Profile photo for Dr. Burma.


Neurosurgery, Biochemistry & Structural Biology

Sandeep Burma, Ph.D.

Professor, Vice Chair (Research), Mays Family Foundation Distinguished Chair in Oncology

Personal Statement:

Dr. Burma holds the Mays Family Foundation Distinguished Chair in Oncology, is Professor of Neurosurgery and Biochemistry & Structural Biology, and the Vice Chair for Research in the Department of Neurosurgery. He is also a member of the Mays MD Anderson Cancer Center at UT Health San Antonio.  Before moving to San Antonio, he spent fourteen years at the UT Southwestern Medical Center where he developed a strong research program in DNA repair and glioblastoma therapy resistance. Dr. Burma obtained his doctoral degree from the National Institute of Immunology in India. After postdoctoral research in the fields of transcription and DNA repair at Yale University, Pennsylvania State University, and the Los Alamos National Laboratory, he worked as a Career Scientist at the Lawrence Berkeley National Laboratory. He started his own research laboratory at UT Southwestern in 2005 and rose through the ranks there to become Professor of Radiation Oncology in 2019. Dr. Burma’s research has made many seminal contributions to our understanding of basic mechanisms of DNA repair and therapy resistance in glioblastoma. He is committed to translation of his research findings to improve cancer therapy, especially that of glioblastoma. Dr. Burma’s research has been continuously funded by the NIH and NASA. He serves on many grant review committees for the NIH, DOD, and NASA. He is on the editorial board of the Journal of Biological Chemistry, DNA Repair, and Annals of Translational Medicine. Dr.  Burma is an accomplished mentor and teacher. At UT Southwestern, Dr. Burma helped develop Core and Cancer Biology courses in the Graduate School and taught in these courses. Notably, as the Course Director of Advanced Concepts in Cancer Biology, Dr. Burma played a crucial role in curriculum development for the Cancer Biology graduate program.  He was also a lead instructor in the Macromolecules module taken by all medical students at UT Southwestern, and he taught in the Radiation Oncology Resident Training Program as well. At UT Health San Antonio, Dr. Burma will be deeply involved in the scientific and educational missions of the institution through his research and his mentorship of students in the Graduate School of Biomedical Sciences, and students and residents in the Long School of Medicine.

Academic Appointments:

1999-2005, Scientist Biologist, Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA
2005-2012, Assistant Professor (Tenure Track), Radiation Oncology, UT Southwestern Medical Center, Dallas, TX
2012-2019, Associate Professor (With Tenure), Radiation Oncology, UT Southwestern Medical Center, Dallas, TX
2019, Promoted to Professor (With Tenure), Radiation Oncology, UT Southwestern Medical Center, Dallas, TX
2019-Present, Professor (With Tenure), Neurosurgery, Biochemistry & Structural Biology, UT Health San Antonio, TX
2019-Present, Vice Chair (Research), Neurosurgery, UT Health San Antonio, TX
2019-Present, Mays Family Foundation Distinguished Chair in Oncology, UT Health San Antonio MD Anderson Cancer Center, TX


When it comes to DNA repair, it’s not one tool fits all

Dr. Burma honored by Society for NeuroOncology


B.Sc. Botany, Zoology, Chemistry (Honors in Zoology), Banaras Hindu University, India
M.Sc. Zoology (Specialization in Molecular Genetics and Cytogenetics), Banaras Hindu University, India
Ph.D. Molecular Biology, National Institute of Immunology, India
Postdoctoral Associate, Transcription Regulation, Dept. of Mol. Biophysics & Biochemistry, Yale University
Postdoctoral Associate, Transcription Regulation, Dept. of Biochemistry & Mol. Biology, Pennsylvania State University
Postdoctoral Associate, DNA Repair, Life Sciences Division, Los Alamos National Laboratory


Research in our laboratory is focused on the responses of mammalian cells to DNA double-strand breaks (DSBs) and the carcinogenic implications of these breaks. Cellular responses to DSBs 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 radiation or chemotherapy to treat the disease. Our laboratory is involved in studying DNA repair and damage signaling events triggered by genomic insults such as ionizing radiation and chemotherapeutic drugs. There are three synergistic and overlapping research projects in my laboratory with the overarching goal of comprehensively understanding cellular responses to DSBs and their carcinogenic implications. The three projects are structured such that basic results (from project 1) are being used to devise translational strategies to improve cancer therapy with genotoxic agents (project 2), and to understand how these very same agents can trigger primary or therapy-induced cancers (project 3):

