Abstract: This disclosure includes the identification of molecular markers, including ASPM, ATP9A, ACOX3, CD-C45L, SLC40A1, AGR2, and those found in TABLE 2, that are associated with the differentiation and the clinical prognosis of pancreatic cancer. More specifically, the disclosure includes the identification of sets of gene markers whose expression levels can be used to distinguish pancreatic cancers with higher degrees of differentiation from those with lower degrees of differentiation. These markers can be used to predict clinical prognosis of pancreatic cancer, including disease progression, recurrence or death of the hosts. The disclosure also provides methods of treating glandular cancers and kits for assaying glandular cancers, such as pancreatic cancer, breast cancer, and prostate cancer, by inhibiting the expression of ASPM or its ability to activate or maintain the Wnt signaling activity and/or the cancer stem cell populations of said glandular cancers.

Abstract: The present application provides a method for predicting clinical prognosis for a human subject diagnosed with prostate cancer, comprising: detecting an expression level of a marker gene selected from a group consisting of ABCG1, PDCD4, KLF6, ST6, BTD, BANF1, IRS1, ZNF185, ANXA11, DUSP2, KLF4 and DSC2, in a biological sample containing prostate cancer cells obtained from the human subject; and predicting a likehood of the clinical prognosis by comparing the expression level of the marker gene with a reference level. The present application also provides a combination of molecular markers and a kit containing thereof.

Abstract: The present invention relates to methods for prognosis, diagnosis, and treatment of malignant tumors that were treatment resistant. The present invention provides methods of prognosis and diagnosis of multidrug resistant tumors through detection of the expression levels of nuclear co-repressor 2 (“N-CoR2”), histone deacetylases 3 (“HDAC3”), and their associated gene expression biomarkers. The present invention also provides methods of sensitizing tumors to anti-tumor therapeutics by disrupting HDAC3 activation, abrogating the N-CoR2-HDAC3 interaction, inhibiting the activity of either protein, or by downregulating the expression of either protein.

Abstract: The present invention relates to methods for prognosis, diagnosis, and treatment of malignant tumors that were treatment resistant. The present invention provides methods of prognosis and diagnosis of multidrug resistant tumors through detection of the expression levels of nuclear co-repressor 2 (“N-CoR2”), histone deacetylases 3 (“HDAC3”), and their associated gene expression biomarkers. The present invention also provides methods of sensitizing tumors to anti-tumor therapeutics by disrupting HDAC3 activation, abrogating the N-CoR2-HDAC3 interaction, inhibiting the activity of either protein, or by downregulating the expression of either protein.

Abstract: The present invention relates to methods for prognosis, diagnosis, and treatment of malignant tumors that were treatment resistant. The present invention provides methods of prognosis and diagnosis of multidrug resistant tumors through detection of the expression levels of nuclear co-repressor 2 (“N-CoR2”), histone deacetylases 3 (“HDAC3”), and their associated gene expression biomarkers. The present invention also provides methods of sensitizing tumors to anti-tumor therapeutics by disrupting HDAC3 activation, abrogating the N-CoR2-HDAC3 interaction, inhibiting the activity of either protein, or by down-regulating the expression of either protein.

Abstract: The present invention relates to methods for prognosis, diagnosis, and treatment of malignant tumors that were treatment resistant. The present invention provides methods of prognosis and diagnosis of multidrug resistant tumors through detection of the expression levels of nuclear co-repressor 2 (“N-CoR2”), histone deacetylases 3 (“HDAC3”), and their associated gene expression biomarkers. The present invention also provides methods of sensitizing tumors to anti-tumor therapeutics by disrupting HDAC3 activation, abrogating the N-CoR2-HDAC3 interaction, inhibiting the activity of either protein, or by down-regulating the expression of either protein.