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Overexpression of LEF1-AS1 and miR-221 promoted cancer cell proliferation and inhibited apoptosis. PTEN played an opposite role and reduced the effects of overexpressing LEF1-AS1 and miR-221. Conclusion LEF1-AS1 may promote the proliferation and induce apoptosis of NSCLC cells by regulating miR-221/PTEN signaling.Objective This study set out to institute an effective nomogram to predict the prognosis of nasopharyngeal carcinoma (NPC) using magnetic resonance imaging (MRI)-detected residual tumor at the end of intensity-modulated radiotherapy (IMRT). Background This study retrospectively analyzed the prognostic factors of NPC using MRI-detected residual tumor at the end of IMRT, in order to individualize the treatment of patients with poor prognosis as early as possible. Methods Overall, 162 NPC patients with local or regional residual tumor at the end of IMRT were retrospectively analyzed. Based on multivariate Cox regression analysis using the backward stepwise method, a nomogram was generated to predict the prognosis of these patients. Identification, calibration, clinical applicability and reproducibility were evaluated by C-index, time-dependent AUC, calibration curve and bootstrap verification. According to the best cut-off value of total score of prognoses calculated by X-tile software, all patients were separatndividual risk, clinicians can start treatment decisions as early as possible for high-risk patients with poor prognosis.Purpose Anlotinib is a newly developed oral multitarget tyrosine kinase inhibitor. We retrospectively evaluated the toxicity and clinical efficacy of chemotherapy combined with anlotinib versus chemotherapy alone for metastatic/advanced non-small cell lung cancer (NSCLC) in patients who failed first- or second-line systemic treatment in China. click here Patients and methods In this retrospective trial, ninety-four advanced NSCLC patients received chemotherapy combined with anlotinib (n = 41) or chemotherapy alone (n = 53) in Henan Cancer Hospital. We recorded the objective response rate (ORR), disease control rate (DCR), progression-free survival (PFS) and adverse events (AEs). Results In the anlotinib plus chemotherapy group, eleven patients (27%) achieved a PR (partial response), and twenty-one patients (51%) achieved SD (stable disease), with an ORR of 27% and a DCR of 78%. In the chemotherapy alone group, eight patients (15%) achieved a PR, and nineteen patients (36%) had SD, with an ORR of 15% and a DCR of 51%. The ORR in the combination arm was slightly, but not obviously, higher than that in the chemotherapy arm (27% vs 15%, p > 0.05). In addition, the DCR was significantly higher in the combination arm than in the chemotherapy alone arm (78% vs 51%, p=0.007). At the end of follow-up, patients in the combination arm had a 1.5-month longer median PFS than patients in the chemotherapy arm; this difference was statistically significant (5.0 vs 3.5, p=0.002). The median OS was not achieved at the final analysis. The hematological and nonhematological toxicities were well tolerated and controlled. In general, most toxicity was limited to grade I or II, well tolerated and controlled. Conclusion Our study suggests that anlotinib combined with chemotherapy may be an effective and well-tolerated treatment for advanced NSCLC in patients who fail first- or second-line therapy.Background Prophylactic transarterial chemoembolization (p-TACE) is strongly recommended for hepatocellular carcinoma (HCC) patients with microvascular invasion (MVI), but the potential beneficiaries remain controversial. Methods Data of HCC patients with MVI who underwent R0 resection between December 2013 and December 2015 were identified through the primary liver cancer big data. Disease-free survival (DFS) and overall survival (OS) were compared between patients who received p-TACE or not using Kaplan-Meier survival curves before and after propensity scoring match (PSM). Results A total of 695 patients were eligible for this study, including 199 patients (28.6%) receiving p-TACE and 496 patients (71.4%) receiving resection alone. In the crude cohort, median DFS and OS were longer in the p-TACE group than those in the non-TACE group without significant differences (25.0 months vs 24.2 months, P=0.100; 48.0 months vs 46.5 months, P=0.150; respectively), but significant differences were observed both in DFS and OS (both P less then 0.05) after 11 PSM. p-TACE was identified as one of the independent risk factors of both DFS and OS using multivariate analysis in the matched cohort (HR=0.69, 95% CI=0.54-0.88; HR=0.66, 95% CI=0.50-0.88; respectively). Subgroup analysis showed that p-TACE could beneficiate patients if they were male, aged ≥50 years old, had HBV infection, preoperative AFP level ≥400 ng/mL, Child-Pugh grading A, no transfusion, single tumor, tumor diameter ≥5cm, Edmondson-Steiner grading I/II, capsule, or BCLC stage A, CNLC stage Ib, AJCC stage II both in DFS and OS (all P less then 0.05). Conclusion With the current data, we concluded that not all HCC patients with MVI would be benefited from p-TACE, and p-TACE could benefit patients with "middle risk" according to the current staging systems.Background/objective Topoisomerases type IIA (TOP2A) was identified to present with a high-expression pattern in cervical cancer. However, TOP2A role in the progression of cervical cancer remains unknown. Here, we aimed to explore the effect and reveal the underlying mechanism of TOP2A in the migration, invasion and epithelial-mesenchymal transition (EMT) of cervical cancer. Materials and methods The expression profiles of TOP2A in 20 paired cervical cancer tissues and the paracancerous normal tissues were detected by using Western blotting assay. Transwell chambers were used to test cell migration and invasion abilities. Cell morphology and the expressions of E-cadherin and N-cadherin were detected to assess cell EMT. LY294002 was used to inhibit the activation of PI3K/AKT signaling. Results Compared with the paracancerous normal tissues, TOP2A was overexpressed in 85% (17/20) cervical cancer tissues. Repression of TOP2A expression in SiHa cells significantly weakened cell migration and invasion abilities, reduced cell numbers in shuttle shape and increased E-cadherin expression while decreased E-cadherin expression.
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