1. DNA double-strand break sensing, signaling, and repair. We are examining early cellular events that occur in response to DNA breaks, with an emphasis on DNA end resection. Our early research from UTSW re-defined our understanding of the cellular responses to DSBs with regard to the exact roles of the three kinases that are activated by these breaks – ATM, ATR, and DNA-PKcs. Our research uncovered the existence of an “ATM-independent” pathway of ATR activation and cell cycle checkpoint implementation involving DSB resection by a 5’-3’ exonuclease, EXO1. Subsequently, we established that DNA end resection by EXO1 is a critical step which influences the choice that a cell makes between DNA repair pathways (NHEJ vs HR) and between cell cycle checkpoint activation modes (ATM vs ATR). Importantly, we established that EXO1 was phosphorylated and regulated by CDKs 1/2 in S/G2 phases of the cell cycle. This work is significant as it demonstrates that CDKs in S/G2 phases also regulate the “long range” resection step in HR via EXO1. Most recently, we established that DNA-damage induced degradation of EXO1 is a mechanism by which the cell negatively regulates DNA end resection. This work is significant because mechanisms terminating end resection are critical for promoting optimal HR and preventing genomic instability. Regulatory mechanisms impinging on EXO1 are of significance from a carcinogenesis standpoint as multiple SNPs in EXO1 have been linked to a host of human cancers. Moreover, disrupting accurate repair pathway choice can be an effective cancer therapeutic strategy as shown by us in the context of gliomas.

2. Targeting DNA repair pathways to augment glioblastoma therapy. An important translational goal of our research is to understand the genetic basis of glioblastoma (GBM) radio- and chemo-resistance with the objective of developing rational therapeutic-sensitization strategies for these lethal brain tumors. We systematically examined the contributions of key GBM-specific genetic alterations to therapy resistance using state-of-the-art transgenic mouse models, with a focus on two key events driving gliomagenesis – amplification of EGFRvIII and loss of PTEN. This research helped formulate an important concept in radiation oncology, i.e., key genetic changes occurring during carcinogenesis impact DNA repair pathways in specific ways. Specifically, EGFRvIII amplification and activation of the PI3K-Akt pathway augments NHEJ via DNA-PKcs while PTEN loss results in attenuated HR. Importantly, we discovered that the dual PI3K/mTOR inhibitor NVP-BEZ235 blocks both ATM and DNA-PKcs activation, thereby attenuating both NHEJ and HR pathways of DSB repair in glioma cells. Using pre-clinical mouse models, we showed that the drug can cross the blood-brain-barrier, and block DSB repair in gliomas thus sensitizing these tumors to IR. Most recently, we established that GBMs being treated with the chemotherapeutic agent TMZ acquire chemo-resistance, in part, due to augmented HR, and that such tumors can be re-sensitized using CDK inhibitors (based upon results from our EXO1 project). Our research established that GBMs (or other cancers) may be vulnerable to tailored therapies with specific DNA repair inhibitors based upon their DNA repair status. Our work has resulted in the development of several novel approaches that can be used to augment GBM therapy, illustrating how results from our basic DNA repair project can synergize with our translational GBM project.

3. Heavy ion-induced glioblastoma development. Complementing our research on ionizing radiation as a therapeutic agent, a third project in our laboratory focuses on the carcinogenic effects of radiation, especially particle radiation. Under the auspices of grants from NASA, we are studying cellular responses to complex DNA damage inflicted by the HZE (High-Z, High-Energy) particles and their gliomagenic consequenes. We analyzed HZE-induced GBM development in compound transgenic mouse models with brain-restricted tumor suppressor deletions. Our research established that low doses of HZE particles are highly transforming while gamma or X-rays are also very gliomagenic but only at higher doses. We discovered that loss of the Ink4a-Rb and Arf-p53 tumor suppressor axes and amplification of the MET proto-oncogene are critical events in the transformation process. We also found a linear correlation between atomic number of charged particles and GBM development in these mouse models. These findings are very pertinent to NASA as the decision to launch future long-duration space missions hinges upon the accurate estimation of cancer risks to astronauts from these particles. Moreover, this research is also very relevant to cancer therapy due to the increasing use of charged particles (protons and carbon) for targeted tumor therapy in the clinic which raises the specter of secondary tumors triggered by radiation therapy. This project has led to the development of valuable mouse models that could be used to understand mechanisms underlying radiation-induced GBM development and recurrence.

