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Tej K. Pandita, PhD

Professor of Radiation Oncology, Institute for Academic Medicine
Full Member, Research Institute
Scientific Director, Department of Radiation Oncology
Houston Methodist
Weill Cornell Medical College


Biography

Dr. Pandita earned his Ph.D. in Cytogenetics from Panjab University in 1980. He held faculty appointments at Columbia University in New York, Washington University in St.  Louis, Missouri, and The University of Texas Southwestern Medical Center in Dallas, Texas before becoming a member of the Houston Methodist Research Institute in 2014.  As a member of the Cancer Research Program, he directs a research program focusing on DNA repair and radiotherapy.  Dr. Pandita was elected the Fellow of the American Association of Advancement of Science in 2013. He has also been a member of several NIH study sections and review boards. He is the past Chairman of A-T Workshop 2012 (ATW2012) International meeting. Dr. Pandita serves on the editorial board for the journals Cancer Research, Genomic Integrity, BMC Genomics, and served as a chartered member of the CMAD NIH Study Section.

Description of Research

Dr. Pandita's research employs radiation genetics and biology to study the relationships between DNA sequence, chromatin structure and sensitivity to IR. The long-term goal of the research projects is to understand the mechanistic role of chromatin structure in regulating the cell survival response to IR-induced DNA damage. This knowledge base will be used by the laboratory to develop clinically relevant methods to increase tumor cell response to IR-based therapies while decreasing injury to adjacent, normal tissue.

Dr. Pandita's main areas of research are the following:
-To define, at the chromatin level, the function of H4K16ac in DNA DSB repair.
-To determine the role of ATM dependent MOF phosphorylation in the cellular response to IR.
-To determine the pathobiology of mutant mice defective for MOF T392 phosphorylation in order to test the hypothesis that Mof plays a critical role in oncogenic transformation in vivo.
-To determine the mechanisitic basis for enhanced tumor cell radiosensitivity following HP1ß loss or hyperthermia.

Areas Of Expertise

DNA damage response DNA DSB repair Radiation Signaling Telomere metabolism Chromatin structure
Education & Training

MSc , Kashmir University, Srinagar
Postdoctoral Fellowship , National Botanical Research Institute, Council of Scientific and Industrial Research, Lucknow
PhD , Punjab University, Chandigarh
Publications

MiR-15a/miR-16 down-regulates BMI1, impacting Ub-H2A mediated DNA repair and breast cancer cell sensitivity to doxorubicin
Patel, N, Garikapati, KR, Pandita, RK, Singh, DK, Pandita, TK, Bhadra, U & Bhadra, MP 2017, Scientific Reports, vol 7, no. 1, 4263. DOI:

Ssb1 and Ssb2 cooperate to regulate mouse hematopoietic stem and progenitor cells by resolving replicative stress
Shi, W, Vu, T, Boucher, D, Biernacka, A, Nde, J, Pandita, RK, Straube, J, Boyle, GM, Al-Ejeh, F, Nag, P, Jeffery, J, Harris, JL, Bain, AL, Grzelak, M, Skrzypczak, M, Mitra, A, Dojer, N, Crosetto, N, Cloonan, N, Becherel, OJ, Finnie, J, Skaar, JR, Walkley, CR, Pandita, TK, Rowicka, M, Ginalski, K, Lane, SW & Khanna, KK 2017, Blood, vol 129, no. 18, pp. 2479-2492. DOI:

Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis
Valerio, DG, Xu, H, Chen, C-W, Hoshii, T, Eisold, ME, Delaney, C, Cusan, M, Deshpande, AJ, Huang, C-H, Lujambio, A, Zheng, YG, Zuber, J, Pandita, TK, Lowe, SW & Armstrong, SA 2017, Cancer Research, vol 77, no. 7, pp. 1753-1762. DOI:

Aurora kinase B dependent phosphorylation of 53BP1 is required for resolving merotelic kinetochore-microtubule attachment errors during mitosis
Wang, H, Peng, B, Pandita, RK, Engler, DA, Matsunami, RK, Xu, X, Hegde, PM, Butler, EB, Pandita, TK, Mitra, S, Xu, B & Hegde, ML 2017, Oncotarget, vol 8, no. 30, pp. 48671-48687. DOI:

Histone acetyltransferase KAT8 is essential for mouse oocyte development by regulating reactive oxygen species levels
Yin, S, Jiang, X, Jiang, H, Gao, Q, Wang, F, Fan, S, Khan, T, Jabeen, N, Khan, M, Ali, A, Xu, P, Pandita, TK, Fan, HY, Zhang, Y & Shi, Q 2017, Development (Cambridge), vol 144, no. 12, pp. 2165-2174. DOI:

