In BMC Cancer this week, researchers in Ohio say oncostatin M promotes STAT3 activation, VEGF production, and invasion in osteosarcoma cell lines. Using RT-PCR and western blotting to interrogate the consequences of oncostatin M and IL-6 stimulation in osteosarcoma cells, the researchers found that the oncostatin receptor is expressed by all human osteosarcoma cells lines, and that treatment of the cell lines with the oncostatin "induced phosphorylation of STAT3, Src, and JAK2. OSM stimulation also resulted in a dose dependent increase in MMP2 activity and VEGF expression that was markedly reduced following treatment with the small molecule STAT3 inhibitor LLL3." Oncostatin M and its receptor may prove to be a novel therapeutic target for osteosarcoma, the authors add.
Also in BMC Cancer this week, researchers in Italy present their findings of a study on erbB2 copy number variations in the plasma of patients with esophageal carcinoma. Mortality in esophageal carcinoma is high, so the research team sought to find isolates of cell-free DNA in the plasma of esophageal carcinoma patients, and found that the real-time PCR assays for erbB2 showed "significant" CNVs in patients as compared with healthy individuals. "These variations in erbB2 were negatively correlated to the progression free survival of these patients, and revealed a further risk category stratification of patients with low VEGF expression levels," the authors write. "The copy number variation of erbB2 gene from plasma can be used as prognostic marker for early detection of patients at risk of worse clinical outcome."
And finally in BMC Cancer this week, researchers in Israel present their findings on a study of inflammatory mediators in breast cancer. The inflammatory chemokines CCL2 and CCL5, and the inflammatory cytokines TNFalpha and IL-1beta have been shown to contribute to the development and metastasis of breast cancer. In their study, which looked to determine whether these factors affect breast cancer progression, the team found that levels of CCL2, CCL5, TNFalpha, and IL-1beta were very low in normal breast tissue and "significantly elevated" in tumor cells. "These results suggest progression-related roles for TNFalpha and IL-1beta in breast cancer," the authors write. "Our findings suggest that the coordinated expression of CCL2 & CCL5 and TNFalpha & IL-1beta may be important for disease course, and that TNFalpha & IL-1beta may promote disease relapse."