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Enhanced recovery after surgery (ERAS) protocol has widely gained acceptance in gynecological surgery. Its safety and efficacy should be evaluated fully via well-designed, randomized, control trials. The main objective of our study is to compare the ERAS protocol with the conventional perioperative care program after gynecological oncology. Furthermore, the secondary objectives of our study are the identification of markers that allow us to evaluate the effectiveness of the application of ERAS elements in the modulation of the body’s response to surgical stress.

Patients with gynecological tumors indicated for surgery were randomly assigned to either the ERAS group or the conventional group. The ERAS protocol included short fasting time, fluid restriction, early oral feeding, reduced opioid consumption and immediate mobilization after surgery. The primary endpoint was the reduction of hospital stay in the ERAS group. The day of first flatus, postoperative nausea and vomiting (PONV), maximum pain score by how ERAS protocols modulate gynecological oncology surgery.

The trial was registered in ClinicalTrials.gov (NCT03629626).

The trial was registered in ClinicalTrials.gov (NCT03629626).

The survival outcome of lung cancer patients with coexisting liver cirrhosis has thus far received limited attention in the literature. In this study, we evaluated whether liver cirrhosis is an independent risk factor for the survival of patients with lung cancer.

We conducted a retrospective, multicenter, propensity-matched study of lung cancer patients with and without liver cirrhosis. To determine differences in survival, we sought to identify risk factors associated with poor outcomes using Kaplan-Meier survival analysis and Cox proportional hazards regression.

There were no statistically significant differences in the baseline clinical characteristics of patients between the cirrhosis and non-cirrhosis groups. The median overall survival of patients with and without cirrhosis was 13.07 months (95% confidence interval [CI] 10.56-16.84) and 13.67 months (95% CI 10.42-16.91), respectively (p=0.76). Cox proportional hazards regression analysis revealed that liver cirrhosis was not an independent risk factor for poor outcome (hazard ratio [HR] 1.057, 95% CI 0.805-1.388, p=0.690). In patients with cirrhosis, lower serum albumin levels, higher Charlson Comorbidity Index score, advanced-stage lung cancer, and treatment modality were factors associated with poor outcome. Increase in serum albumin by 1 g was associated with a 30% reduction in the risk of mortality (HR 0.700, 95% CI 0.494-0.993, p=0.045). Mirdametinib While every point increase in the Charlson Comorbidity Index score by 1 point was linked to a 9% higher risk of mortality (HR 1.090, 95% CI 1.023-1.161, p=0.007).

The survival rates of lung cancer patients with and without cirrhosis did not differ significantly. Higher serum albumin levels and lower Charlson Comorbidity Index scores were associated with improved survival.

The survival rates of lung cancer patients with and without cirrhosis did not differ significantly. Higher serum albumin levels and lower Charlson Comorbidity Index scores were associated with improved survival.

Grape seed proanthocyanidins (GSPs) have been shown to inhibit the progression of many cancers, including cutaneous squamous cell carcinoma (CSCC). Circular RNA (circRNA) is a key regulator for cancer progression. However, it is unclear whether GSPs can mediate the progression of CSCC by regulating circRNA.

Quantitative real-time PCR was conducted to determine the expression of hsa_circ_0070934, microRNA (miR)-136-5p and prenylated Rab acceptor family 2 (PRAF2). MTT assay and colony formation assay were used to assess cell proliferation. Cell cycle process and apoptosis were detected by flow cytometry, and cell migration and invasion were measured by transwell assay. Western blot analysis was utilized to examine protein expression. In addition, dual-luciferase reporter assay and RIP assay were used to evaluate the interaction between miR-136-5p and hsa_circ_0070934 or PRAF2. Subcutaneous xenograft models were constructed to explore the function of GSPs on CSCC tumor growth in vivo.

GSPs could reduce hsa_circ_0070934 expression and inhibit CSCC cell proliferation, cell cycle process, migration, invasion, while promote apoptosis. Overexpressed hsa_circ_0070934 could reverse the suppressive effect of GSPs on CSCC cell progression. MiR-136-5p could be sponged by hsa_circ_0070934, and its overexpression also abolished the positively regulation of hsa_circ_0070934 on the progression of GSPs-induced CSCC cells. PRAF2 was a target of miR-136-5p, and its expression could be decreased by GSPs and increased by hsa_circ_0070934. The inhibitory effect of miR-136-5p on CSCC cell progression could be reversed by PRAF2 overexpression. Additionally, GSPs also could inhibit CSCC tumor growth in vivo.

Our data showed that GSPs regulated the hsa_circ_0070934/miR-136-5p/PRAF2 axis to restrain CSCC progression.

Our data showed that GSPs regulated the hsa_circ_0070934/miR-136-5p/PRAF2 axis to restrain CSCC progression.The canonical model for hereditary cancer predisposition is a cancer predisposition gene (CPG) that drives either one or both of two fundamental hallmarks of cancer, defective genomic integrity and deregulated cell proliferation, ultimately resulting in the accumulation of mutations within cells. Thus, the genes most commonly associated with cancer-predisposing genetic syndromes are tumor suppressor genes that regulate DNA repair (eg, BRCA1, BRCA2, MMR genes) and/or cell cycle (eg, APC, RB1). In recent years, however, the spectrum of high-penetrance CPGs has expanded considerably to include genes in non-canonical pathways such as oncogenic signaling, metabolism, and protein translation. We propose here that, given the variety of pathways that may ultimately affect genome integrity and cell proliferation, the model of cancer genetic predisposition needs to be expanded to account for diverse mechanisms. This synthesis calls for modeling and multi-omic studies applying novel experimental and computational approaches to understand cancer genetic predisposition.