DNA DAMAGE AND REPAIR IN CANCER

Year 2017, Volume: Volume 2 Issue: İssue 1 (1) - 2.İnternational Congress Of Forensic Toxicology, 60 - 60, 16.02.2017

Miral Dızdaroglu

Abstract

 

Oxygen- and nitrogen-derived reactive species are constantly generated in
living organisms by endogenous and exogenous sources. Reactions of reactive
species such as free radicals with DNA cause the formation of multiple
mutagenic and cytotoxic lesions, leading to genetic instability, which is a
hallmark of cancer. DNA repair mechanisms exist in living organisms to repair
DNA lesions. Most effective cancer treatments work by causing DNA damage in
malignant tumors. Just like in normal cells, however, DNA repair also exist in
cancer cells. Thus, understanding of how DNA lesions are repaired is essential
for the understanding of cancer development and treatment. Cancer cells develop
greater DNA repair capacity than normal cells by overexpressing DNA repair
proteins. Increased DNA repair capacity that removes DNA lesions before they
become toxic is a major mechanism for development of resistance to therapy.
Knowledge of DNA repair capacity and levels of DNA repair proteins may be a
predictive biomarker for patient response to therapy, and guide development of
novel treatments. DNA repair proteins constitute targets for inhibitors to
overcome the therapy resistance. Inhibitors of DNA repair proteins for
combination therapy or for monotherapy as single drugs may help selectively
kill tumors, potentially leading to personalized therapy. Over the past decade,
a variety of inhibitors have been developed for various DNA repair proteins and
are being tested in clinical trials. The efficacy of some inhibitors in therapy
has been successfully demonstrated in patients. More developments of inhibitors
of DNA repair proteins are globally underway to help eradicate cancer.

Keywords

DNA DAMAGE AND REPAIR IN CANCER

References

• Miral DIZDAROGLU National Institute of Standards and Technology, Gaithersburg, Maryland, USA