In Cancer this week, researchers in China identify a gene-expression signature for predicting lymph-node metastasis in patients with early-stage cervical carcinoma. The team studied 88 women with cervical carcinoma — 23 with pelvic lymph-node metastasis, and 65 without — divided into a training group and a test group. The team developed a gene expression signature for predicting pelvic lymph-node metastasis from the training group that includes 11 genes. "In the test group, the signature's accuracy, sensitivity, specificity, positive predictive value, and negative predictive value were 91 percent, 90.9 percent, 93.9 percent, 83.3 percent, and 96.9 percent, respectively, for predicting pelvic lymph-node metastasis," the team writes. "A multivariate analysis demonstrated that patients with 11-gene high-risk scores [had] a 33-fold increased risk for pelvic lymph-node metastasis compared with patients who had low-risk scores. The 5-year overall and disease-free survival rates for patients who had 11-gene high-risk scores were marginally significantly lower than the rates for patients who had 11-gene low-risk scores."
Also in Cancer this week, an international group of researchers presents findings from a study of the association between an aromatase promoter gene polymorphism and the risk of non-viral hepatitis-related hepatocellular carcinoma. Experimental studies shows that sex hormones may induce or promote the development of hepatocellular carcinoma, the team writes, and androgens are converted to estrogens by aromatase, a product of the CYP19 gene. "Hepatic aromatase level and activity have been shown to be markedly elevated in HCC. Aromatase expression in liver tumors is driven by a promoter upstream of CYP19 exon I.6," the authors add. In this study, they identified a polymorphism in CYP19 and found epidemiological evidence "for the role of hepatic aromatization of androgen into estrogen in the development of nonviral hepatitis-related HCC."
And finally in Cancer this week, researchers in Taiwan write that a novel exon 15-deleted, splicing variant of Slit2 shows potential to inhibit growth and invasion in lung cancer. The team analyzed Slit2 expression in 27 lung adenocarcinomas and found that "exon 15 modulates Slit2 function in growth inhibition of lung cancer cells." Because the splice variant is present in low invasive cancer cells and non-cancerous lung tissue, the authors say that loss of this variant contributes significantly to tumor progression and invasion.