In BMC Cancer this week, researchers in China and the US examine the association of proteasome activator REGgamma and multiple oncogenic pathways in four human cancers. The team found over-expression of REGgamma in each of those cancers. "We verified elevated REGgamma gene expression in the four types of cancers and identified genes significantly correlated with REGgamma expression, including genes in p53, Myc pathways, and multiple other cancer-related pathways," the authors write. "Our results indicate potentially important pathogenic roles of REGgamma in multiple cancer types and implicate REGgamma as a putative cancer marker."
Also in BMC Cancer this week, researchers in Argentina and Chile report a study on the clinical relevance of ErbB-2 nuclear expression in breast cancer. The team analyzed tissue from 273 primary invasive breast carcinomas — 33.6 percent of the samples were positive for nuclear ErbB-2 and 14.2 percent were positive for membrane ErbB-2. "We identified NuclErbB-2 positivity as a significant independent predictor of worse [overall survival] in patients with MembErbB-2 overexpression," the authors write. "NuclErbB-2 was also a biomarker of lower OS in tumors that overexpress MembErbB-2 and lack steroid hormone receptors. … Patients presenting NuclErbB-2 may need new therapeutic strategies involving specific blockage of ErbB-2 nuclear migration."
Finally, researchers in the US and Norway report that cytoplasmic BRMS1 expression is associated with increased disease-free survival in malignant melanoma patients. The team examined 155 primary melanoma samples, 60 metastases, and 15 nevi for BRMS1 expression — 87 percent of nevi expressed BRMS1 in the nucleus, compared to 20 percent of primary melanomas and 48 percent of metastases. "When intensity and percentage BRMS1 positive cells were analyzed separately, intensity remained associated with tumor thickness and ulceration but was inversely associated with expression of proliferation markers," the authors write. "Our data suggest that BRMS1 is localized in cytoplasm and nucleus of melanocytic cells and that cellular localization determines its in vivo effect. We hypothesize that cytoplasmic BRMS1 restricts melanoma progression while nuclear BRMS1 possibly promotes melanoma cell invasion."