Awards & Accomplishments

Ph.D. Fellowship, Council for Scientific and Industrial Research, India
Prof. SRV Rao Oration Award, 16th All India Cell Biology Conference
Best Abstract Award, 8th International Ataxia Telangiectasia Workshop
Travel Award, Gordon Research Conference
Concept Award, Dept. of Defense Breast Cancer Research Program
Lecture-Tour of Japan, Japan Society for Promotion of Science
Individual Investigator Award, Cancer Prevention & Research Institute of Texas
DNA Poster Prize, 1st Exploring DNA Repair Pathways as Targets for Cancer Therapy Conference
Award for Excellence in Adult Basic Science, 24th Annual Meeting of the Society for Neuro-Oncology


Radiation Research Society (RRS)
American Association for the Advancement of Science (AAAS)
American Association of Cancer Research (AACR)
Society for Neuro-Oncology (SNO)
American Society for Therapeutic Radiology and Oncology (ASTRO)
The Radiosurgery Society (RSS)
American Society of Biochemistry and Molecular Biology (ASBMB)


Original Research Articles:

Specificity of end resection pathways for double-strand break regions containing ribonucleotides and base lesions. J.M. Daley, N. Tomimatsu, G. Hooks, W. Wang, A.S. Miller, X. Xue, K.A. Nguyen, H. Kaur, E. Williamson, B. Mukherjee, R. Hromas, S. Burma*, and P. Sung. Nature Communications June 18;11:3088 (2020) *Burma is a corresponding author

EGFR inhibition triggers an adaptive response driven by cooptation of antiviral signaling pathways in lung cancer. K. Gong, G. Guo, S. Panchani, M. Bender, D.E. Gerber, J.D. Minna, F. Fattah, B. Gao, M. Peyton, K. Kernstine, B. Mukherjee, S. Burma, C.M. Chiang, Z. Zhang, A.A. Sathe, C. Xing, K.H. Dao, D. Zhoa. E.A. Akbay, and A.A. Habib Nature Cancer (2020) In Press

Radiation-induced DNA damage cooperates with heterozygosity of TP53 and PTEN to generate high grade gliomas. P.K. Todorova, E. Fletcher-Sananikone, B. Mukherjee, R. Kollipara, V. Vemireddy, X.J. Xie, P. Guida, M.D. Story, K.J. Hatanpaa, A.A. Habib, R. Kittler, R.M. Bachoo, R. Hromas, J. Floyd, and S. Burma Cancer Research 79:3749-3761 (2019)

MiR223-3p promotes synthetic lethality in BRCA1-deficient cancers. G. Srinivasan, E.A. Williamson, K. Kong, A.S. Jaiswal, G. Huang, H.S. Kim, O. Schärer, W. Zhao, S. Burma, P. Sung, and R. Hromas Proc Natl Acad Sci U S A. 116:17438-17443 (2019)

Efficacy of EGFR plus TNF inhibition in a preclinical model of temozolomide-resistant glioblastoma. G. Guo, K. Gong, V.T. Puliyapaddamba, N. Panchani, E. Pan, B. Mukherjee, Z. Damanwalla, S. Bharia, K.J. Hatanpaa, D. E. Gerber, B.E. Mickey, T.R. Patel, J.N. Sarkaria, D. Zhao, S. Burma, and A.A. Habib Neuro Oncology 21:1529-1539 (2019)

TNF drives an adaptive response that mediates resistance to EGFR inhibition in lung cancer. K. Gong, G. Guo, D.E. Gerber, B. Gao, M. Peyton, C. Huang, J.D. Minna, K.J. Hatanpaa, K. Kernstine, L. Cai, Y. Xie, H. Zhu, F.J. Fattah, S. Zhang, M. Takahashi, B. Mukherjee, S. Burma, J. Dowell, K. Dao, V.A. Papadimitrakopoulou, V. Olivas, T.G. Bivona, M. Ma, K. Politi, D. Zhao, and A. A. Habib Journal of Clinical Investigation 128:2500-2518 (2018)

BRD4 promotes DNA repair and mediates the formation of TMPRSS2ERG gene rearrangements in prostate cancer. X. Li, G-H. Baek, S.G. Ramanand, A. Sharp, Y. Gao, W. Yuan, J. Welti, D.N. Rodrigues, D. Dolling, I. Figueiredo, S. Sumanasuriya, M. Crespo, A. Aslam, R. Li, Y. Yin, B. Mukherjee, M. Kanchwala, A.M. Hughes, W.S. Halse, C-M. Chiang, C Xing, G.V. Raj, S. Burma, J. de Bono, and R.S. Mani Cell Reports 22:796-808 (2018)

