Toronto, Nov 07: Though the environment is full of cancer-causing carcinogens because of sun`s ultraviolet rays, tobacco smoke and other factors, the human body`s DNA repair mechanisms stops them from producing tumours, says a new study.
In their study, scientists from Montreal University and its affiliated Maisonneuve-Rosemont Hospital Research Centre also say that they have identified a biochemical process behind this DNA repair mechanism.
``Our study is the first to identify a regulatory role for the ATR protein (which triggers DNA damage checkt response) in a specific DNA repair system, which is called nucleotide excision repair or NER,`` said study author Elliot Drobetsky of Montreal University in a statement Thursday.
``NER is a critical DNA repair system that removes pieces of damaged DNA before these pieces can destroy the function of tumour-preventing proteins in the body. Characterizing how the NER system is turned on or off is critical to understanding how tumours develop. In this system, ATR is the key that turns on the repair machinery,`` he said.
The scientific team used cultured lung cells to investigate the role of ATR in NER function, the university statement said.
``They found that inhibiting ATR protein resulted in a dysfunctional NER system and, during a certain period of the cell`s growth cycle, damaged DNA was not repaired at all.
``What`s more, they discovered that some tumour cell lines are completely deficient in the ATR-mediated repair pathway, providing solid evidence that this protein`s DNA repair function may be pivotal in cancer development,`` the statement said.
``Our study reveals an original mechanism to explain how exposure to environmental carcinogens initiate and promote cancer,`` said Drobetsky.
``Our findings open a whole new area of research. Our data harbour critical implications not only for understanding how cancer develops but also for devising new strategies to greatly improve cancer treatment,`` he said.
The study has been published in the online edition of Proceedings of the National Academy of Sciences of the USA (PNAS).
IANS
