BMC Cancer最新文献

Background: Checkpoint inhibitor pneumonitis (CIP) is an uncommon but clinically severe adverse event that can seriously compromise the quality of life and can be potentially life-threatening in lung cancer patients receiving immune checkpoint inhibitors (ICI). However, there is still a lack of effective predictive models to predict the occurrence of CIP. The aim of this study was to develop a novel scoring system for predicting the risk of CIP based on a nomogram model.

Methods: We retrospectively screened patients with lung cancer who received ICI treatment at our hospital. The independent risk factors of CIP were identified by the univariable and multivariable analysis of the COX hazard regression model and were integrated to develop a nomogram predictive model. The receiver operating characteristic (ROC) curve, the concordance index (C- index), and the calibration curve were used to evaluate the discrimination and prediction accuracy of the model. The clinical utility of the model was evaluated by decision curve analysis (DCA).

Results: A total of 2,082 cancer patients were included in the analysis. In the final multivariate Cox regression analysis identified that sex, body mass index (BMI), chemotherapy, radiotherapy, C-reactive protein (CRP), CD4/CD8, white blood cell (WBC), ALB/GLB, platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), neutrophil-to-platelet ratio (NPR), platelet-to-albumin ratio (PAR), and CRP-to-lymphocyte ratio (CLR) were the independent predictive factors for CIP. Based on these risk factors, a predictive nomogram model was constructed. The C-index for the nomogram model in predicting the probability of CIP at 1 year, 1.5 years, and 2 years was 0.704, 0.718, and 0.725, respectively. The average C-index (SD) was 0.712 (0.004), and the average AUC (SD) was 0.733 (0.005), calculated through 100 iterations of 10-fold cross-validation. The calibration curves demonstrated good concordance, and the DCA indicated that the model had good clinical utility.

Conclusions: The nomogram was accurate in predicting the occurrence of CIP in patients with lung cancer. This study provides a reference for screening CIP high-risk patients and for individualized treatment strategies.

Introduction: Wilms tumor (WT) is a highly treatable form of childhood cancer, with five-year survival rates greater than 90% in high-income countries. In low- and middle-income countries, survival is still low. Delayed surgery is one of the leading factors for poor survival, as it leads to tumor complications, making subsequent treatment more complex. However, there is a paucity of information in Uganda on the prevalence and factors associated with delayed surgery. This study aimed to determine the prevalence and factors associated with delayed surgery, and to explore the barriers and facilitators of timely surgery among children with WT at Mulago Hospital.

Methods: The study employed a convergent concurrent mixed-methods design. The quantitative component involved a retrospective cross-sectional design using 261 patient records selected through consecutive sampling and reviewed via a data abstraction tool. Modified Poisson regression was used to assess associated factors. The qualitative component included in-depth interviews with 10 healthcare workers and 10 caregivers selected purposively and was analyzed via inductive thematic analysis.

Results: The prevalence of delayed surgery was 63.6% (95% confidence interval (CI) 57.0-68.7). The year of diagnosis (2021: adjusted prevalence ratio (aPR) 2.26, 95% CI 1.40-3.65, p value 0.001; 2022: aPR 1.78, 95% CI 1.07-2.99, p value 0.026; and 2023: aPR 2.01, 95% CI 1.24-3.25, p value 0.004), tumor laterality (aPR 1.41, 95% CI 1.07-1.85, p value 0.014), hemoglobin level after preoperative chemotherapy (POPC; aPR 1.22, 95% CI 1.05-1.51, p value 0.032), and chemotherapy regimen (VAD: aPR 1.32, 95% CI 1.11-1.57, p value 0.02; and AV/CE: aPR 1.46, 95% CI 1.07-1.99) were associated with delayed surgery. Qualitative findings revealed systemic, patient-level, chemotherapy, and tumor-related barriers to and facilitators of timely surgery.

Conclusion: The prevalence of delayed surgery was high among children with WT. Delayed surgery results from a complex interplay of clinical, systemic, and patient-related factors. Addressing barriers at both the institutional and patient levels may help reduce surgical delays and improve outcomes.

Background: ITGA5 is an oncogene that performs its biological function by integrating the intracellular structure and extracellular matrix. We found that ITGA5 is highly expressed in gastric tumors and is closely related to proliferation and metastasis. Multiple miRNAs regulate the ITGA5 gene during the occurrence and development of tumors. This study aimed to explore the role of targeting miRNAs upstream of ITGA5 in the regulation of the proliferation, invasion, and migration of gastric cancer cells.

Methods: Target miRNA molecules regulating the ITGA5 gene were predicted using four bioinformatics databases (TargetScan、miRDB、miRTarBase and mirDIP). The unreported miRNAs with high correlation were selected, and their expression in gastric cancer was assessed using qRT-PCR and western blot. The miRNAs with potential targeting abilities were further verified by dual luciferase reporter gene experiment. The effects of miR-330-5p and ITGA5 on the proliferation, invasion, and migration of gastric cancer cells were evaluated using CCK8, clonogenic assay, and Transwell chamber assay, respectively.

Results: Six miRNAs (miR-26a-5p、miR-92a-3p、miR-148a-3p、miR-148b-3p、miR-330-5p and miR-152-3p) were identified. miR-330-5p was found to target and regulate ITGA5. In vitro experiments demonstrated that miR-330-5p mimic significantly inhibited the proliferation, invasion, and migration of gastric cancer cells compared with the control group (p < 0.05). Transfection of miR-330-5p mimic into gastric cancer cells overexpressing ITGA5 (OE-ITGA5) significantly prevented the ability of OE-ITGA5 to promote the proliferation, invasion, and migration of gastric cancer cells (P < 0.05). In addition, miR-330-5p mimic reduced ITGA5 expression in gastric cancer cells and partially prevented FAK/AKT signaling pathway activated by the ITGA5 gene. An miR-330-5p inhibitor increased ITGA5 expression in gastric cancer cells, and partially prevented blockage of the FAK/AKT signaling pathway by sh-ITGA5.

Conclusions: miR-330-5p was shown to affect the proliferation, invasion, and migration of gastric cancer cells by mediating ITGA5 through a mechanism possibly associated with the regulation of the FAK/AKT signaling pathway.