Objective. To assess the effectiveness and safety of extracorporeal shockwave therapy (ESWT) for the treatment of chronic low back pain (CLBP). Methods. This was a systematic review and meta-analysis of randomized controlled trials (RCTs) designed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-analysis statement standard. We identified relevant studies by searching multiple electronic databases, trial registries, and websites up to April 30, 2021, and examining reference lists. We selected RCTs that compared ESWT, in unimodal or multimodal therapeutic approaches, with sham ESWT or other active therapies. Two investigators independently extracted data and assessed the risk of bias and quality of the evidence. The main outcomes were pain intensity and disability status, examined as standardized mean differences (SMD) with 95% confidence intervals (CI). The risk of bias was assessed by using Cochrane Back and Neck (CBN) Group risk of bias tool and Jadad score, and GRADE was applied to determine the confidence in effect estimates. Heterogeneity was explored using sensitivity analysis and meta-regression. Results. Ten RCTs, including a total of 455 young to middle-aged individuals (29.2–55.8 years), were identified. Compared with control, the ESWT group showed lower pain intensity at month 1 ( SMD = − 0.81 , 95% CI −1.21 to −0.42), as well as lower disability score at month 1 ( SMD = − 1.45 , 95% CI −2.68 to −0.22) and at month 3 ( SMD = − 0.69 , 95% CI −1.08 to −0.31). No serious shockwave-related adverse events were reported. Conclusion. The use of ESWT in CLBP patients results in significant and quantifiable reductions in pain and disability in the short term. However, further well-conducted RCTs are necessary for building high-quality evidence and promoting the application of ESWT in clinical practice.

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Background: Brain metastasis (BM) is a very serious event in patients with breast cancer. The aim of this study was to establish a nomogram to predict the risk of BM in patients with de novo stage IV breast cancer. Methods: We gathered female patients diagnosed with de novo stage IV breast cancer between 2010 and 2015 from the Surveillance, Epidemiology, and End Results (SEER) database. After randomly allocating the patients to the training set and verification set, we used univariate and multivariate logistic regression to analyze the relationship between BM and clinicopathological features. Finally, we developed a nomogram which was validated by the analysis of calibration curve and receiver operating characteristic curve. Results: Of 7,154 patients with de novo stage IV breast cancer, 422 developed BM. Age, tumor size, subtype, and the degree of lung involvement were significantly correlated with BM. The nomogram had discriminatory ability with an area under curve (AUC) of 0.640 [95% confidence interval (CI): 0.607 to 0.673] in the training set, and 0.644 (95% CI: 0.595 to 0.693) in the validation set. Conclusions: Our study developed a nomogram to predict BM for de novo stage IV breast cancer, thus helping clinicians to identify patients at high-risk of BM and implement early preventive interventions to improve their prognoses.

Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are a standard treatment for patients with advanced non-small-cell lung cancer (NSCLC) harboring classic EGFR mutations. However, resistance to TKIs remains a major clinical challenge. The transformation from adenocarcinoma to small-cell lung cancer (SCLC) is a rare resistance mechanism to EGFR-TKIs. In this article, we report on 2 lung adenocarcinoma patients with EGFR mutations who developed EGFR-TKI resistance. In case one, the patient was initially diagnosed as lung adenocarcinoma with EGFR L858R, RB1 R445*, and TP53 Y205C mutations. EGFR-TKI failed to bring satisfactory curative effect with the emergence of EGFR T790M mutation and MET amplification and finally passed away. In case two, the patient was diagnosed with lung cancer harboring EGFR L747 and TP53 R342* mutations, and EGFR-TKIs brought a progression-free survival for nine month. However, EGFR-TKI resistance was acquired, and adenocarcinoma transformed into a complex of neuroendocrine carcinoma, SCLC, and lung adenocarcinoma, with the emergence of the EGFR L747, TP53 R342*, and RB1 mutations. Follow-up treatments failed to prevent tumor progression, and the patient died These 2 cases expand our understanding of EGFR-TKI resistance, SCLC transformation, and highlight the importance of histopathology and molecular characteristics for therapeutic strategies for transformed SCLC patients.