A TNF-JNK-Axl-ERK signaling axis mediates primary resistance to EGFR inhibition in glioblastoma. G. Guo, K. Gong, S. Ali, N. Ali, S. Shallwani, K.J. Hatanpaa, E. Pan, B. Mickey, S. Burma, S. Kesari, Dawen Zhao, and A.A. Habib Nature Neuroscience 8:1074-1084 (2017)

EGFR mutations compromise hypoxia-associated radiation resistance through impaired replication fork-associated DNA damage repair. M. Saki, H. Makino, P. Javvadi, N. Tomimatsu, L. Ding, J. Clark, E. Gavin, K. Takeda, J. Andrews, D. Saha, M.D. Story, S. Burma, and C. Nirodi Molecular Cancer Research 22:796-808 (2017)

Androgen receptor variants mediate DNA repair following radiation in prostate cancer. Y. Yin, R. Li, K. Xu, S. Ding, J. Li, G.H. Baek, S. Ramanand, S. Ding, Z. Liu, Y. Gao, M. Kanchwala, X. Li, R. Hutchinson, X. Liu, S. Woldu, C. Xing, N. Desai, F. Feng, S. Burma, J. de Bono, S. Dehm, R. Mani, B. Chen, and G. Raj Cancer Research 77:4745-4753 (2017)

DNA damage-induced Degradation of EXO1 Exonuclease Limits DNA End Resection to Ensure Accurate DNA Repair. N. Tomimatsu, B. Mukherjee, J.L. Harris, F.L. Boffo, M. Hardebeck, P.R. Potts, K.K. Khanna, and S. Burma Journal of Biological Chemistry 292:10779-10790 (2017)

Enhanced dependency of KRAS-mutant colorectal cancer cells on RAD51-dependent homologous recombination repair identified from genetic interactions in Saccharomyces cerevisiae. M. Kalimutho, A. L. Bain, B. Mukherjee, P. Nag, D.M. Nanayakkara, S.K. Harten, J.L. Harris, G.N. Subramanian, D. Sinha, S. Shirasawa, S. Srihari, S. Burma, and K.K. Khanna Molecular Oncology 11:470-490 (2017)

Endonuclease EEPD1 is a gatekeeper for repair of stressed replication forks. H.S. Kim, J.A. Nickoloff, Y. Wu, E.A. Williamson, G.S. Sidhu, B.L. Reinert, A.S. Jaiswal, G. Srinivasan, B. Patel, K. Kong, S. Burma, S.H. Lee, and R.A. Hromas Journal of Biological Chemistry 292:2795-2804 (2017)

INT6/EIF3E Controls the RNF8-Dependent Ubiquitylation Pathway and Facilitates DNA Double-Strand Break Repair in Human Cells. C. Morris, N. Tomimatsu, S. Burma, and P. Jalinot Cancer Research 76:6054-6065 (2016)

Augmented HR Repair Mediates Acquired Temozolomide Resistance in Glioblastoma. C.R. Gil Del Alcazar, P.K. Todorova, A.A. Habib, B. Mukherjee, and S. Burma Molecular Cancer Research 14:928-940 (2016) Cover Image of Molecular Cancer Research October 2016 issue. Included in Molecular Cancer Research Must-Read 2016

EEPD1 Rescues Stressed Replication Forks and Maintains Genome Stability by Promoting End Resection and Homologous Recombination Repair. Y. Wu, S.H. Lee, E.A. Williamson, B.L. Reinert, J.H. Cho, F. Xia, A.S. Jaiswal, G. Srinivasan, B. Patel, A. Brantley, D. Zhou, L. Shao, R. Pathak, M. Hauer-Jensen, S. Singh, K. Kong, X. Wu, H.S. Kim, T.S. Beissbarth, J. Gaedcke, S. Burma, J.A. Nickoloff, and R.A. Hromas PLoS Genetics 11:e1005675 (2015)

DNA double-strand breaks cooperate with loss of Ink4 and Arf tumor suppressors to generate glioblastomas with frequent Met amplification. C.V. Camacho, P.K. Todorova, M.C. Gillam, N. Tomimatsu, C.R. Gil del Alcazar, M. Ilcheva, B. Mukherjee, B. McEllin, V. Vemireddy, K. Hatanpaa, M.D. Story, A.A. Habib, V.V. Murty, R. Bachoo, and S. Burma  Oncogene 34:1064-72 (2015)

