RESUMO
Objective To explore the prognostic factors of primary mediastinal large B-cell lymphoma (PMBCL) and the effects of chemoradiotherapy versus chemotherapy alone on patients' prognosis before and after rituximab era. Methods We extracted the data of PMBCL patients diagnosed from 2001 to 2015 from SEER database. SEER Stat software was used to calculate the incidence rate. Kaplan-Meier method and Cox regression model were used to analyze the impact of various clinical variables on prognosis. Results We included 635 patients with PMBCL. Multivariate Cox regression analysis showed that age, stage and chemotherapy were independent prognostic factors. Kaplan-Meier survival analysis showed that OS of the patients receiving chemotherapy only in 2006-2015 was significantly better than that in 2001-2005 (χ2=10.002, P=0.002). The patients who received chemoradiotherapy had better OS than those who received chemotherapy alone from 2001 to 2005. The OS and DSS of patients receiving chemoradiotherapy were not significantly different from those of chemotherapy alone from 2006 to 2015. Conclusion The application of rituximab improves the long-term survival of PMBCL patients. The prognosis of patients who received chemoradiotherapy is comparable to that of chemotherapy alone from 2006 to 2015.
RESUMO
In contrast to the well-established genomic 5-methylcytosine (5mC), the existence of N6-methyladenine (6 mA) in eukaryotic genomes was discovered only recently. Initial studies found that it was actively regulated in cancer cells, suggesting its involvement in the process of carcinogenesis. However, the contribution of 6 mA in tongue squamous cell carcinoma (TSCC) still remains uncharacterized. In this study, a pan-cancer type analysis was first performed, which revealed enhanced 6 mA metabolism in diverse cancer types. The study was then focused on the regulation of 6 mA metabolism, as well as its effects on TSCC cells. To these aspects, genome 6 mA level was found greatly increased in TSCC tissues and cultured cells. By knocking down 6 mA methylases N6AMT1 and METTL4, the level of genomic 6 mA was decreased in TSCC cells. This led to suppressed colony formation and cell migration. By contrast, knockdown of 6 mA demethylase ALKBH1 resulted in an increased 6 mA level, enhanced colony formation, and cell migration. Further study suggested that regulation of the NF-κB pathway might contribute to the enhanced migration of TSCC cells. Therefore, in the case of TSCC, we have shown that genomic 6 mA modification is involved in the proliferation and migration of cancer cells.