＜Editors' Choice＞ Efficacy of pectoral nerve block type-2 (Pecs II block) versus serratus plane block for postoperative analgesia in breast cancer surgery: a retrospective study.

Thoracic wall nerve blocks reduce postoperative acute pain after breast cancer surgery (BCS); however, their short-term effects and the most effective technique remain unclear. To compare the effects of pectoral nerve block type-2 (Pecs II block) and serratus plane block for postoperative short-term analgesia, we retrospectively reviewed 43 BCS patients who underwent Pecs II block (n=22) or serratus plane block (n=21). The primary outcome was the proportion of patients with no complaints of pain 2 months post-BCS. The odds ratio (OR) was assessed, adjusting for axillary lymph node dissection. The secondary outcomes were pain severity 24 hours and 2 months post-operation using the numerical rating scale score, and morphine consumption within 24 hours. The proportion of patients without pain 2 months post-BCS was significantly less with Pecs II block than in patients with serratus plane block (55% vs. 19%, adjusted OR, 5.04; 95% confidence interval, 1.26-20.07; P=0.02); the median [interquartile range] score for pain 2 months post-operation was also significantly lower with Pecs II block (Pecs II block 0.5 [0-1] vs. serratus plane block 1 [1-2]); P=0.03). Regarding post-BCS acute analgesia, the median [interquartile range] postoperative 24-hour pain score was 2 [1-3] and 3 [1.5-3.5], and the median morphine consumption within 24 hours was 1.5 [0.75-5.5] and 3 [1.5-10] mg in Pecs II block and serratus plane block (P=0.47 and P=0.11), respectively. This study suggests that Pecs II block prevents short-term post-BCS pain better than serratus plane block. However, further studies are needed in order to support this finding.

TGF-beta downregulates PTEN via activation of NF-kappaB in pancreatic cancer cells.

TGF-beta utilizes receptor-activated SMAD signaling to mediate growth suppression; however, non-SMAD signaling that modulates the TGF-beta response in epithelial cells become apparent when the SMAD signaling is abrogated, a common occurrence in pancreatic cancers. Here, we examined whether TGF-beta utilized NF-kappaB to downregulate PTEN, a gene that is rarely mutated in pancreatic cancers. SMAD4-null BxPc3 and CAPAN-1 pancreatic cancer cells were treated with TGF-beta (10 ng/ml) and lysed, and cellular proteins were analyzed by Western blots using p-IkappaB, p65, and PTEN antibodies. PTEN promoter and NF-kappaB activities were assessed by PTEN-luc and p-NF-luc constructs, respectively. Dominant negative p-IkappaB-alpha-M (NF-kappaB superrepressor) was used to block activation of NF-kappaB. Cell motility was assessed by Boyden chamber migration assay. TGF-beta induced IkappaB-alpha phosphorylation followed by NF-kappaB p65 subunit nuclear translocation and increased NF-kappaB activity. IkappaB-alpha-M blocked TGF-beta-induced NF-kappaB activity, reversed downregulated PTEN promoter activity and PTEN expression, and prevented augmentation of cell motility induced by TGF-beta. SMAD4 restoration, but not knockdown of SMAD2 and/or 3, reversed TGF-beta-induced NF-kappaB activity. Thus TGF-beta suppresses PTEN in pancreatic cancer cells through NF-kappaB activation and enhances cell motility and invasiveness in a SMAD4-independent manner that can be counteracted when TGF-beta-SMAD signaling is restored. The TGF-beta/NF-kappaB/PTEN cascade may be a critical pathway for pancreatic cancer cells to proliferate and metastasize.