Abstract: The present invention features methods of diagnosing and prognosticating ovarian tumors by detecting increased expression of an ovarian tumor marker gene in a subject or in a sample from a subject. Also featured are kits for the aforementioned diagnostic and prognostic methods. In addition, the invention features methods of treating and preventing ovarian tumors, and methods of inhibiting the growth or metastasis of ovarian tumors, by modulating the production or activity of an ovarian tumor marker polypeptide. Further featured are methods of inhibiting the growth or metastasis of an ovarian tumor by contacting an ovarian tumor cell with an antibody that specifically binds an ovarian tumor marker polypeptide.

Abstract: The present invention features methods of diagnosing and prognosticating ovarian tumors by detecting increased expression of an ovarian tumor marker gene in a subject or in a sample from a subject. Also featured are kits for the aforementioned diagnostic and prognostic methods. In addition, the invention features methods of treating and preventing ovarian tumors, and methods of inhibiting the growth or metastasis of ovarian tumors, by modulating the production or activity of an ovarian tumor marker polypeptide. Further featured are methods of inhibiting the growth or metastasis of an ovarian tumor by contacting an ovarian tumor cell with an antibody that specifically binds an ovarian tumor marker polypeptide.

Abstract: The present invention features methods of diagnosing and prognosticating ovarian tumors by detecting increased expression of an ovarian tumor marker gene in a subject or in a sample from a subject. Also featured are kits for the aforementioned diagnostic and prognostic methods. In addition, the invention features methods of treating and preventing ovarian tumors, and methods of inhibiting the growth or metastasis of ovarian tumors, by modulating the production or activity of an ovarian tumor marker polypeptide. Further featured are methods of inhibiting the growth or metastasis of an ovarian tumor by contacting an ovarian tumor cell with an antibody that specifically binds an ovarian tumor marker polypeptide.

Abstract: The present invention features methods of diagnosing and prognosticating ovarian tumors by detecting increased expression of an ovarian tumor marker gene in a subject or in a sample from a subject. Also featured are kits for the aforementioned diagnostic and prognostic methods. In addition, the invention features methods of treating and preventing ovarian tumors, and methods of inhibiting the growth or metastasis of ovarian tumors, by modulating the production or activity of an ovarian tumor marker polypeptide. Further featured are methods of inhibiting the growth or metastasis of an ovarian tumor by contacting an ovarian tumor cell with an antibody that specifically binds an ovarian tumor marker polypeptide.

Abstract: Nonsteroidal anti-inflammatory drugs cause a dramatic increase in intracellular ceramide, which induces apoptosis. The ceramide increase is likely mediated by cyclooxygenase inhibition, which elevates arachidonic acid, which stimulates sphingomyelinase, which produces ceramide. Contacting members of this pathway with test compounds and observing their effects provides a method of screening for potential cancer chemopreventative agents.

Abstract: The APC tumor suppressor protein binds to .beta.-catenin, a protein recently shown to interact with Tcf/Lef transcription factors. Here, the gene encoding a Tcf family member that is expressed in colonic epithelium (hTcf-4) was cloned and characterized. hTcf-4 transactivates transcription only when associated with .beta.-catenin. Nuclei of APC.sup.-/- colon carcinoma cells were found to contain a stable .beta.-catenin-hTCF-4 complex that was constitutively active, as measured by transcription of a Tcf reporter gene. Reintroduction of APC removed .beta.-catenin from hTcf4 and abrogated the transcriptional transactivation. Constitutive transcription of TCF target genes, caused by loss of APC function, may be a crucial event in the early transformation of colonic epithelium. It is also shown here that the products of mutant APC genes found in colorectal tumors are defective in regulating .beta.-catenin/Tcf-4 transcrpitional activation.