No abstract

No abstract

Background and Objectives: Data on associations between soy food intake after cancer diagnosis with breast cancer survival are conflicting, so we conducted this meta-analysis for more accurate evaluation. Methods: Comprehensive searches were conducted to find cohort studies of the relationship between soy food intake after cancer diagnosis and breast cancer survival. Data were analyzed with comprehensive meta-analysis software.

No abstract

BackgroundMiR-133b is a muscle-specific microRNA; it has a role in the formation of cardiocytes and the expression of myocardium ion channels by regulating target genes. Many human malignant tumors demonstrate a low expression of miR-133b, as noted in colorectal, lung, esophagus and bladder cancers, but the role of miR-133b in bladder cancer is unknown.MethodsThe expression of miR-133b in clinical bladder cancer specimens and adjacent normal tissues was confirmed by stem-loop RT-PCR. We also analyzed the relationship between miR-133b expression and clinicopathological factors of bladder cancer. Bcl-w and Akt1 protein expression in 41 bladder cancer specimens and adjacent normal tissues was detected by Western blot. After transfection of miR-133b mimics or inhibitor into a T24 human bladder cancer cell line, Bcl-w and Akt1 protein and mRNA expression were examined by Western blot and RT-PCR, respectively. The effect of miR-133b on T24 cell proliferation and apoptosis was measured by CCK-8 tests and flow cytometry, respectively.ResultsThe expression of miR-133b in bladder cancer tissues from 41 patients was significantly down-regulated (P < 0.01); low expression of miR-133b was strongly associated with high-grade bladder cancer (P < 0.01). Bcl-w and Akt1 proteins were significantly overexpressed in bladder cancer tissues versus adjacent normal tissues (P < 0.01 for both). The expression of Akt1 and Bcl-w proteins and Akt1 mRNA, in T24 cells was significantly down-regulated or up-regulated after transfection of miR-133b mimics or inhibitor, respectively; however, there was no significant difference in Bcl-w mRNA expression. Transfection of HEK-293 T cells with miR-133b significantly suppressed a luciferase-reporter containing the Bcl-w or Akt 1 3′-untranslated regions. MiR-133b mimics significantly inhibited T24 cell proliferation, as well as increased T24 cell apoptosis (P < 0.05 and P < 0.01, respectively) while the miR-133b inhibitor increased and decreased these, respectively (P < 0.05 for both).ConclusionsMiR-133b may play a very important role in the proliferation and apoptosis of T24 cells by regulating the expression of Bcl-w and Akt1.

Background: B and T lymphocyte attenuator (BTLA) is a novel immune checkpoint with an unclear role in non-small-cell lung cancer (NSCLC). In contrast, the programmed death-1 (PD-1)/programmed death ligand-1 (PD-L1) checkpoint is a potentially curative immunotherapy target in NSCLC. Our study investigated BTLA expression and its relationship with PD-1/PD-L1, tumor-infiltrating lymphocytes (TILs), and clinicopathological features. Methods: The protein expressions of BTLA, PD-1, and PD-L1 were evaluated by immunohistochemistry (IHC) and TIL abundance was scored in paraffin-embedded tissues from surgically resected specimens from 87 patients with stage I-III NSCLC. Results: BTLA was expressed in tumor cells in 35 patients with NSCLC (40.2%). In addition, 42 patients (48.3%) were positive for PD-1 in TILs and 31 (35.6%) were positive for PD-L1 in tumor cells. BTLA was overexpressed in patients with lymphatic invasion (P=0.045) and an advanced tumor stage (P=0.034). High expression of BTLA was positively correlated with a high level of PD-L1 (P=0.011). Patients with positive BTLA expression had a shorter relapse-free survival (RFS) than those with negative BTLA expression (P=0.029). Moreover, patients negative for both BTLA and PD-L1 had a longer RFS than patients who were positive for BTLA or PD-L1 or for both checkpoints (P=0.012). The same pattern was shown for overall survival (P=0.031). Conclusion: High BTLA expression may predict poor prognosis in patients with NSCLC and may represent a new immunotherapy target.

BackgroundTo evaluate the clinical and oncological outcomes and to identify prognostic factors for survival in Chinese patients with renal cell carcinoma (RCC) and venous tumor thrombus (VTT).MethodsA total of 86 patients who underwent nephrectomy and tumor thrombectomy for RCC and venous tumor thrombus extension from 2003 to 2013 were included in this retrospective study. The records of these patients were reviewed. Kaplan-Meier analysis was used to determine cancer-specific survival (CSS). Prognostic factors for CSS were identified by univariate and multivariate analyses using the Cox proportional hazards regression mode.ResultsAll patients in this cohort received radical nephrectomy and tumor thrombectomy. Median follow-up period was 27.0 months (range 3–111). No patients died intraoperatively, and the complication rate was 36.0%. The 1-, 3-, and 5-year CSS rates for all patients were 93.0%, 70.9%, and 58.1%, respectively, and those for patients without distant metastasis at presentation were 95.3%, 82.6%, and 68.6%, respectively. Multivariate Cox regression analysis showed that lymph node invasion, distant metastasis at presentation, and invasion of the inferior vena cava (IVC) wall were the independent prognostic factors for CSS in all patients. For patients without distant metastasis, tumor grade, lymph node invasion, and perinephric fat invasion were significantly associated with CSS on multivariate analysis.ConclusionsSurvival rates for patients with RCC and VTT were still poor. Our results indicated that lymph node invasion, distant metastasis at presentation, and invasion of the IVC wall were independent negative prognostic factors.

Special AT-rich sequence-binding protein-1 (SATB1) has been recently reported to be overexpressed in various cancers and associate with the malignant behavior of cancer cells. However, the expression and potential roles of SATB1 in bladder cancer remains unclear. In the present study, SATB1 expression was analyzed in 85 archived bladder cancer specimens using immunohistochemistry and the correlations between SATB1 expression and clinicopathological parameters were evaluated. To further explore the biological functions of SATB1 in bladder cancer, siRNA knockdown was performed in 5637 and T24 bladder cancer cell lines. We then carried out CCK8 assay and examined cisplatin-induced apoptosis to address the roles of SATB1 in proliferation and apoptosis. We found that SATB1 was overexpressed in 33 of 85 (38.8 %) bladder cancer specimens. SATB1 overexpression associated with tumor grade (p = 0.002) and tumor stage (p = 0.027). SATB1 depletion in 5637 and T24 cells decreased cell proliferation while upregulating cisplatin-induced apoptosis. Further study demonstrated that SATB1 knockdown decreased cyclin D1 and cyclin E expression and upregulated caspase3 cleavage. In conclusion, SATB1 is overexpressed in bladder cancer and regulates malignant cell growth and apoptosis, which makes SATB1 a therapeutic target candidate for bladder cancer.