Abstract: Provided herein are methods related to methods of predicting sensitivity to NER-targeting agents for the treatment of cancer. In one aspect, provided herein is a method for treating cancer in a subject) of at least 0.70 and the anti-cancer treatment comprises an alkylating chemotherapeutic agent.

Abstract: The present invention is based, in part, on the identification of novel methods for defining predictive biomarkers of response to anti-cancer drugs.

Abstract: The present invention is based, in part, on the identification of novel methods for defining predictive biomarkers of response to anti-cancer drugs.

Abstract: The present disclosure provides methods of identifying or characterizing prostate cancer comprising detecting in a biological sample the presence or absence of a genomic rearrangement that results in a deletion of an LSAMP gene and detecting in a biological sample the presence or absence of a genomic rearrangement that results in a deletion of a CHD1 gene. In certain embodiments, the patient self-identifies as being of African descent. Also disclosed herein are methods of testing for the presence of genomic rearrangements in an LSAMP gene and a CHD1 gene in a biological sample. The LSAMP and CHD1 genomic rearrangements serves as a biomarker for prostate cancer and can be used to stratify prostate cancer based on ethnicity or the severity or aggressiveness of prostate cancer and/or identify a patient for prostate cancer treatment. Also provided are kits for diagnosing and prognosing prostate cancer and methods of selecting a targeted prostate cancer treatment for a patient.

Abstract: The present invention is based, in part, on the identification of novel methods for defining predictive biomarkers of response to anti-cancer drugs.

Abstract: The present invention is based, in part, on the identification of novel methods for defining predictive biomarkers of response to anti-cancer drugs.

Abstract: The present invention is based, in part, on the identification of novel methods for defining predictive biomarkers of response to anti-cancer drugs.

Abstract: The present invention is based, in part, on the identification of novel methods for defining predictive biomarkers of response to anti-cancer drugs.

Abstract: The present invention is based, in part, on the identification of novel methods for defining predictive biomarkers of response to anti-cancer drugs.

Abstract: Provided is a method of predicting the prognosis of a patient with ovarian cancer by determining the total number of somatic exome mutations per genome (Nmut) and status of the BRCA1 and/or BRCA2 in the subject.

Abstract: The present invention is based, in part, on the identification of novel methods for defining predictive biomarkers of response to anti-cancer drugs.

Abstract: The present invention is based, in part, on the identification of novel methods for defining predictive biomarkers of response to anti-cancer drugs.

Abstract: The present teachings provide methods for predicting the clinical outcome of the treatment of human solid tumors. In some embodiments, the method includes measuring in the cells of a tumor the expression level of a set of genes whose change is related to chromosomal instability; taking a statistical measure of the expression level of the set of measured genes; and if the statistical measure of the expression level of the set of measured genes is elevated, determining that the prognosis is poor. Another aspect of the present teachings is the sets of genes, which are useful in predicting the outcome of treatment of solid tumors.

Abstract: Disclosed are modified bryostatins and their use as anticancer drugs.

Abstract: The present invention relates to a method of inhibiting a protein kinase C-mediated biological response, such as, hyperplasia. The method comprises administering to a mammal a non-tumor promoting 12-deoxyphorbol ester. Phorbol esters suitable for use in the method include 12-deoxyphorbol 13-monoesters wherein the ester is a formate, acetate, propionate, butyrate, pentanoate, hexanoate, benzoate or phenylacetate ester.

Abstract: The present invention relates to a method of inhibiting the protein kinase C-mediated biological response inflammation. The method comprises administering to a mammal a non-tumor promoting 12-deoxyphorbol ester. Phorbol esters suitable for use in the method include 12-deoxyphorbol 13-monoesters wherein the ester is a formate, acetate, propionate, butyrate, pentanoate, hexanote, benzoate or phenylacetate ester. The invention also relates to novel 12-deoxyphorbol 13-monoesters, wherein the ester can be a formate, propionate, butyrate or pentanoate ester, and to pharmaceutical compositions comprising same.

Abstract: The present invention provides a method of inhibiting neoplasia and tumor promotion. The method comprises administering to a mammal, particularly a human, in need thereof an effective amount of a 12-deoxyphorbol ester, particularly a 12-deoxyphorbol 13-monoester such as 12-deoxyphorbol 13-acetate (prostratin) and 12-deoxyphorbol 13-phenylacetate (dPP).

Abstract: The present invention relates to labelled resiniferatoxin and congeners thereof. Preferably, the labelled compounds of the invention are radio or fluorescently labelled. The invention is further directed to compositions comprising these labelled compounds, as well as to methods of using these compounds.