Abstract: An adenoviral vector which expresses a dominant negative form of Stat3 called Stat3-EVA for the treatment of non-small cell lung carcinoma. This construct has two mutations in the DNA binding site of Stat3 which prevents binding to DNA but has no effect on tyrosine phosphorylation or dimerization.

Abstract: Provided is a method and vector for modulating apoptosis in a target cell population. Flavopiridol treatment leads to apoptosis via a mechanism associated with downregulation of Mcl-1. E2F1 leads to transcriptional repression of Mcl-1 and subsequently apoptosis. Given the ability of cyclin/cyclin-dependent kinase 2 antagonists to kill transformed cells, flavopiridol may stabilize E2F1 and enhance apoptosis via repression of Mcl-1. Flavopiridol is associated with a dose-dependent increase in E2F1 protein levels, a corresponding reduction in Mcl-1, and apoptosis in lung carcinoma cells. Treatment of cells with 200 nM flavopiridol results in the rapid elevation of E2F1 and reduction in Mcl-1 levels within 12 hours of treatment. The elevation of E2F1 and reduction in Mcl-1 clearly precedes the induction of apoptosis.

Abstract: Methods are provided for predicting responsiveness of cancer cells to chemotherapy by measuring the level of phosphorylated Stat or the level of expression of Survivin in a cancer and comparing the level in the cancer cell to the respective level in a control. Also provided are methods of selecting a chemotherapeutic treatment for a subject diagnosed with cancer by measuring the level of phosphorylated Stat or the level of expression of Survivin in a cancer and comparing the level in the cancer cell to the respective level in a control. Kits for performing the methods are also provided. Methods for modulating Survivin-dependent apoptosis in a cancer cell are also disclosed.