Abstract: The present invention relates to the identification of marker genes useful in the diagnosis and prognosis of clinically problematic subsets of primary breast cancers. More specifically, the invention relates to the identification of two sets of marker genes that are differentially expressed in and useful for the diagnosis and prognosis of subsets of hormone receptor-negative (HRneg; i.e., ER and PR negative) and triple-negative (Tneg; i.e., ER, PR and HER2 negative) primary breast cancers at highest risk for early metastatic relapse. The invention further provides methods for determining the best course of treatment for patients having one of these clinically problematic subsets of primary breast cancers. The invention also provides methods for identifying compounds that prevent or treat a subtype of breast cancer based on their ability to modulate the activity or expression level of one or more marker genes identified herein.

Abstract: The present invention provides for immunoliposomes that optimizes internalization of a drug into target cells bearing a characteristic cell surface marker. The immunoliposomes comprise an Fab? domain of an antibody that specifically binds the characteristic marker, an amphipathic vesicle-forming lipid, and a polyethylene glycol derivatized lipid. The invention also provides for growth-inhibiting immunoliposomes that lack growth-inhibiting therapeutic agents and yet are capable of inhibiting the growth and proliferation of target cells.

Abstract: This invention pertains to the identification of two novel epithelial signaling pathways in ER-positive breast cancer s and the discovery that the cellular biology and (likely also the clinical outcome) of ER-positive breast cancer cells is unexpectedly altered when these signaling pathways are activated. The first pathway pertains to the discovery that NF-?B activation and/or DNA binding is implicated in the etiology of ER-positive breast (and other) cancers. The second pathway involves ligand-independent quinine-mediated ER activation by posphorylation (e.g. on SER-118 and SER-167 residues of ER) and nuclear translocation of full-length (67 kDA) ER as well as the phorphorylating activation of a truncated and nuclear-localized ER variant (˜52 kDa).

Abstract: This invention pertains to the development of a screening system to identify (screen for) HER2 promoter silencing agents. Such agents are expected to be of therapeutic value in the treatment of cancers characterized by HER2 amplification/upregulation. In addition, this invention pertains to the discovery that histone deacetylase (HDAC) inhibitors like sodium butyrate and trichostatin A (TSA), in a time and dose dependent fashion can silence gnomical.ly integrated and/or amplified/overexpressing promoters, such as that driving the HER2/ErbB2/neu oncogene, resulting in inhibition of gene products including transcripts and protein, and subsequent production of tumor/cell growth inhibition, apoptosis and/or differentiation. In another embodiment, this invention provides novel SNPs associated with the coding region of the ErbB2. proto-oncogene.