Combination therapy with ATO and PTL has an augmented anticancer effect on pancreatic cancer in vitro and in vivo, which provides a novel promising approach in the treatment of pancreatic cancer. The mechanism of growth-suppressive effect of combination therapy was correlated with its ability to induce reactive oxygen species generation and apoptosis via the mitochondrial pathway.

Background: Epidemiological evidence supports a role for the insulin-like growth factors (IGFs) and their receptor, IGF-IR, in the induction and progression of various cancers. Estrogen receptor alpha (ERΑ), which plays a role in the etiology of ovarian cancer, both regulates and is influenced by the IGF family. Patients and Methods: We present a case control study conducted in the Northeast region of China between 2007 and 2008. Fresh specimens were collected from ovarian cancer patients and matched controls who underwent surgery for benign diseases. IGF-I, IGF-IR, and ERΑexpression was analyzed using quantitative real-time polymerase chain reaction. Results: Expression of IGF-I and IGF-IR was increased in ovarian cancer compared to benign tumors. The association was dose-dependent and was more evident in premenopausal women than in postmenopausal women. Both IGF-I and IGF-IR expression were found to be higher in tumors with poor prognosis. Patients with either suboptimal debulking or with residual tumor after surgery had slightly higher IGF-IR expression. Intratumoral IGF-I expression was positively correlated with the expression of IGF-IR, but not with ERΑ. Conclusion: The increased intratumoral IGF-I and IGF-IR expression suggests an involvement of the IGF-I/IGF-IR axis in the biological behavior of ovarian cancers in this population and could define a potential therapeutic target.

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