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t factors impacting the outcome identified here should be considered in future cancer research on disparities.The purpose of this article was to explore the association of tumor size with lymph node metastases (LNM) risk in patients with clear cell renal cell carcinoma (ccRCC). Based on the Surveillance, Epidemiology, and End Result (SEER) database, patients diagnosed with ccRCC from 1988 to 2015 were included in this study. For each patient, personal characteristics, clinicopathological data, and survival outcomes were, respectively, collected. Subsequently, the odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to investigate the potential risk factors for LNM in ccRCC. Finally, Kaplan-Meier (KM) survival plots of overall survival (OS) and ccRCC-specific survival (CSS) were evaluated on the basis of different tumor sizes. A total of 8,292 patients were finally enrolled in the study, 1,170 of whom (14.11%) had LNM. According to the heatmap, we could intuitively interpret that larger tumor size was related to an increased risk of LNM obviously. The risk of LNM was evidently greater for larger tumor size (4-7 cm OR = 2.415, 95% CI = 1.708-3.415; 7-10 cm OR = 3.746, 95% CI = 2.677-5.242; and >10 cm OR = 4.617, 95% CI = 3.302-6.457) compared with smaller tumor size (≤4 cm). According to the KM survival plots of OS and CSS, we observed a gradual decline in survival with increasing tumor size, while the smallest tumor size had the best survival outcomes. These results indicated the positive relationship of tumor size with risk of LNM in ccRCC. And we also noticed continual decrease survival rates of OS and CSS with increasing tumor size.The aim is to evaluate the clinical consequences of coinfection between HPV 16 and other high-risk HPVs among women with a histological diagnosis of CIN or invasive cervical cancer. A total of 2985 women, with a diagnosis of either CIN or cancer ( less then IB) on cervical or cone biopsy, were included. HPV genotypes were identified using the INNO-LiPA HPV genotyping assay, version EXTRA, on cervical scraping, before the colposcopic evaluation and the colposcopic biopsies or conization. In the overall population, HPV16 interacted positively with HPV18 (RR = 2, 95% CI 1.5-2.6) and negatively with HPV33, 51, 52, and 66, in log-linear analysis. There was an excess of CIN3 diagnoses among subjects coinfected with HPV16 and HPV18 or HPV52, although the absolute number of cases was relatively small. In a logistic model, the odds ratio of CIN3+ associated with coinfection of HPV16 and HPV18 (OR = 3.8, 95% CI 2.5-5.7, p=0.004 compared to single HPV16) or HPV52 (OR = 3.6, 95% CI 2.6-5.1, p=0.009 compared to single HPV) was higher than that associated with single HPV 16 infections. selleck chemical Finally, multiple infections had no effect on residual disease and did not influence the recurrence of high-grade CIN during a median follow-up of 25 months (IR 17-41). HPV16 interacted positively with HPV18 and negatively with HPV33, 51, 52, and 66 supporting the notion that HPV16 interacts mostly negatively with other HR-HPVs in CIN lesions. Among specimens coinfected with HPV16 and 18 or 52, there was an excess of CIN3+ although the impact on the prevalence of severe cervical lesions was limited.

Chronic liver disease (CLD) of different etiologies leads to hepatocellular carcinoma (HCC) by multiple mechanisms that may be translated into clinicopathological differences. We evaluated the tissue expression of the MAPK and PI3K/Akt/mTOR pathway proteins and their association with long-term outcome and other parameters, according to the etiology of the CLD, in HCC patients.

Clinicopathological data from 80 patients who underwent orthotopic liver transplantation for HCC treatment in a Brazilian referral center were compared according to CLD etiology. Event (tumor recurrence or death from any cause) occurrence and event-free survival (EFS) were analyzed. Pathway protein expression was assessed by immunohistochemistry (IHQ) in both tumor and underlying cirrhosis and by RT-PCR in tumor tissue.

Strong expression (SE) of KRAS was more frequent in tumors arising from viral (26.8%) than the nonviral group of liver disease (7.7%,

=0.024) and also than cirrhotic parenchyma (0%,

=0.004). SE of PI3K was more frequent in tumor than in cirrhosis (

=0.048,

< 0.01), without differences in its tumor expression among etiologic groups (

=0.111). mRNA of ERK, PI3K, and BRAF was expressed in the tumor, without differences between CLD etiologies, and there was no association with IHQ findings. Older age and microvascular invasion (MIV) were the only parameters independently associated with the event. MIV was also associated with shorter EFS.

Hepatitis B and C virus can lead to HCC by different mechanisms compared with nonviral hepatopathy. KRAS and PI3K may have a role in carcinogenesis. The prognostic and therapeutic implications need to be investigated.

Hepatitis B and C virus can lead to HCC by different mechanisms compared with nonviral hepatopathy. KRAS and PI3K may have a role in carcinogenesis. The prognostic and therapeutic implications need to be investigated.Dysregulation of Rab11a has been implicated in the progression of several cancers. However, there have been no such studies for human gastric cancers. In the current study, we examined Rab11a protein expression and found it was upregulated in 49 of 108 gastric cancer tissues and correlated with local invasion, nodal metastasis, and advanced stage. Rab11a protein was higher in gastric cancer cell lines than normal gastric cell line. We transfected Rab11a plasmid and siRNA in both MGC803 and AGS cell lines. Rab11a overexpression increased the cell growth rate, colony numbers, and invasion ability in both MGC803 and AGS cell lines. Downregulation of Rab11a using siRNA decreased the cell proliferation rate, colony numbers, and inhibited invasion. Rab11a overexpression also conferred cisplatin resistance. Annexin V/PI staining showed that Rab11a overexpression suppressed cisplatin-induced apoptosis, while Rab11a depletion promoted cell apoptosis. We also showed that Rab11a overexpression maintained mitochondrial membrane potential.