The human AP-endonuclease (APE1/Ref-1), an essential
multifunctional protein, plays a central role in the repair of
oxidative base damage via the DNA base excision repair (BER)
pathway. The mammalian AP-endonuclease (APE1) overexpression is
often observed in tumor cells, and confers resistance to various
anticancer drugs; its downregulation sensitizes tumor cells to
those agents via induction of apoptosis. Disruption of APE1
function has been shown to have a detrimental effect on cancer cell
viability and its elevated level in certain cancers has been
implicated in resistance to chemo/radiotherapy and cell killing.
Thus, level of APE1 may prove to have a prognostic importance in
cancer management. APE1 has been seen to be elevated in prostrate,
lung and cervical cancers. However, no study has been carried out
on gall bladder cancer correlating with oxidative damage and level
of APE1. Thus, any possible role of oxidative stress induced DNA
damage and up-regulation of APE1 remains to be elucidated in the
gall bladder cancer. This is a novel study in its type carried out
with the intention of seeking for any possible co-relation between
APE and Carcinoma bladder.
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