To identify major coregulators in ER-a or mutated ER-a mediated breast cancer development and their anti-estrogen resistance.
To determine whether the altered association coregulators with ER-a and alterations in their crosstalk is responsible for hypersensitivity of ER-a.
To determine whether any change in target promoters of ER-a of and investigate their possible implications for the global effect of hypersensitive ER-a.
To identify the important altered associations and altered targets (promoter) as the mechanism underlying ER-a hypersensitivity.
To manipulate such alterations at the molecular level in an effort to reverse the hypersensitivity of ER-a and its resistance to anti-estrogen.