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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