Aurora kinase B dependent phosphorylation of 53BP1 is required for resolving merotelic kinetochore-microtubule attachment errors during mitosis
Wang, H, Peng, B, Pandita, RK, Engler, DA, Matsunami, RK, Xu, X, Hegde, PM, Butler, BE, Pandita, TK, Mitra, S, Xu, B & Hegde, ML 2017, Oncotarget, vol 8, no. 30, pp. 48671-48687. DOI:

Nuclear functions of ß2-Spectrin in genomic stability
Mujoo, K, Hunt, CR & Pandita, T 2016, Aging, vol 8, no. 12, pp. 3151-3152. DOI:

Critical role of the POT1 OB domain in maintaining genomic stability
Pandita, TK 2016, Oncogene. DOI:

Histone acetyltransferase activity of MOF is required for adult, but not early fetal hematopoiesis in mice
Valerio, DG, Xu, H, Eisold, ME, Woolthuis, CM, Pandita, TK & Armstrong, SA 2016, Blood. DOI:

MCL-1 depletion impairs DNA DSB repair and re-initiation of stalled DNA replication forks
Mattoo, AR, Pandita, RK, Chakraborty, S, Charaka, V, Mujoo, K, Hunt, CR & Pandita, TK 2016, Molecular and Cellular Biology. DOI:

The DNA damage response during induced pluripotent and embryonic stem cell differentiation
Mujoo, K & Pandita, T 2016, . in Third Ataxia-Telangiectasia clinical Research Conference 2016., A-T 2016, pp. 97.

Classical non-homologous end-joining pathway utilizes nascent RNA for error-free double-strand break repair of transcribed genes
Chakraborty, A, Tapryal, N, Venkova, T, Horikoshi, N, Pandita, RK, Sarker, AH, Sarkar, PS, Pandita, TK & Hazra, TK 2016, Nature communications, vol 7, pp. 13049. DOI:

Endocrine disrupting chemical, bisphenol-A, induces breast cancer associated gene HOXB9 expression in vitro and in vivo
Deb, P, Bhan, A, Hussain, I, Ansari, KI, Bobzean, SA, Pandita, TK, Perrotti, LI & Mandal, SS 2016, Gene, vol 590, no. 2, pp. 234-43. DOI:

HOXC10 expression supports the development of chemotherapy resistance by fine tuning DNA repair in breast cancer cells
Sadik, H, Korangath, P, Nguyen, NK, Gyorffy, B, Kumar, R, Hedayati, M, Teo, WW, Park, S, Panday, H, Munoz, TG, Menyhart, O, Shah, N, Pandita, RK, Chang, JC, DeWeese, T, Chang, HY, Pandita, TK & Sukumar, S 2016, Cancer Research, vol 76, no. 15, pp. 4443-4456. DOI:

Pluripotent stem cells and DNA damage response to ionizing radiations
Mujoo, K , Butler, EB, Pandita, RK, Hunt, CR & Pandita, TK 2016, Radiation Research, vol 186, no. 1, pp. 17-26. DOI:

ß2-spectrin depletion impairs DNA damage repair
Horikoshi, N, Pandita, RK, Mujoo, K, Hambarde, S, Sharma, D, Mattoo, AR, Chakraborty, S, Charaka, V, Hunt, CR & Pandita, TK 2016, Oncotarget, vol 7, no. 23, pp. 33557-33570. DOI:

The TIP60 Complex Regulates Bivalent Chromatin Recognition by 53BP1 through Direct H4K20me Binding and H2AK15 Acetylation
Jacquet, K, Fradet-Turcotte, A, Avvakumov, N, Lambert, JP, Roques, C, Pandita, RK, Paquet, E, Herst, P, Gingras, AC, Pandita, TK, Legube, G, Doyon, Y, Durocher, D & Côté, J 2016, Molecular Cell, vol 62, no. 3, pp. 409-421. DOI:

Torin2 suppresses ionizing radiation-induced DNA damage repair
Udayakumar, D, Pandita, RK, Horikoshi, N, Liu, Y, Liu, Q, Wong, KK, Hunt, CR, Gray, NS, Minna, JD, Pandita, TK & Westover, KD 2016, Radiation Research, vol 185, no. 5, pp. 527-538. DOI:

Emerging therapeutic targets in esophageal adenocarcinoma
Gaur, P, Hunt, CR & Pandita, TK 2016, Oncotarget. DOI:

The many faces of histone H3K79 methylation
Farooq, Z, Banday, S, Pandita, TK & Altaf, M 2016, Mutation Research - Reviews in Mutation Research, vol 768, pp. 46-52. DOI: