These results suggest that combination therapy with cisplatin and gefitinib may increase the therapeutic efficacy of cisplatin by blocking EGFR downstream signaling and/or inhibiting DNA repair in ovarian cancer.
EGFR gene mutations were frequently observed in not only non-small-cell lung cancer (NSCLC), but also in ovarian cancer in Japanese patients. the selective EGFR inhibitor Gefitinib might therefore offer some benefit in patients with EGFR mutations in ovarian cancer.
Although anti-EGFR-targeted therapy has shown limited clinical activity in ovarian cancer to date, a recent report suggests that activation of ErbB3, one of the members of the EGFR family, may support the growth and proliferation of ovarian cancer cells and that ErbB3 may therefore serve as a potential therapeutic target in this disease.
This new integral pathway in the EGFR-driven mitogenic cell response, which through its key player E2F3a was found to be essential in triggering proliferation in ovarian cancer cells, provides new insights into EGFR signaling and could represent the basis for appealing new therapeutic approaches in ovarian cancer.
Importantly, overexpression of the epidermal growth factor receptor (EGFR) in ovarian cancer correlates with poor disease outcome and induces EMT in ovarian cancer cells.
Upregulation of the EGF-R by integrin alphavbeta3, both receptor molecules with a well-defined role as targets for cancer treatment, might represent an additional mechanism to adapt synergistic receptor signaling and crosstalk in response to an altered tumor cell microenvironment during ovarian cancer progression.
We hypothesize short AR allelotypes promote aggressive ovarian cancer phenotype through modulation of epidermal growth factor receptor (EGFR) signaling.
This data suggests that EGFR-inhibitors, such as gefitinib, have the potential to modulate common mechanisms of drug resistance and may have a role in optimizing chemotherapy regimens for the treatment of ovarian cancer.
The over-expression of the epidermal growth factor receptor (EGFR) is associated with the majority of ovarian cancer and has been implicated in the process of malignant transformation by promoting cell proliferation, survival, and motility.
Collectively, our data indicate that EGFR and TrkB crosstalk each other in response to EGF and BDNF, leading to cell survival pathway activation in ovarian cancer cells.