Tumor-selective use of DNA base excision repair inhibition in pancreatic cancer using the NQO1 bioactivatable drug, β-lapachone. G. Chakrabarti, M.A. Silvers, M. Ilcheva, Y. Liu, Z.R. Moore, X. Luo, J. Gao, G. Anderson, L. Liu, V. Sarode, D.E. Gerber, S. Burma, R.J. DeBerardinis, S.L. Gerson, and D.A. Boothman Science Reports 5:17066 (2015)

Targeting glutamine metabolism sensitizes pancreatic cancer to PARP-driven metabolic catastrophe induced by ß-lapachone. G. Chakrabarti, Z.R. Moore, X. Luo, M. Ilcheva, A. Ali, M. Padanad, Y. Zhou, Y. Xie, S. Burma, P.P. Scaglioni, L.C. Cantley, R.J. DeBerardinis, A.C. Kimmelman, C.A. Lyssiotis, and D.A Boothman Cancer Metabolism 3:12 (2015)

Phosphorylation of EXO1 by CDKs 1 and 2 regulates DNA end resection and repair pathway choice. N. Tomimatsu, B. Mukherjee, M. Gillam, M. Ilcheva, M.C. Hardebeck, C.V. Camacho, J.L. Harris, M. Porteus, B. Llorente, K.K. Khanna, and S. Burma Nature Communications 5:3561-71 (2014)

Inhibition of DNA double-strand break repair by the dual PI3K/mTOR inhibitor NVP-BEZ235 as a strategy for radiosensitization of glioblastoma. C. Gil Del Alcazar, M. Gillam, B. Mukherjee, N. Tomimatsu, X. Gao, J. Yan, X.J. Xie, R. Bachoo, L. Li, A.A. Habib, and S. Burma Clinical Cancer Research 20:1235-48 (2014)

EGFR wild type antagonizes EGFRvIII-mediated activation of Met in glioblastoma. L. Li, V.T. Puliyappadamba, S. Chakraborty, A. Rehman, V. Vemireddy, D. Saha, R.F. Souza, K.J. Hatanpaa, P. Koduru, S. Burma, D.A. Boothman, and A.A.  Habib Oncogene 34:129-134 (2014)

An EGFR wild type-EGFRvIII-HB-EGF feed-forward loop regulates the activation of EGFRvIII. L. Li, S. Chakraborty, C.R. Yang, K.J. Hatanpaa, D.J. Cipher, V.T. Puliyappadamba, A. Rehman, A.J. Jiwani, B. Mickey, C. Madden, J. Raisanen, S. Burma, D. Saha, Z. Wang, S.C. Pingle, S. Kesari, D.A. Boothman, and A.A. Habib Oncogene 33:4253-64 (2014)

Opposing effect of EGFRWT on EGFRvIII-mediated NF-kB activation with RIP1 as a cell death switch. V.T. Puliyappadamba, S. Chakraborty, S.S. Chauncey, L. Li, K.J. Hatanpaa, B. Mickey, S. Noorani, H.K. Shu, S. Burma, D.A. Boothman, and A.A. Habib Cell Reports 4:764-75 (2013)

Cytoplasmic TRADD confers a worse prognosis in glioblastoma. S. Chakraborty, L. Li, H. Tang, Y. Xie, V.T. Puliyappadamba, J. Raisanen, S. Burma, D.A. Boothman, B. Cochran, J. Wu, and A.A.  Habib Neoplasia 15:888-97 (2013)

The yeast Fun30 and human SMARCAD1 chromatin remodelers promote DNA end resection. T. Costelloe*, R. Louge*, N. Tomimatsu*, B. Mukherjee, B. Khadaroo, K. Dubois, W. Wiegant, E. Martini, A. Thierry, S. Burma, H. van Attikum, and B. Llorente Nature 489:581-584 (2012) *equal contribution

INT6/EIF3E interacts with ATM and is required for proper execution of the DNA damage response in human cells. C. Morris, N. Tomimatsu, D.J. Richard, D. Cluet, S. Burma, K.K. Khanna, and P. Jalinot Cancer Research 72:2006-2016 (2012)

Exo1 plays a major role in DNA end resection in humans and influences DNA repair and damage signaling decisions. N. Tomimatsu, B. Mukherjee, K. Deland, A. Kurimasa, E. Bolderson, K.K. Khanna, and S. Burma DNA Repair 11:441-448 (2012)

The dual PI3K/mTOR inhibitor NVP-BEZ235 is a potent inhibitor of ATM- and DNA-PKcs-mediated DNA damage responses. B. Mukherjee, N. Tomimatsu, K. Amancherla, C.V. Camacho, N. Pichamoorthy, and S. Burma Neoplasia 14:34-43 (2012)

