Dr. Sandeep Burma obtained his PhD in Molecular Biology from the National Institute of Immunology, New Delhi, India in 1995. After postdoctoral training at Yale University, Pennsylvania State University and Los Alamos National Laboratory, he joined the Lawrence Berkeley National Laboratory as a Scientist Biologist in 1999. He joined the UT Southwestern Medical Center in 2005 where he is currently Associate Professor of Radiation Oncology. Dr. Burma is member of the Harold C. Simmons Comprehensive Cancer center and member of the Cancer Biology and Genetics and Development graduate programs of UT Southwestern.
Research in the Burma laboratory is focused on the responses of mammalian cells to DNA double-strand breaks (DSBs), collectively called the DNA damage response (DDR). These responses are of paramount importance in the field of cancer biology - on one hand, DSBs cause cancer, while, on the other hand, these breaks are induced by ionizing radiation or chemotherapies commonly used to treat the disease. The Burma lab is involved in studying DDR events triggered by ionizing radiation and their carcinogenic and cancer therapeutic implications.
|Undergraduate||Banaras Hindu University (1988), Zoology|
|Graduate School||Banaras Hindu University (1990), Molecular Genetics|
|Graduate School||National Inst of Immunology (1995), Molecular Biology|
- DNA double-strand breaks - sensing, signaling and repair
- Glioblastoma radioresistance - genetic basis and therapeutic targeting
- Radiation-induced gliomagenesis - genetic events underlying transformation
- DNA double-strand breaks cooperate with loss of Ink4 and Arf tumor suppressors to generate glioblastomas with frequent Met amplification.
- Camacho CV, Todorova PK, Hardebeck MC, Tomimatsu N, Gil Del Alcazar CR, Ilcheva M, Mukherjee B, McEllin B, Vemireddy V, Hatanpaa K, Story MD, Habib AA, Murty VV, Bachoo R, Burma S Oncogene 2014 Mar
- Inhibition of DNA Double-Strand Break Repair by the Dual PI3K/mTOR Inhibitor NVP-BEZ235 as a Strategy for Radiosensitization of Glioblastoma.
- Gil Del Alcazar CR, Hardebeck MC, Mukherjee B, Tomimatsu N, Gao X, Yan J, Xie XJ, Bachoo R, Li L, Habib AA, Burma S Clin. Cancer Res. 2014 Feb
- Phosphorylation of EXO1 by CDKs 1 and 2 regulates DNA end resection and repair pathway choice.
- Tomimatsu N, Mukherjee B, Catherine Hardebeck M, Ilcheva M, Vanessa Camacho C, Louise Harris J, Porteus M, Llorente B, Khanna KK, Burma S Nat Commun 2014 5 3561
- The yeast Fun30 and human SMARCAD1 chromatin remodellers promote DNA end resection.
- Costelloe T, Louge R, Tomimatsu N, Mukherjee B, Martini E, Khadaroo B, Dubois K, Wiegant WW, Thierry A, Burma S, van Attikum H, Llorente B Nature 2012 Sep 489 7417 581-4
- PTEN Loss Compromises Homologous Recombination Repair in Astrocytes: Implications for Glioblastoma Therapy with Temozolomide or PARP Inhibitors
- B. McElliin, C.V. Camacho, B. Mukherjee, B. Hahm, N. Tomimatsu, R.M. Bachoo, and S. Burma Cancer Research July 2010 70 5457-5464
- Distinct roles of ATR and DNA-PKcs in triggering DNA damage responses in ATM-deficient cells
- N. Tomimatsu, B. Mukherjee, and S Burma EMBO Reports June 2009 10 629-635
- EGFRvIII and DNA Double-Strand Break Repair: A Molecular Mechanism for Radioresistance in Glioblastoma
- B. Mukherjee, B. McEllin, C.V. Camacho, N. Tomimatsu, S. Sirasanagandala, S. Nannepaga, K.J. Hatanpaa, B. Mickey, C. Madden, E. Maher, D.A. Boothman, F. Furnari, W.K. Cavenee, R.M. Bachoo, and S. Burma Cancer Research May 2009 69 4252-4259
- EGFR wild type antagonizes EGFRvIII-mediated activation of Met in glioblastoma.
- Li L, Puliyappadamba VT, Chakraborty S, Rehman A, Vemireddy V, Saha D, Souza RF, Hatanpaa KJ, Koduru P, Burma S, Boothman DA, Habib AA Oncogene 2013 Dec
- An EGFR wild type-EGFRvIII-HB-EGF feed-forward loop regulates the activation of EGFRvIII.
- Li L, Chakraborty S, Yang CR, Hatanpaa KJ, Cipher DJ, Puliyappadamba VT, Rehman A, Jiwani AJ, Mickey B, Madden C, Raisanen J, Burma S, Saha D, Wang Z, Pingle SC, Kesari S, Boothman DA, Habib AA Oncogene 2013 Sep
- Opposing Effect of EGFRWT on EGFRvIII-Mediated NF-?B Activation with RIP1 as a Cell Death Switch.
- Puliyappadamba VT, Chakraborty S, Chauncey SS, Li L, Hatanpaa KJ, Mickey B, Noorani S, Shu HK, Burma S, Boothman DA, Habib AA Cell Rep 2013 Aug
Honors & Awards
- Cancer Prevention and Research Institute of Texas (CPRIT)
Individual Investigator Award (2010)
- Japan Society for Promotion of Science (JSPS)
Fellowship for Lecture-Tour of Japan (2009)
- Department of Defense Breast Cancer Research Program (DOD BCRP)
Concept Award (2003)
- Eighth International Workshop for Ataxia Telangiectasia (ATW)
Best Abstract Award (1999)
- Council for Scientific and Industrial Research of India (CSIR)
Research Fellowship (1990)
- American Association for Cancer Research (AACR)
- American Association for the Advancement of Science (AAAS)
- Radiation Research Society (RRS)