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1.

Objective

Comparative survival between neoadjuvant chemotherapy and adjuvant chemotherapy for patients with cT2-4N0-1M0 non–small cell lung cancer has not been extensively studied.

Methods

Patients with cT2-4N0-1M0 non–small cell lung cancer who received platinum-based chemotherapy were retrospectively identified. Exclusion criteria included stage IV disease, induction radiotherapy, and targeted therapy. The primary end point was disease-free survival. Secondary end points were overall survival, chemotherapy tolerance, and ability of Response Evaluation Criteria In Solid Tumors response to predict survival. Survival was estimated using the Kaplan–Meier method, compared using the log-rank test and Cox proportional hazards models, and stratified using matched pairs after propensity score matching.

Results

In total, 330 patients met the inclusion criteria (n = 92/group after propensity-score matching; median follow-up, 42 months). Five-year disease-free survival was 49% (95% confidence interval, 39-61) for neoadjuvant chemotherapy versus 48% (95% confidence interval, 38-61) for adjuvant chemotherapy (P = .70). On multivariable analysis, disease-free survival was not associated with neoadjuvant chemotherapy or adjuvant chemotherapy (hazard ratio, 1.1; 95% confidence interval, 0.64-1.90; P = .737), nor was overall survival (hazard ratio, 1.21; 95% confidence interval, 0.63-2.30; P = .572). The neoadjuvant chemotherapy group was more likely to receive full doses and cycles of chemotherapy (P = .014/0.005) and had fewer grade 3 or greater toxicities (P = .001). Response Evaluation Criteria In Solid Tumors response to neoadjuvant chemotherapy was associated with disease-free survival (P = .035); 15% of patients receiving neoadjuvant chemotherapy (14/92) had a major pathologic response.

Conclusions

Timing of chemotherapy, before or after surgery, is not associated with an improvement in overall or disease-free survival among patients with cT2-4N0-1M0 non–small cell lung cancer who undergo complete surgical resection.  相似文献   
2.

Background

There were few studies assessed the postoperative sarcopenia in patients with cancers. The objective of present study was to assess whether postoperative development of sarcopenia could predict a poor prognosis in patients with adenocarcinoma of esophagogastric junction, (AEG) and upper gastric cancer (UGC).

Methods

Patients with AEG and UGC who were judged as non-sarcopenic before surgery were reassessed the presence of postoperative development of sarcopenia 6 months after surgery. Patients were divided into the development group or non-development group, and clinicopathological factors and prognosis between these two groups were analyzed.

Results

The 5-year overall survival rates were significantly poorer in the development group than non-development group (68.0% vs. 92.6%, P?=?0.0118). Multivariate analyses showed that postoperative development of sarcopenia was an independent prognostic factor for poor overall survival (P?=?0.0237).

Conclusions

Postoperative development of sarcopenia was associated with a poor prognosis in patients with AEG and UGC.  相似文献   
3.
Mammary carcinoma (MC) is one of most common malignancy in women, and ring finger protein 2 (RNF2) possesses various roles in vast human tumors. In MC tissues as well as in cell lines RNF2 exhibited high expression, had significant association with tumor size, lymph node status, TNM stage, patients’ poor survival, and promoted cell proliferation, colony formation, cell migration and invasion of MC cell lines which was mediated by downregulation of E-cadherin protein. These data reveal that RNF2 protein plays a vital role in the development of MC and may be a potential therapy target of MC.  相似文献   
4.
目的研究正常国人新鲜尸体股骨上端松质骨的拉伸粘弹性力学性质,为临床提供生物力学参数。方法对股上端松质骨试样纵向进行拉伸应力松弛及蠕变实验。得到股骨上端松质骨纵向的应力松弛及蠕变数据和曲线。对实验数据进行归一化处理。结果分别用对数、指数一元回归分析的方法处理数据,得出了归一化应力松弛、归一化蠕变函数及曲线。结论股骨上端松质骨拉伸应力松弛7200s应力松弛量为0.422MPa,7200s蠕变量为0.784%。  相似文献   
5.
Hypertrophic cardiomyopathy (HCM) is the most common genetic cardiac disease and is an important cause of sudden death in patients of all ages. The aim of this study was to find out whether Toll-like receptor-4 (TLR4) polymorphism is associated with HCM. To explore the association between TLR4 gene polymorphisms and HCM, 486 HCM patients and 214 healthy controls were enrolled in a case–control study of Chinese Han population. Two single nucleotide polymorphisms (SNPs) in the promoter region of TLR4 gene, ?728G > C (rs11536865) and ?2081G > A (rs10983755), were genotyped by PCR restriction fragment length polymorphism (PCR-RFLP). The associations between TLR4 SNPs and overall survival (OS) of HCM patients were analyzed by the Kaplan–Meier estimation method and Cox proportional hazards regression analysis. Serum TLR4 level was determined by ELISA. Our results showed that the C allelic frequency of ?728G > C and A allelic frequency of ?2081G > A were higher in HCM patients than those in controls (P < 0.001). The ratios of genotype frequencies for both SNPs were associated with HCM susceptibility under three genetic models (P < 0.01). Two SNPs were also associated with the OS in HCM patients (P < 0.001). The CC genotype of ?728G > C and AA genotype of ?2081G > A were associated with poor prognosis of HCM (P < 0.001). Moreover, HCM patients had a higher serum TLR4 level compared with the controls (242.6 pg/ml versus 135.7 pg/ml, P = 0.027). In addition, significant associations were observed between CC genotype of ?728G > C or AA genotype of ?2081G > A and plasma TLR4 level (P < 0.01). The results of this study indicated that TLR4 polymorphisms may be a genetic susceptibility factor for HCM in the Han Chinese population.  相似文献   
6.
7.
The field of mechanistic chemical carcinogenesis has evolved with the advent and advances in genomic, proteomic and metabolomic technologies. These advances allow mechanistic events along the process of exposure to frank tumors to be studied in great detail. Herein is reviewed an example of this approach using, propiconazole, a triazole-containing antifungal agent that is a mouse hepatocarcinogen. This review will highlight those toxicological, genomic, proteomic and metabolomic findings in mice that were used to describe a set of linked events that lead to propiconazole-induced hepatocarcinogenesis. Independent experimental proof of many of these events is presented that solidified this proposed mechanism of carcinogenic action for propiconazole.  相似文献   
8.