Nucleolin participates in DNA double-strand break-induced damage response through MDC1-dependent pathway. J. Kobayashi, H. Fujimoto, J. Sato, I. Hayashi, S. Burma, S. Matsuura, D.J. Chen, K. Komatsu PLoS One 7:e49245 (2012)

AZD5438, an inhibitor of Cdk1, 2, and 9, enhances the radiosensitivity of non-small cell lung carcinoma cells. P. Raghavan, V. Tumati, L. Yu, N. Chan, N. Tomimatsu, S. Burma, R.G. Bristow, and D. Saha Int. J. Radiation Oncology Biol. Phys. 84:507-5014 (2012)

Epothilone B confers radiation dose enhancement in DAB2IP gene knock-down radioresistant prostate cancer cells. Z. Kong, P. Raghavan, D. Xie, T. Boike, S. Burma, D.J. Chen, A. Chakraborty, J-T. Hsieh and D. Saha Int. J. Radiation Oncology Biol. Phys. 78:250-257 (2010)

Loss of p15/Ink4b accompanies tumorigenesis triggered by complex DNA double-strand breaks. C. V. Camacho, B. Mukherjee, B. McEllin, L-H. Ding, B. Hu, A. Habib, X-J. Xie, C. Nirodi, D. Saha, M. Story, A. Balajee, R. M. Bachoo, D. A. Boothman, and S. Burma Carcinogenesis 31:1889-1896 (2010)

WRN participates in translesion synthesis pathway through interaction with NBS1. J. Kobayashi, M. Okui, A. Asaithamby, S. Burma, B. Chen, K. Tanimoto, S. Matsuura, K. Komatsu, D.J. Chen Mech Ageing Dev. 131:436-444 (2010)

Down-regulation of human DAB2IP gene expression in prostate cancer cells results in resistance to ionizing radiation. Z. Kong, D. Xie, T. Boike, P. Raghavan, S. Burma, D.J. Chen, A.A. Habib, A. Chakraborty, J-T. Hsieh and D. Saha Cancer Research 70:2829-2839 (2010)

PTEN loss compromises homologous recombination repair in astrocytes: implications for glioblastoma therapy with temozolomide or PARP inhibitors. B. McEllin, C.V. Camacho, B. Mukherjee, B. Hahm, N. Tomimatsu, R.M. Bachoo, and S. Burma Cancer Research 70:5457-5464 (2010)

RIP-1 activates PI3K-Akt via a dual mechanism involving NF-kB-mediated inhibition of mTOR-S6K-IRS1 negative feedback loop and down-regulation of PTEN. S. Park, D. Zhao, K.J. Hatanpaa, B.E. Mickey, D. Saha, D.A. Boothman, M.D. Story, E.T. Wong, S. Burma, M-M. Georgescu, V.M. Rangnekar, S.S. Chauncey, and A.A. Habib Cancer Research 69:4107-4111 (2009)

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 69:4252-4259 (2009)

Histone H2AX participates in the DNA damage-induced ATM activation through interaction with Nbs1. J. Kobayashi, H. Tauchi, B. Chen, S. Burma, S. Tashiro, S. Matsuura, K. Tanimoto, D.J. Chen, K. Komatsu Biochem. Biphys. Res. Commun. 380:752-757 (2009)

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 10:629-635 (2009)

Phosphorylation of Exo1 modulates homolgous recombination repair of DNA double-strand breaks. E. Bolderson, N. Tomimatsu, D.J. Richards, D. Boucher, R. Kumar, T.K. Pandita, S. Burma, K.K. Khanna Nucleic Acids Res. 38:1821-1831 (2009)

Modulation of the DNA-damage response to HZE particles by shielding. B. Mukherjee, C.V. Camcho, N. Tomimatsu, J. Miller, and S. Burma DNA Repair 7:1717-1730 (2008)

Repair of HZE-partcle-induced DNA double-strand breaks in normal human fibroblasts. A. Asaithamby, N. Uematsu, A. Chatterjee, M.D. Story, S. Burma, and D.J. Chen Radiation Research 169:437-446 (2008)

Ku70/80 modulates ATM and ATR signaling pathways in response to DNA double-strand breaks.N. Tomimatsu, G.G. Tahimic, A. Otsuki, S. Burma, A. Fukuhara, K. Sato, G. Shiota, M. Oshimura, D.J. Chen, and A. Kurimasa Journal of Biological Chemistry 282:10138-10145 (‘07)

