Role of glutathione-S-transferase gene P1 in the diagnosis of prostate cancer in patients with 'grey level' prostate-specific antigen values.

Prostate cancer (PC) represents the second most frequent cancer diagnosis in men and, at the same time, is one of the top six causes of death worldwide. The aim of the present study was to evaluate the diagnostic value of glutathione-S-transferase gene P1 (GST-P1) in patients that fall within the 'grey area' of the prostate-specific antigen (PSA) values. A retrospective observational study on 80 patients with prostate abnormal volumes and PSA values in the range 4-10 ng/ml was performed. The prostate gland was extracted following transrectal ultrasonography, and GST-P1 gene expression was analysed. A histopathological examination was considered the gold standard for PC diagnosis. Among the 53 patients diagnosed with PC, 69.8% (n=37) were GST-P1-positive, whereas, among the 27 patients diagnosed with benign prostatic hyperplasia, 18.5% (n=5) were GST-P1-positive. The sensitivity for diagnosing PC in patients with PSA values between 4 and 10 ng/ml was 69.81%, and the specificity was 81.48%. The positive predictive value was 88.1% [95% confidence interval (CI), 74.37-96.02%] and the negative predictive value was 57.89% (95% CI, 40.82-73.69%). Collectively, these results show the potential of using GST-P1 gene expression in patients who are suspected of having PC, but where the PSA values are inconclusive.

A review of NTRK fusions in cancer.

The family of the neurotrophic tropomyosin kinase receptors (NTRK or TRK) is a part of the transmembrane tyrosine kinases responsible for neuronal development. The members of this receptor family are TRKA, TRKB and TRKC and they are encoded by the genes NTRK1, NTRK2 and NTRK3. Alterations of NTRK genes can induce carcinogenesis both in neurogenic and non-neurogenic cells. The prevalence of NTRK gene fusion is under 1% in solid tumors, but is highly encountered in rare tumors. The presence of NTRK 1 gene fusion is associated, in some types of neoplasia, with a favorable evolution, but the presence of NTRK 2 may be associated with a poor prognosis. The identification of cancer patients harboring NTRK gene fusions is constantly growing, especially with the advent of NTRK inhibitors. This has promisingly provided a rationale for personalized therapeutics that improved outcomes in settings with this signature.