Abstract: The present invention provides methods and reagents for treating cancer cells for therapeutic purposes, by contacting with a sumoylation inhibitor in a dose effective to block sumoylation of TFAP2A. In breast cancer cells the sumoylation inhibitor induces a basal to luminal shift in phenotype. Sumoylation inhibitors also reduce the number of cancer stem cells in a cancer cell population. Inhibition of sumoylation makes cancer cells more responsive to conventional chemotherapeutic therapy and radiation therapy and decreases recurrence or development of metastases.

Abstract: Neurological dysfunction is prevented or treated by the administration of ligands that activate the GPR30 receptor. Ligands include estrogens and structurally related molecules. Preferably the GPR30 ligand is an orally available drug that can cross into the brain from blood. Screening methods are provided for ligands that do not activate other estrogen receptors, and therefore do not have the classical estrogenic effects attributable to these receptors.

Abstract: Neurological dysfunction is prevented or treated by the administration of ligands that activate the GPR30 receptor. Ligands include, but are not limited to, estrogens and structurally related molecules. In a preferred embodiment, the GPR30 ligand is an orally available drug that can cross into the brain from blood. Of particular interest are ligands that do not activate other estrogen receptors, and therefore do not have the classical estrogenic effects attributable to these receptors.

Abstract: Neurological dysfunction is prevented or treated by the administration of ligands that activate the GPR30 receptor. Ligands include, but are not limited to, estrogens and structurally related molecules. In a preferred embodiment, the GPR30 ligand is an orally available drug that can cross into the brain from blood. Of particular interest are ligands that do not activate other estrogen receptors, and therefore do not have the classical estrogenic effects attributable to these receptors.

Abstract: ERF-1 is shown to be a transcriptional regulator of the expression of the estrogen receptor, where elevated ERF-1 is related to elevated expression of the estrogen receptor. By monitoring the level of ERF-1, one can relate phenotypic characteristics of carcinomas expressing ERF-1 as prognostic of the response of the tumor to various therapies. In addition, ERF-1 may be used for screening therapeutic drugs which may act as antagonists to initiation of estrogen receptor transcription.