| Guang Peng, M.D.,Ph.D. |
Present Title & Affiliation
Primary Appointment
Bio Statement
The overall goal of my laboratory is to apply the basic knowledge of genome maintenance mechanisms to early detection and cancer prevention. More specifically, by understanding and targeting the DNA repair network, our research aim to address two key questions: (1) Can we identify genetic alterations in the DNA repair network at early stages of carcinogenesis, particularly during the transition from premalignant lesions to cancer? (2) Can we identify targeted prevention strategies for the premalignant lesions with particular genetic alterations? Several research topics are currently investigated in the lab.
1. Identify genetic alterations in the DNA repair network that occur at early stage of carcinogenesis
We aim to investigate the novel functions of human nucleases/helicases such as DNA2 in promoting tumorigenesis by both in vitro and in vivo studies, which may lead to identification of a new class of markers for early detection and intervention. We will also focus our studies on novel chromatin remodeling factors in the DNA repair network to understand how environmental and endogenous factors reshape the landscape of cellular genome by targeting epigenetic regulatory machineries.
2. Discover novel agents targeting the DNA repair network by genetic and chemical approaches
We aim to utilize chemical screening approach to systematically identify chemical compounds, particularly natural products and FDA-approved drugs that target the DNA repair network. In addition, we will also use bioinformatics’ tools as a drug-discovery platform to identify chemical agents modulating DNA repair process. These candidate compounds will be tested for their cancer preventive and therapeutic effects.
3. Assess synthetic lethality approach as a new strategy for personalized cancer prevention
We aim to test the hypothesis whether the reduction of cellular tolerance to replication stress by modulating DNA repair process would lead a synthetic lethality interaction in premalignant cells with hyperactive DNA replication. This study will help us identify novel targeted preventive strategy based on the genetic alterations in the premalignant cells, leading to our ultimate goal of personalized cancer prevention.
Office Address
Basic Science Research Building
1515 Holcombe Blvd.
Unit Number: 1013
Houston, TX 77030
Room Number: S7.8336B
Phone: 713-834-6151
Fax: 713-834-6350
Email: gpeng@mdanderson.org
Education & Training
Degree-Granting Education | |
| 2005 | University of South Carolina School of Medicine, Columbia, SC, PHD, Biomedical Sciences |
| 2002 | Tongji Medical University, Wuhan, China, MD, Medicine |
Postgraduate Training | |
| 10/2006-6/2010 | Research Fellowship, Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, Dr. Shiaw-Yih Lin |
| 5/2005-9/2006 | Research Fellowship, Human Genetics, Fox Chase Cancer Center, Philadelphia, PA, Dr. Davide Ruggero |
Experience/Service
Academic Appointments
Selected Publications
Peer-Reviewed Original Research Articles | |
| 1. | Zhang W, Peng G, Lin SY, Zhang P. DNA damage response is suppressed by high CDK1 activity in mitotic mammalian cells. J Biol Chem 286(41). e-Pub 8/2011. PMCID: PMCPMC3195557. |
| 2. | Pan MR, Peng G, Hung WC, Lin SY. Monoubiquitination of H2AX Protein Regulates DNA Damage Response Signaling. J Biol Chem 286(32):28599-607, 8/2011. e-Pub 6/2011. PMCID: PMC3151101. |
| 3. | Hu R, Peng G, Dai H, Breuer EK, Stemke-Hale K, Li K, González-Angulo AM, Mills GB, Lin SY. ZNF668 functions as a tumor suppressor by regulating p53 stability and function in breast cancer. Cancer Res 71:6524-6534, 2011. e-Pub 8/2011. PMCID: PMCPMC3193577. |
| 4. | Tian L, Peng G, Parant JM, Leventaki V, Drakos E, Zhang Q, Parker-Thornburg J, Shackleford TJ, Dai H, Lin SY, Lozano G, Rassidakis GZ, Claret FX. Essential roles of Jab1 in cell survival, spontaneous DNA damage and DNA repair. Oncogene. e-Pub 8/2010. PMID: 20802511. |
| 5. | Bellodi C, Krasnykh O, Haynes N, Theodoropoulou M, Peng G, Montanaro L, Ruggero D. Loss of function of the tumor suppressor DKC1 perturbs p27 translation control and contributes to pituitary tumorigenesis. Cancer Res 70(14):6026-35, 7/2010. e-Pub 6/2010. PMCID: PMC2913864. |
| 6. | Peng G, Yim EK, Dai H, Jackson AP, Burgt I, Pan MR, Hu R, Li K, Lin SY. BRIT1/MCPH1 links chromatin remodelling to DNA damage response. Nat Cell Biol 11(7):865-72, 7/2009. e-Pub 6/2009. PMCID: PMC2714531. |
| 7. | Yim EK,Peng G, Dai H, Hu R, Li K, Lu Y, Mills GB, Meric-Bernstam F, Hennessy BT, Craven RJ, Lin SY. Rak functions as a tumor suppressor by regulating PTEN protein stability and function. Cancer Cell 15(4):304-14, 4/2009. PMCID: PMC2673492. |
| 8. | Peng G, Wargovich MJ, Dixon DA. Anti-proliferative effects of green tea polyphenol EGCG on Ha-Ras-induced transformation of intestinal epithelial cells. Cancer Lett 238(2):260-70, 7/2006. e-Pub 9/2005. PMID: 16157446. |
| 9. | Peng G, Dixon DA, Muga SJ, Smith TJ, Wargovich MJ. Green tea polyphenol (-)-epigallocatechin-3-gallate inhibits cyclooxygenase-2 expression in colon carcinogenesis. Mol Carcinog 45(5):309-19, 5/2006. PMID: 16508969. |
| 10. | Yoon A, Peng G, Brandenburger Y, Brandenburg Y, Zollo O, Xu W, Rego E, Ruggero D. Impairments in IRES-mediated translational control underlie X-linked dyskeratosis congenita. Science 312(5775):902-906, 5/2006. PMID: 16690864. |
Grant & Contract Support
| Title: | Understanding and Targeting DNA Repair Network in Cancer |
| Funding Source: | NIH/NCI |
| Role: | Principal Investigator |
| Duration: | 7/18/2011 - 6/30/2013 |
| Title: | Genetic and Chemical Screens for Suppressors of Oct4 Expression in Breast Cancer |
| Funding Source: | Susan G. Komen Breast Cancer Foundation |
| Role: | Principal Investigator |
| Duration: | 8/20/2008 - 8/19/2010 |
Last updated: 3/8/2013
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