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OBJECTIVE: Gene mutation is closely related to the occurrence of tumor. Renal cell carcinoma is a malignant tumor, seriously threatening patients' life quality. Regulatory T cells (Treg) play important roles in the development of several cancers. This study aimed to investigate whether CD18 affects renal carcinoma cell proliferation. MATERIALS AND METHODS: Thirty mice with renal cell carcinoma were constructed using gene-engineering mouse with CD18 deficiency, and another 30 normal C57 mice were used as control. Ki67 and micro-vessel density were detected by using immunohistochemistry (IHC) and immunofluorescence, respectively. The expression of CD3, CD4 and CD8 were detected in blood and spleen by quantitative PCR (q-PCR). Flow cytometry was used to detect the changes of Treg cells. RESULTS: The expression of Ki67 in C57 was significantly higher than that in CD18-/- mice (p<0.05). IHC results showed that CD31 was also significantly downregulated in CD18-/- group compared to control group (p<0.05). It was found that only high expression of CD4 in mesenteric lymph nodes of CD18-/- was considered as non-tumor- bearing. Flow cytometry results showed that Treg cells were significantly decreased in CD18-/- compared to C57 group (p<0.05). CONCLUSIONS: CD18-/- down-regulates Treg cells and inhibits the pathogenesis of renal cell carcinoma. [ABSTRACT FROM AUTHOR]

This study aims to investigate the role of diffusion-weighted magnetic resonance imaging (DWMRI) in ESCC patients receiving neoadjuvant concurrent chemoradiotherapy (CCRT), and the efficacy of apparent diffusion coefficient (ADC) values in predicting pathologic response to neoadjuvant CCRT. Twenty-eight locally advanced ESCC patients treated with neoadjuvant CCRT followed by radical resection were prospectively enrolled. DW-MRI was recommended to be performed within 2 weeks before and 4-6 weeks after neoadjuvant CCRT. The calculated ADCs pre- (ADC1) and post- (ADC2) neoadjuvant CCRT, the definite (ΔADC) and percentage changes (ΔADC%) were analyzed for the efficacy of predicting pathologic response to neoadjuvant CCRT. Twenty patients had been identified as responders (tumor regression grade 1-2). Among them, ADC2 (3.02 ± 0.84 vs. 2.12 ± 0.44 × 10-3 mm²/s, P = 0.001) and ΔADC (1.22 ± 0.78 vs 0.64 ± 0.26 × 10-3 mm²/s, P = 0.007) were significantly higher than those of nonresponders (tumor regression grade: 3-5). Receiver operating characteristic analysis revealed that ADC2 exhibited an overall accuracy of in 71.4% in predicting pathologic response, with a sensitivity of 60.0%, a specificity of 100%, a positive predictive value of 100%, and a negative predictive value of 50.0%, when 3.04 × 10-3 mm²/s was used as the cutoff value. ADC value could be useful in predicting pathologic response to neoadjuvant CCRT in ESCC patients. High postneoadjuvant CCRT ADC is a predictive indicator for good response. [ABSTRACT FROM AUTHOR]

OBJECTIVE: PI3K/AKT/mTOR signaling pathway plays a crucial role in tumorigenesis and development. It was shown that mTOR overexpression was associated with the pathogenesis of renal cancer. Down-regulation of MiR-182 was found in renal carcinoma tissue. This study thus aims to investigate the influence of miR-182 in regulating mTOR expression and renal carcinoma cell proliferation, invasion, and apoptosis. PATIENTS AND METHODS: The targeted regulatory relationship between miR-182 and mTOR was tested by dual luciferase assay. Renal carcinoma tissue and benign renal tissue were collected to detect miR-182 and mTOR expressions. MiR-182, mTOR, p-mTOR, and Survivin levels were compared between HK-2 and A498 cells. Renal carcinoma A498 cells were divided into four groups, including miR-NC, anti-miR-182 mimic, si-NC, and si-mTOR groups. Cell apoptosis and proliferation were evaluated by flow cytometry. Cell invasion was determined by transwell assay. RESULTS: Bioinformatics analysis revealed the complementary relationship between miR- 182 and the 3'-UTR of mTOR mRNA. The level of miR-182 was significantly reduced, while mTOR expression was upregulated in renal carcinoma tissue compared with that in benign lesion, which was associated with TNM stage. MiR-182 expression was markedly declined, whereas mTOR, p-mTOR, and Survivin levels were apparently upregulated in A498 cells compared with that in HK-2 cells. The treatment of miR-182 mimic or si-mTOR transfection significantly downregulated mTOR, p-mTOR, and Survivin expressions, restrained cell proliferation and invasion, and enhanced cell apoptosis. CONCLUSIONS: The decreasing level of miR- 182 plays a role in enhancing mTOR expression and promoting renal carcinoma pathogenesis. Overexpression of miR-182 inhibited mTOR expression and weakened cell proliferation and invasion, which provides leads to the future therapy of renal cancer. [ABSTRACT FROM AUTHOR]

The correlations of murine double minute 2 ( MDM2) T309 G and esophageal cancer were elucidated because the association between MDM2 expression states and clinicopathological parameters of esophageal squamous cell carcinoma ( ESCC) is controversial. We conducted a meta-analysis on studies screened from Pub Med, Web of Science, Embase, the Cochrane Library, and the Chinese Biomedical Literature Databases that were published before October 2014. All studies describing the association between MDM2 and ESCC were traced. Meta-analysis was performed using the STATA software ( Stata Corp., College Station, TX, USA). A total of 9 studies with 707 cases and 324 controls were included. MDM2 expression was higher in ESCC than in normal esophageal epithelium (odds ratio [ OR] 10.38, 95% confidence interval [ CI] 6.42-16.78, P < 0.001). High MDM2 expression was associated with early primary tumor stage ( T1/ T2 vs. T3/ T4, OR 0.59, 95% CI 0.38-0.92, P = 0.018) and increased risk of regional lymph node metastasis ( N0 vs. N1, OR 1.66, 95% CI 1.03-2.67, P = 0.039). However, no relationship was observed between MDM2 expression and the risk of distant metastasis ( OR = 2.09, 95% CI 1.00-4.36, P = 0.050), and MDM2 was not significantly correlated with TP53 expression ( OR 1.22, 95% CI 0.53-2.77, P = 0.643). Our analysis suggests that MDM2 acts as a potent marker of early primary tumor stage but higher risk of regional lymph node metastasis in ESCC. However, because of the limited number of studies included, the result should be further clarified by well-designed prospective studies. [ABSTRACT FROM AUTHOR]

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