Nucleophosmin suppresses oncogene-induced apoptosis and senescence and enhances oncogenic cooperation in cells with genomic instability. J. Li, D.P. Sejas, S. Burma, D.J. Chen, and Q. Pang Carcinogenesis 28:1163-1170 (2007)

DNA-PK phosphorylates histone H2AX during apoptotic DNA fragmentation in mammalian cells. B. Mukherjee, C. Kessinger, J. Kobayashi, B.P. Chen, D.J. Chen, A. Chatterje, and S. Burma DNA Repair 5:575-590 (2006)

Effect of Ku proteins on IRES-mediated translation. D. Silvera, N. Koloteva-Levine, S. Burma, and O. Elroy-Stein Biology of the Cell 98:353-361 (2006)

Gene expression profiles of normal human fibroblasts after ionizing radiation: a comparative study with low and high doses. L.-H. Ding, M. Shingyoji, F. Chen, J.-J. Hwang, S. Burma, J.-F. Cheng, and D. J. Chen Radiation Research 164:17-26 (2005)

Cell cycle dependence of DNA-PK phosphorylation in response to DNA double-strand breaks. B. Chen, D.W. Chan, J. Kobayashi, S. Burma, A. Asaithamby, K. Morotomi-Yano, E. Botvinick, J. Qin, and D.J. Chen Journal of Biological Chemistry 280:14709-14715 (2005)

Amplification and overexpression of oncogene Mdm2 and orphan receptor gene Nrlh4 in immortal PRKDC knockout cells. R. Ai, A. Sandoval, D.J. Chen, S. Burma, and P. Labhart Molecular Biology Reports 31:91-96 (2004)

Lethality in PARP-1/Ku80 double mutant mice reveals physiological synergy during early embryogenesis. M.S. Henrie, A. Kurimasa, S.Burma, J. Menissier-de Murcia, G. de Murcia, G.C. Li, and D.J. Chen DNA Repair 2:151-158 (2003)

DNA damage-induced apoptosis requires the DNA-dependent protein kinase, and is mediated by the latent population of p53. R.A. Woo, M.T. Jack, Y. Xu, S. Burma, D.J. Chen, and P.W. Lee EMBO Journal 21:3000-3008 (2002)

Differing responses of Nijmegen breakage syndrome and ataxia telangiectasia cells to ionizing radiation. J. Little, H. Nagasawa, W.K. Dahlberg, M.Z. Zdzienicka, S. Burma , and D.J.Chen Radiation Research 158:319-326 (2002)

ATM phosphorylates histone H2AX in response to DNA double-strand breaks. S. Burma, B.P. Chen, M. Murphy, A. Kurimasa, and D.J. Chen Journal of Biological Chemistry 276:42462-42467 (2001) “Of outstanding interest”-Current Opinions in Genetics & Development (2002), Citations > 1,100

DNA-dependent protein kinase–independent activation of p53 in response to DNA damage.S. Burma, A. Kurimasa, G. Xie, Y. Taya, R. Araki, H.A. Crissman, M. Abe, H. Ouyang, G.C. Li, and D.J. Chen Journal of Biological Chemistry 274:17139-17143 (1999)

Enhanced phosphorylation of p53 serine18 following DNA damage in DNA-dependent protein kinase catalytic subunit-deficient cells. R. Araki, R. Fukumura, A. Fujimori, Y. Taya, Y. Shiloh, A. Kurimasa, S. Burma, G.C. Li, D.J. Chen, K. Satoh, Y. Hoki, K. Tatsumi, and M. Abe Cancer Research 59:3543-3546 (1999)

TFIIA regulates TBP and TFIID dimers. R.A. Coleman, A.K. Taggart, S. Burma, J.J. Chicca 2nd, and B.F. Pugh Molecular Cell 4:451-457 (1999)

Dimer dissociation and thermosensitivity kinetics of the Saccharomyces cerevisiae and human TATA binding proteins. *A.J. Jackson-Fisher, *S. Burma, *M. Portnoy, L.A. Schneeweis, R.A. Coleman, M. Mitra, C. Chitikila, and B.F. Pugh Biochemistry 38:11340-11348 (1999) [*Equal contribution]

Increase in p202 expression during skeletal muscle differentiation: Inhibition of MyoD protein expression and activity by p202. B. Datta, W. Min, S. Burma, and P. Lengyel Molecular and Cellular Biology 18:1074-1083 (1998)

