Screening of differentially expressed genes and identification of AMACR as a prognostic marker in prostate cancer.

Prostate cancer, the second most common cancer found in male over the world, was estimated to have 191,930 new cases and 33,330 deaths in 2020 in the United States. Prostate cancer is very common in male, about 12.1% of men will acquire this cancer in their lifetime, and a higher risk was reported in older men and African American men. Gene deregulations have been found to be extensively associated with cancer development. To gain further insight into how gene deregulation affects prostate cancer, we analysed three gene profiling datasets of prostate cancer from Gene Expression Omnibus (GEO) applying bioinformatic tools in our study. Firstly, we identified common differently expressed genes (DEGs) shared by the three gene profiling datasets, constructed protein-protein interaction network and determined top 10 hub genes. Further DEGs validation in TCGA and Human Protein Atlas Database identified AMACR as the core gene. We then analysed the role of AMACR in prostate cancer cell lines and found that AMACR-knockdown resulted in the decreased cell proliferation and increased apoptosis. These results suggest an oncogenic role of AMACR in prostate cancer, and it could be a potential biomarker for the diagnosis of prostate cancer.

Associations between body mass index and the risk of mortality from lung cancer: A dose-response PRISMA-compliant meta-analysis of prospective cohort studies.

BACKGROUND: Whether body mass index (BMI) is associated with the risk of mortality from lung cancer (LC) is controversial, and the shape of dose-response relationship on this topic is not well-established. Thus, a dose-response meta-analysis was performed to clarify this association. METHODS: A search of PubMed and EMBASE was conducted, and 2-stage random-effect dose-response model was used to yield summary relative risks and its shape. RESULTS: Fifteen prospective cohort studies were eligible for inclusion criteria. The combined relative risks per 5 kg/m in BMI for risk of LC mortality is 0.94 (95% confidence interval] 0.92-0.96), and nonlinear association was found (Pnonlinearity < .0001), which indicated that compared with higher BMI, lower BMI showed higher LC mortality risk. Subgroup analyses revealed that this obesity paradox remained regardless of number of cases, follow-up duration, and study location, but this relationship was not observed among nonsmokers. CONCLUSION: A nonlinear association between BMI and the risk of LC mortality was found, and higher BMI participants have a lower risk of LC death than slim people.