RESUMEN
Background: In recent years, several studies have investigated the relationship between platelet to lymphocyte ratio (PLR) and the prognosis of patients with laryngeal cancer, but the results remain controversial. This study aimed to evaluate the prognostic significance of pretreatment PLR in patients with laryngeal cancer. Methods: Up to July 2023, we searched PubMed, PubMed Central, Web of Science, Embase, CNKI and Wanfang databases to collect relevant articles evaluating the relationship between PLR and the prognosis of laryngeal cancer. The pooled hazard ratio (HR) and 95% confidence interval (CI) were calculated using the random effect-model. Results: A total of 14 included studies involving 3220 patients with laryngeal cancer were included. The combined results suggested that elevated PLR was associated with poorer overall survival (HR = 2.21, 95% CI, 1.67 - 2.93, p < 0.001), progression-free survival (HR = 2.54, 95% CI, 1.76-3.66, p < 0.001), recurrence-free survival (HR = 1.87, 95% CI,1.45 - 2.42, p < 0.001), and disease-free survival (HR = 1.46, 95% CI, 1.08-1.98, p < 0.001). Subgroup analysis further confirmed that pretreatment PLR was an independent predictor of OS in laryngeal cancer patients. Conclusion: Higher pretreatment PLR is strongly related to poor prognosis of laryngeal cancer patients. This indicates that PLR has the potential to serve as a valuable biomarker for predicting the prognosis of laryngeal cancer. However, further validations in large prospective cohorts are necessary to confirm its clinical utility and reliability.
RESUMEN
Osteoarthritis (OA) is a highly prevalent joint disorder that is tightly correlated with age. As the body ages, cell replication and function decline until homeostasis can no longer be maintained. This process involves cellular senescence as well as replicative senescence. Telomere length, cell cycle arrest, expression of p16 and p53, and the release of senescence-associated ß-galactosidase (SA-ß-Gal) are all markers of cell senescence. In OA joints, chondrocytes undergo cellular senescence prematurely, thereby ceasing to synthesize and maintain cartilage tissue. Upregulation of proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), and oxidative stress induced by overproduction of reactive oxygen species (ROS) are key events in the pathogenesis of OA. In the present study, we investigated the effects of pinitol, a naturally occurring compound, on the effects of TNF-α on chondrocyte senescence and cell cycle arrest. We found that pinitol has a favorable safety profile in terms of cell viability. Pinitol significantly inhibited cellular senescence and cell cycle arrest in the G0/G1 phase induced by TNF-α. We also found that pinitol could inhibit TNF-α-induced increased telomerase activity and expression of p16 and p53. Importantly, we found that the effects of pinitol may be mediated through rescue of Nrf2 signaling, which is recognized as a key protective factor in OA. This finding was verified through a Nrf2 silencing experiment using Nrf2 siRNA. Together, our findings reveal the potential of pinitol as a safe therapeutic option for the prevention of OA-associated chondrocyte senescence and oxidative stress.