Bifunctionality of the AcMNPV homologous region sequence (hr1): enhancer and ori functions have different sequence requirements. S. Habib, S. Pandey, U. Chatterjee, S. Burma, R. Ahmed, A. Jain, and S.E. Hasnain  DNA and Cell Biology 15:737-747 (1996)

Transcriptional regulation of cell line-dependent, baculovirus-mediated expression of foreign genes. B. Mukherjee, S. Burma, G.P. Talwar, and S.E. Hasnain  DNA and Cell Biology 14:7-14 (1995)

The 30-kDa protein binding to the ‘initiator’ of the baculovirus polyhedrin promoter also binds specifically to the coding strand. B. Mukherjee, S. Burma, and S. E. Hasnain Journal of Biological Chemistry 270:4405-4411 (1995)

An unusual 30-kDa protein binding to the polyhedrin gene promoter of the Autographa californica nuclear polyhedrosis virus. S. Burma, B. Mukherjee, A. Jain, S. Habib, and S.E. Hasnain Journal of Biological Chemistry 269:2750-2757 (1994)


Reviews and Monographs:

MET signaling promotes DNA repair and radiation resistance in glioblastoma stem-like cells. P.K. Todorova, B. Mukherjee, and S. Burma Annals of Translational Medicine 5:61-64 (2017)

Mouse models of radiation-induced glioblastoma. B. Mukherjee, P.K. Todorova, and S. Burma Oncoscience 2:934-935 (2015)

Concepts and challenges in cancer risk prediction for the space radiation environment. M.H. Barcellos-Hoff, E.A. Blakely, S. Burma, A.J. Fornace Jr, S. Gerson, L.Hlatky, D.G. Kirsch, IU. Luderer, J. Shay, Y. Wang, M.M. Weil Life Sci Space Res (Amst). 6:92-103 (2015)

Immunofluorescence-based methods to monitor DNA end resection. B. Mukherjee, N. Tomimatsu, and S. Burma Methods in Molecular Biology 1292:67-75 (2015)

DNA double-strand breaks make bedfellows of ATM and AKT. B. Mukherje and S. Burma Cell Cycle 10:3230 (2011)

Epidermal growth factor receptor in glioma: signal transduction, neuropathology, imaging, and radioresistance. K.J. Hatanpaa, S. Burma, D. Zhao, A.A. Habib Neoplasia 12:675-684 (2010)**

Targeting Non-Homologous End-Joining Through Epidermal Growth Factor Receptor Inhibition: Rationale and Strategies for Radiosensitization. B. Mukherjee, H. Choy, C. Nirodi, and S. Burma Seminars in Radiation Oncology 20:250-257 (2010)

Role of non-homologous end joining (NHEJ) in maintaining genomic stability in mammalian cells. S. Burma, B.P. Chen, and D.J. Chen DNA Repair 5:1042-1048 (2006)** Listed in “most downloaded/most cited DNA Repair articles”

Role of DNA-PK in the cellular response to DNA double-strand breaks. S. Burma, and D.J.Chen DNA Repair 3:909-918 (2004)**

Host factor with single-stranded DNA-binding activity involved in transcription from the baculovirus polyhedrin promoter. S.E. Hasnain, S. Habib, A. Jain, S. Burma, and B. Mukherjee Methods in Enzymology: RNA polymerase and associated factors (S. Adhya, volume editor), Academic Press, New York, 274:20-32 (1996)

Baculovirus vector-mediated expression of heterologous genes in insect cells. P. Sridhar, C.A. Azim, S. Burma, S. Habib, A. Jain, B. Mukherjee, A. Ranjan, and S.E. Hasnain Journal of Biosciences 19: 603-614 (1994)

The baculovirus expression vector system: Regulation of the polyhedrin gene promoter. S. Burma and S.E. Hasnain Proceedings of the India National Science Academy B60:365-374 (1994)


Book Chapters:

Role of non-homologous end joining in the repair of DNA double-strand breaks. S. Burma, B. Chen, D.J. Chen in DNA Repair Genetic Instability and Cancer (Q. Wei, L. Li, and D.J. Chen, eds), World Scientific Publishing Co., p157-175 (2007)

Transcriptional regulation of the AcNPV polyhedrin gene promoter. S. Habib, S. Burma, U. Chatterjee, P. Das, A. Jain, B. Mukherjee, K. Natarajan, A.  Ranjan, and S.E. Hasnain in Current Developments in Animal Virology (E.K. Wagner and S. Jameel, eds.), Oxford and IBH Publishing Co., New Delhi, India and Science Publishers Inc., Lebanon, NH, USA, p205-210 (1996)