damage response, DNA recombination and repair, telomere biology, genomic instability, cell regulation, chromatin modification in cancers, and regulators of cell proliferation and apoptosis. The faculty use genetic and biochemical assays, animal models and human samples to understand the normal and abnormal mechanisms that govern cell proliferation and death. Trainees will choose a research mentor of their choice, and submit their applications to open training grant positions. If highly qualified, they will be selected and supported for a maximum of three years with annual review. Trainees will attend classes and receive instruction in the responsible conduct of research. They will attend seminars, journal clubs, and the annual program retreat. They will learn presentation and grant writing skills. They will be encouraged to attend and present at national meetings. The faculty and the interactive environment of MDACC and the Texas Medical Center will stimulate trainees to achieve a life long commitment to Making Cancer History"""""""".

Public Health Relevance

An estimated 565,000 Americans will die of cancer this year. The complexity and heterogeneity of the cancer phenotype, the existence of multiple pathways that control cell proliferation and death suggest that cancer is an individual disease. We have much to learn.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Institutional National Research Service Award (T32)
Project #
2T32CA009299-31A1
Application #
7941363
Study Section
Subcommittee G - Education (NCI)
Program Officer
Lim, Susan E
Project Start
1978-09-30
Project End
2015-06-30
Budget Start
2010-08-06
Budget End
2011-06-30
Support Year
31
Fiscal Year
2010
Total Cost
$411,822
Indirect Cost
Name
University of Texas MD Anderson Cancer Center
Department
Genetics
Type
Other Domestic Higher Education
DUNS #
800772139
City
Houston
State
TX
Country
United States
Zip Code
77030
Im, Seol Hee; Patel, Atit A; Cox, Daniel N et al. (2018) Drosophila Insulin receptor regulates the persistence of injury-induced nociceptive sensitization. Dis Model Mech 11:
Mullen, Rachel D; Wang, Ying; Liu, Bin et al. (2018) Osterix functions downstream of anti-Müllerian hormone signaling to regulate Müllerian duct regression. Proc Natl Acad Sci U S A 115:8382-8387
Larsson, Connie A; Moyer, Sydney M; Liu, Bin et al. (2018) Synergistic and additive effect of retinoic acid in circumventing resistance to p53 restoration. Proc Natl Acad Sci U S A 115:2198-2203
Vue, Zer; Gonzalez, Gabriel; Stewart, C Allison et al. (2018) Volumetric imaging of the developing prepubertal mouse uterine epithelium using light sheet microscopy. Mol Reprod Dev 85:397-405
McCarthy, Ryan L; Duncan, Aundrietta D; Barton, Michelle C (2017) Sample Preparation for Mass Cytometry Analysis. J Vis Exp :
Jo, Juyeon; Im, Seol Hee; Babcock, Daniel T et al. (2017) Drosophila caspase activity is required independently of apoptosis to produce active TNF/Eiger during nociceptive sensitization. Cell Death Dis 8:e2786
Tsai, Chang-Ru; Anderson, Aimee E; Burra, Sirisha et al. (2017) Yorkie regulates epidermal wound healing in Drosophila larvae independently of cell proliferation and apoptosis. Dev Biol 427:61-71
Jain, Abhinav K; Xi, Yuanxin; McCarthy, Ryan et al. (2016) LncPRESS1 Is a p53-Regulated LncRNA that Safeguards Pluripotency by Disrupting SIRT6-Mediated De-acetylation of Histone H3K56. Mol Cell 64:967-981
Ungewiss, Christin; Rizvi, Zain H; Roybal, Jonathon D et al. (2016) The microRNA-200/Zeb1 axis regulates ECM-dependent ?1-integrin/FAK signaling, cancer cell invasion and metastasis through CRKL. Sci Rep 6:18652
Riley, M F; You, M J; Multani, A S et al. (2016) Mdm2 overexpression and p73 loss exacerbate genomic instability and dampen apoptosis, resulting in B-cell lymphoma. Oncogene 35:358-65

Showing the most recent 10 out of 74 publications