Sandeep Burma
University of Texas Health Science Center at San Antonio, TX·Biochemistry
Cancer treatments such as radiation and many chemotherapy drugs work by breaking DNA. Cells, including tumor cells, survive by repairing those breaks, and the way a cell chooses to repair them can decide whether a tumor responds to treatment or resists it.
- Fields
Biochemistry
Medicine & Clinical Research
Genetics
- Topics
DNA double-strand break repair
DNA end resection
homology-directed repair
- Grants
- 2 known grants, through Aug 2029
What they work on
- Determine the biological role of the newly found ability of 53BP1, a chromatin-reading DNA repair protein, to bind double-stranded DNA, and how this binding recruits partner proteins and sets which repair pathway a break uses.
- Define how the CST complex (CTC1-STN1-TEN1) physically interacts with and inhibits the resection enzymes EXO1 and BLM-DNA2, which trim broken DNA ends, and how its binding to single-stranded DNA contributes.
- Test whether the BRCA1-BARD1 tumor-suppressor complex overcomes CST's block on DNA end resection by disrupting CST's contacts with resection enzymes and by stimulating those enzymes.
- Investigate whether radiation-induced MET amplification reprograms the transcription factors SOX2 and OLIG2 to produce glioblastoma stem-like cells with stronger DNA repair, using PDX and syngeneic mouse models and human tumor samples.
- Test whether HGF released by radiation-induced senescent astrocytes promotes the growth and radiation resistance of MET-amplified glioblastoma cells.
- Evaluate whether senolytic drugs, which selectively kill senescent cells, can make glioblastoma more sensitive to radiation and delay tumor recurrence in mouse models.
More about the research
The two projects here look at this from two angles. One studies the molecular switches that pick a DNA repair route. The other asks how radiation therapy changes both brain tumor cells and the normal brain tissue around them, so that glioblastoma comes back harder to treat.
Why it matters
Two groups of patients could benefit. For people with BRCA1-deficient and other HDR-deficient cancers, knowing how the 53BP1–CST and BRCA1-BARD1 circuit controls DNA repair could help guide targeted therapies and ways around PARP inhibitor resistance. For people with glioblastoma, the work tests whether senolytic drugs given alongside radiotherapy could improve treatment and delay the return of these lethal brain tumors.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
James Jackson
Tulane University of Louisiana, LA·Genetics
Test whether PD-L1-expressing senescent tumor cells have greater relapse potential than PD-L1-negative cells in chemotherapy-treated mouse mammary tumors, and compare their gene expression.
Joseph J. Loparo
Harvard University, MA·Biochemistry
Determine how core and accessory non-homologous end joining factors cooperate to tether broken DNA ends, using single-molecule imaging of the synaptic complex in a physiological cell-free system.
Zhiyuan Shen
Rutgers University-New Brunswick, NJ·Biochemistry
Reveal how chromatin context, shaped by methylation, sumoylation and ubiquitination tags, controls the recruitment and function of the BRCA1-PALB2-BRCA2 repair complex and regulators such as 53BP1, RNF4 and BARD1.
The school
University of Texas Health Science Center at San Antonio: 15 labs on PI Pages, $313M a year on research, 149 research doctorates a year.
More about University of Texas Health Science Center at San Antonio
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