Abstract: Methods for increasing immune therapy response and predicting likelihood of cancer metastasis by analyzing the expression of genes associated with replication stress response. In some aspects, cancers are treated with immune checkpoint inhibitors and/or MEK inhibitors. Methods for selecting patients by analyzing the expression of genes associated with a defect in replication stress response are also provided.

Abstract: Methods for identifying and treating cancers that are DNA repair, such as homologous recombination (HR) repair, defective or sensitive to PARP inhibitors or platinum-based therapy. In some aspects, DNA repair, such as HR repair, defective cancers are treated with a PARP inhibitor therapy or cisplatin. Methods for sensitizing cancers to a PARP inhibitor therapy are also provided.

Abstract: Methods for increasing immune therapy response and predicting likelihood of cancer metastasis by analyzing the expression of genes associated with replication stress response. In some aspects, cancers are treated with immune checkpoint inhibitors and/or MEK inhibitors. Methods for selecting patients by analyzing the expression of genes associated with a defect in replication stress response are also provided.

Abstract: Methods for identifying and treating cancers that are DNA repair, such as homologous recombination (HR) repair, defective or sensitive to PARP inhibitors or platinum-based therapy. In some aspects, DNA repair, such as HR repair, defective cancers are treated with a PARP inhibitor therapy or cisplatin. Methods for sensitizing cancers to a PARP inhibitor therapy are also provided.

Abstract: Methods for identifying and treating cancers that are homologous recombination (HR)-repair defective. In some aspects, HR defective cancers are treated with a PARP inhibitor therapy. Methods for sensitizing cancers to a PARP inhibitor therapy are also provided.

Abstract: Methods for identifying and treating cancers that are homologous recombination (HR)-repair defective. In some aspects, HR defective cancers are treated with a PARP inhibitor therapy. Methods for sensitizing cancers to a PARP inhibitor therapy are also provided.

Abstract: Cyclin D1 is one of the targets of &bgr;-catenin in breast cancer cells. Transactivation of &bgr;-catenin correlated significantly with cyclin D1 expression both in eight breast cell lines in vitro and in 123 patient samples. More importantly, high &bgr;-catenin activity significantly correlated with poor prognosis of the patients and is a strong and independent prognostic factor in breast cancer (p<0.001). Moreover, by multivariate analyses, the inventors found that activated &bgr;-catenin is a strong prognostic factor which provided additional and independent predictive information on patients survival rate even when other prognostic factors, including lymph node metastasis, tumor size, estrogen receptor and progesterone receptor status, were taken into account (p<0.001). This invention demonstrates that &bgr;-catenin is involved in breast cancer formation and/or progression and may serve as a target for breast cancer therapy.

Abstract: The present invention is directed to association of nuclear receptor tyrosine kinase, such as EGFR, with highly proliferative tissue following its translocation from the cell membrane. The nuclear localization of the receptor tyrosine kinase is affiliated with transcription activity, and the specific sequence associated with such activity, particularly for EGFR, is disclosed.