In BMC Cancer this week, researchers in the US and China report on the role of SOX genes in human prostate cancer. Using gene expression microarray and real-time quantitative reverse transcriptase-PCR, the team found that SOX7, SOX9, and SOX10 were significantly disregulated in four prostate cancer specimens. Further, the team found that SOX7 levels were significantly lower in prostate cancer tissues with higher serum PSA levels and metastasis compared with prostate cancer tissues with low serum PSA levels and no metastasis; increased SOX9 protein expression was found in cancer tissues at higher clinical stage; and SOX10 down-regulation was found in cancer tissues with higher serum PSA levels and advanced pathological stage. "Our data offer the [convincing] evidence that the dis-regulation of SOX7, SOX9 and SOX10 may be associated with the aggressive progression of PCa," the team says. "SOX7 and SOX9 may be potential markers for prognosis in PCa patients. Interestingly, the down-regulation of SOX7 and the up-regulation of SOX9 may be important mechanisms for castration-resistant progression of PCa."
Also in BMC Cancer this week, researchers in Finland report that the rs9282861 polymorphism of the SULT1A1 gene might be a modifier of the efficacy of systemic adjuvant therapy in breast cancer patients. The team used PCR-RFLP to identify the rs9282861 genotypes of 412 early stage breast cancer patients, and then treated 76 patients with adjuvant cyclophosphamide-based chemotherapy, 65 patients with adjuvant tamoxifen, and four patients with both. They found that patients receiving either adjuvant tamoxifen or chemotherapy had a statistically significant improvement in overall survival if they had the rs9282861 homozygous variant AA genotype. "In this prospective study, we observed a previously unreported association between the SULT1A1 rs9282861 genotype and OS of breast cancer patients treated with adjuvant chemotherapy or TAM," the authors write. "This novel finding suggests that the rs9282861 polymorphism modifies the long-term clinical outcome of patients receiving adjuvant TAM or chemotherapy."
Finally in BMC Cancer this week, researchers in Australia and the UK report that the protein menin and p53 have separate effects on tumorigenesis in mice. The team generated mice carrying various combinations of Men1 and Trp53 mutations, and found that homozygous loss of Trp53 in mice resulted in early-onset, aggressive tumors and significantly shorter lifespan, while heterozygous loss of either Trp53 or Men1 caused later onset disease, with a variety of tumors characteristic of each gene. "Simultaneous heterozygous deletion of Men1 in animals with either heterozygous or homozygous deletion of Trp53 did not result in formation of tumors at any new sites, implying additive rather than synergistic effects of these pathways," the authors write. "Mice that were Men1+/- in addition to Trp53+/- had tumors in endocrine as well as other sites, implying that increase in total tumor burden, at sites typically associated with either Men1 or Trp53 loss, contributed to the slight decrease in survival in Men1+/- Trp53+/- animals in comparison with their littermates."