Page 55
Volume 3
August 5-6, 2019 | Singapore
CANCER RESEARCH AND PHARMACOLOGY
STRUCTURAL BIOCHEMISTRY, STEM CELLS AND MOLECULAR BIOLOGY
24
th
International Conference on
International Congress on
&
Cancer Research 2019 & Structural Biochemistry 2019
August 5-6, 2019
Journal of Cancer and Metastasis Research
Clin Psychol Cog Sci, Volume 3
Investigating the nexus between DNArepair pathways and genomic instability in cancer
Sonali Bhattacharjee
Cold Spring Harbor Laboratory, USA
D
NA double-strand breaks are one of the most lethal lesions to a cell that can be repaired by one of the two cellular pathways;
non-homologous end joining or homologous recombination. Homologous recombination genes are particularly attractive
targets for precision cancer therapy because these genes have altered expression patterns in cancer cells when compared with
normal cells and these genetic abnormalities can be targeted for selectively killing cancer cells while leaving normal cells
unscathed. Synthetic lethality is thought to be the new frontier of cancer therapeutics because it overcomes the limitation of
chemotherapy, which is unable to discriminate between cancer cells and normal cells. Two genes are synthetically lethal when
simultaneous disruptions of both genes gives rise to a lethal phenotype, while the disruption of either gene alone is viable. Many
homologous recombination genes have synthetic lethal relationships with oncogenes and tumor suppressor genes, which can
be targeted for the development of cancer therapy- an approach referred to as combination therapy. In my presentation, I will
summarize recent progress in understanding both the functioning and the regulation of the DNA repair machinery and elaborate
on the clinical applications of these proteins in cancer therapy.
sonali@cshl.edu