Successful Treatment of Bronchopulmonary Sequestration by Radiofrequency Ablation of Feeding Artery.

INTRODUCTION: Most cases of bronchopulmonary sequestration (BPS) regress. Prenatal intervention is needed in cases of fetal hydrothorax or hydrops. Laser is commonly used to ablate the feeding artery. CASE PRESENTATION: In a fetus with BPS, radiofrequency ablation (RFA) was used to ablate the feeding artery arising from descending aorta at 29 weeks gestation. There was an extralobar BPS and significant pleural effusion causing mediastinal shift and collapse of lung. The effusion and tumor started decreasing from day 3 after procedure, and by the time patient delivered at 36 weeks gestation, the lesion had almost resolved. CONCLUSION: With proper technique, RFA can be safely used to ablate feeding artery in BPS.

Side population in human non-muscle invasive bladder cancer enriches for cancer stem cells that are maintained by MAPK signalling.

Side population (SP) and ABC transporter expression enrich for stem cells in numerous tissues. We explored if this phenotype characterised human bladder cancer stem cells (CSCs) and attempted to identify regulatory mechanisms. Focusing on non-muscle invasive bladder cancer (NMIBC), multiple human cell lines were used to characterise SP and ABC transporter expression. In vitro and in vivo phenotypic and functional assessments of CSC behaviour were undertaken. Expression of putative CSC marker ABCG2 was assessed in clinical NMIBC samples (n = 148), and a role for MAPK signalling, a central mechanism of bladder tumourigenesis, was investigated. Results showed that the ABCG2 transporter was predominantly expressed and was up-regulated in the SP fraction by 3-fold (ABCG2(hi)) relative to the non-SP (NSP) fraction (ABCG2(low)). ABCG2(hi) SP cells displayed enrichment of stem cell markers (Nanog, Notch1 and SOX2) and a three-fold increase in colony forming efficiency (CFE) in comparison to ABCG2(low) NSP cells. In vivo, ABCG2(hi) SP cells enriched for tumour growth compared with ABCG2(low) NSP cells, consistent with CSCs. pERK was constitutively active in ABCG2(hi) SP cells and MEK inhibition also inhibited the ABCG2(hi) SP phenotype and significantly suppressed CFE. Furthermore, on examining clinical NMIBC samples, ABCG2 expression correlated with increased recurrence and decreased progression free survival. Additionally, pERK expression also correlated with decreased progression free survival, whilst a positive correlation was further demonstrated between ABCG2 and pERK expression. In conclusion, we confirm ABCG2(hi) SP enriches for CSCs in human NMIBC and MAPK/ERK pathway is a suitable therapeutic target.