Purpose

To determine the association of micropapillary urothelial carcinoma (MUC) variant histology with bladder cancer outcomes after radical cystectomy.

Materials and Methods

Information on MUC patients treated with radical cystectomy was obtained from five academic centers. Data on 1,497 patients were assembled in a relational database. Tumor histology was categorized as urothelial carcinoma without any histological variants (UC; n?=?1,346) or MUC (n?=?151). Univariable and multivariable models were used to analyze associations with recurrence-free (RFS) and overall (OS) survival.

Results

Median follow-up was 10.0 and 7.8 years for the UC and MUC groups, respectively. No significant differences were noted between UC and MUC groups with regard to age, gender, clinical disease stage, and administration of neoadjuvant and adjuvant chemotherapy (all, P ≥ 0.10). When compared with UC, presence of MUC was associated with higher pathologic stage (organ-confined, 60% vs. 27%; extravesical, 18% vs. 23%; node-positive, 22% vs. 50%; P < 0.01) and lymphovascular invasion (29% vs. 58%; P < 0.01) at cystectomy. In comparison with UC, MUC patients had poorer 5-year RFS (70% vs. 44%; P < 0.01) and OS (61% vs. 38%; P < 0.01). However, on multivariable analysis, tumor histology was not independently associated with the risks of recurrence (P?=?0.27) or mortality (P?=?0.12).

Conclusions

This multi-institutional analysis demonstrated that the presence of MUC was associated with locally advanced disease at radical cystectomy. However, clinical outcomes were comparable to those with pure UC after controlling for standard clinicopathologic predictors.  相似文献   
9.
BackgroundChronic subdural haematoma (CSDH) is one of the most commonly treated condition in neurosurgery. It affects elderly populations who often have significant medical co-morbidities resulting in poor prognosis. The study aimed at identifying clinical factors influencing the survival following surgical management of CSDH.MethodsRetrospective study included 267 cases that underwent surgery for CSDH and followed over 5-year period (2010–2015); data retrieved with reference to operation details, radiology reports and discharge. Using logistic and Cox regression analysis, the patient survival data was analysed with respect to patient demographics, type of surgery, co-morbidities, anticoagulation treatment, and discharge destination.ResultsThe overall survival in the cohort was 37.0 months (IQR: 20.0–60.0). The median age of the patients was 76 years (IQR: 66–82) and the median length of hospital stay was 10 days (range 1–126 days; IQR: 6–17 days). The recurrence rate was 6.37% (n = 17). Fifty-three (19.85%) patients recorded deceased on the IPM database as of October 2016 and of those 11 died in hospital. Univariate Cox-regression analysis revealed increased age (HR: 1.80; 95%CI: 1.04–3.11), length of hospital stay (HR: 2.50; 95%CI: 1.41–4.41) and number of co-morbidities (HR: 2.19; 95%CI: 1.26–3.79) were associated with poor prognosis. Glasgow coma scale (GCS) at discharge was found to be significantly associated with survival whilst anticoagulation treatment did not. Multivariate analysis confirmed similar findings significant statistically.ConclusionAge at admission, median length of hospital stay, number of co-morbidities, GCS at discharge and discharge destination have been found to influence survival significant statistically.  相似文献   
10.
Cancer cells undergo genetic changes allowing their adaptation to environmental changes, thereby obtaining an advantage during the long metastatic route, disseminated of several changes in the surrounding environment. In particular, plasticity in cell motility, mainly due to epigenetic regulation of cancer cells by environmental insults, engage adaptive strategies aimed essentially to survive in hostile milieu, thereby escaping adverse sites. This review is focused on tumor microenvironment as a collection of structural and cellular elements promoting plasticity and adaptive programs. We analyze the role of extracellular matrix stiffness, hypoxia, nutrient deprivation, acidity, as well as different cell populations of tumor microenvironment.  相似文献   
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