subject: Mechanisms Whereby Mesothelioma Tumors Escape Immunosurveillance [print this page] Another interesting study is called, "Control of cell cycle progression in human mesothelioma cells treated with gamma interferon" - Oncogene 2001, vol. 20, no9, pp. 1085-1093 Here is an excerpt: "Abstract - Recombinant human interferon gamma (r-hu-IFN) exerts both antitumoral activity in the early stages of human malignant mesothelioma and a cytostatic effect in human mesothelioma (HM) cell lines in vitro. The antiproliferative effect of interferons (IFNs) reported in a variety of cells has been attributed to several mechanisms. In order to progress in the understanding of HM cell growth modulation by r-hu-IFN, modifications of cell cycle progression and expression of key cell cycle regulator proteins in response to r-hu-IFN were examined. Nine HM cell lines were studied, including one resistant to the antiproliferative effect of r-hu-IFN. Except in the resistant cell line r-hu-IFN produced an arrest in the G1 and G2-M phases of the cell cycle, associated with a reduction in both cyclin A and cyclin dependent kinase inhibitors (CDKIs) expression. Moreover cyclin B1/cdc2 activity was decreased. The present study provides the first evidence of a G2-arrest in r-hu-IFN-treated HM cell lines and indicates that HM cell lines, despite their tumorigenic origin still support cell cycle control. The cell cycle arrest induced by r-hu-IFN seems to depend on cyclin regulation through p21WAF1/CIP1- and p27Kip1-independent mechanisms and is not directly related to the induced DNA damage."
