Refracture of the cemented vertebrae after percutaneous vertebroplasty: risk factors and imaging findings.

BACKGROUND: To determine the related imaging findings and risk factors to refracture of the cemented vertebrae after percutaneous vertebroplasty (PVP) treatment. METHODS: Patients who were treated with PVP for single vertebral compression fractures (VCFs) and met this study's inclusion criteria were retrospectively reviewed from January 2012 to January 2019. The follow-up period was at least 2 years. Forty-eight patients with refracture of the cemented vertebrae and 45 non-refractured patients were included. The following variates were reviewed: age, sex, fracture location, bone mineral density (BMD), intravertebral cleft (IVC), kyphotic angle (KA), wedge angle, endplate cortical disruption, cement volume, surgical approach, non-PMMA-endplate-contact (NPEC), cement leakage, other vertebral fractures, reduction rate (RR), and reduction angle (RA). Multiple logistic regression modeling was used to identify the independent risk factors of refracture. RESULTS: Refracture was found in 48 (51.6%) patients. Four risk factors, including IVC (P = 0.005), endplate cortical disruption (P = 0.037), larger RR (P = 0.007), and NPEC (P = 0.006) were found to be significant independent risk factors for refracture. CONCLUSIONS: Patients with IVC or larger RR, NPEC, or endplate cortical disruption have a high risk of refracture in the cemented vertebrae after PVP.

Overexpression of MYBL2 promotes proliferation and migration of non-small-cell lung cancer via upregulating NCAPH.

MYB Proto-Oncogene Like 2 (MYBL2) is a highly conserved member of the Myb family of transcription factors and plays a critical role in regulating cell proliferation and survival. Here we show that overexpression of MYBL2 is frequently observed in lung adenocarcinoma (LUAD) and significantly correlates with advanced stage and poor patient survival. Knockdown of MYBL2 induced apoptosis in lung cancer cells and resulted in significant inhibition of cell proliferation, migration, and invasion. Notably, we identified Non-SMC Condensin I Complex Subunit H (NCAPH) gene as a direct target of MYBL2. NCAPH expression is highly correlated with that of MYBL2 in LUAD cases and is tightly affected by MYBL2 knockdown or overexpression in vitro. Chromatin immunoprecipitation (ChIP) assays also showed that MYBL2 directly binds to the transcription start site (TSS) of NCAPH. Moreover, we provided evidence that NCAPH functions as an oncogene in lung cancer and overexpression of NCAPH could partially rescue cell death and migration blockage induced by MYBL2 knockdown. Together, these results suggest that overexpression of MYBL2 promotes proliferation and migration of lung cancer cells via upregulating NCAPH, establishing their roles as novel prognostic biomarkers as well as potential therapeutic targets for the disease.