Retinoic acid and its synthetic derivatives participate in many biological processes including development cellular proliferation and differentiation. Retinoids mediate their actions by binding to the nuclear retinoic acid receptors and retinoid X receptors. Wayne State University researchers found that retinoid induced cell cycle arrest and apoptosis in several human breast carcinoma cell lines is independent of tumor suppressor p53 and estrogen receptor status via an undefined mechanism. This led to the identification of a novel cDNA which encodes a 130 Kda protein referred to as CARP-1 (Cell Cycle and Apoptosis Regulatory Protein-1). CARP-1 is expressed in many cancer cell types including breast and colon carcinoma cells. Working with polyclonal antibodies to CARP-1 it was demonstrated that CARP-1 controls cell cycle progression by inhibiting genes such as c-Myc and cyclin B1. CARP-1 is elevated when cells undergo apoptosis in the presence of CD437 or chemotherapeutic drugs. Additionally CARP-1 is abundant in the benign tissues of colon and breast as well as certain hematopoetic progenitor cells. The polyclonal antibodies to CARP-1 are available for non-exclusive biological materials licensing. A development partner is needed to investigate whether the antibodies may be useful as diagnostic and prognostic tool. Research references: Blood. 2002 Oct 15 100(8):2917-25 J Biol Chem. 2003 Aug 29278(35):33422-35.