Efficacy of the revised Vienna Classification for diagnosing colorectal epithelial neoplasias

AIM： To prospectively investigate the efficacy of the revised Vienna Classification for diagnosing colorectal epithelial neoplastic lesions in cold biopsy specimens.METHODS： Patients were selected for inclusion if they had colorectal epithelial lesions that were not considered suitable for direct endoscopic resection,These included colorectal polyps ≥ 10 mm and lesions suspected of being carcinomas capable of invading the colorectal submucosa or beyond, including strictures, based on the cold biopsies obtained from each lesion prior to resection. We investigated the relationship between diagnoses based on cold biopsy samples using the revised Vienna Classification and resected specimens of the same lesions, and the therapeutic implications of diagnoses made using the revised Vienna Classification. The same cold biopsy specimens were also examined using the Japanese Group Classification guidelines, and compared with the resected specimens of the same lesions for reference.RESULTS： A total of 179 lesions were identified. The sensitivity, specificity, positive and negativepredictive values of the revised Vienna Classification for distinguishing between intramucosal lesions and submucosal invasive carcinomas in cold biopsy specimens was 22.2%, 100%, 100%, and 71.4%,respectively, and for distinguishing between intramucosal lesions and those invading the submucosa or beyond was 59.7%, 100%, 100%, and 37.6%,respectively. The sensitivity, specificity, positive and negative predictive values of the Japanese Group Classification for distinguishing between intramucosal lesions and submucosal invasive carcinomas in cold biopsy specimens was 83.3%, 91.4%, 83.3%. and 91.4%, respectively, and for distinguishing between intramucosal lesions and those invading the submucosa or beyond was 95.1%, 91.4%, 97.9%, and 82.1%, respectively. A total of 137 of 144 carcinomas that had invaded the submucosa or beyond and three high-grade intraepithelial neoplasias were diagnosed as ＂carcinoma＂ using the Japanese Group Classification system.CONCLUSION： The revised Vienna Classification for cold biopsy specimens has high positive predictive value in the diagnosis of colorectal carcinoma invasive to the subrnucosa or beyond.

Moxibustion down-regulates colonic epithelial cell apoptosis and repairs tight junctions in rats with Crohn's disease

AIM: To investigate the effects of moxibustion on down-regulation of the colonic epithelial cell apoptosis and repair of the tight junctions in rats with Crohn's disease (CD). METHODS: Sixty male Sprague-Dawley rats were randomly divided into a normal control (NC) group, a model control (MC) group, an herbs-partitioned moxibustion (HPM) group, a mild-warm moxibustion (MWM) group and a salicylazosulphapyridine (SASP) group, with 12 rats in each group. The CD model rats were treated with trinitrobenzene sulphonic acid to induce intestinal inflammation. The rats in the HPM and MWM groups were treated at the Tianshu (ST25) and Qihai (CV6) acupoints once daily for 14 d, and the SASP group was fed SASP twice daily for 14 d. No additional treatment was given to the MC and NC groups. Themicrostructure of the colonic epithelium was observed under a transmission electron microscope, the transepithelial resistance was measured using a shortcircuit current, colonic epithelial cell apoptosis was determined by terminal deoxynucleotidyl transferasemediated dUTP-biotin nick end labelling assay, and the expression of occludin, claudin-1 and zonula occludens-l (ZO-1) in the colonic epithelial junction was determined by Western blotting and immunofluorescence staining. RESULTS: Compared with the MC group, the microstructure of the colonic epithelial barrier was signifi-cantly improved in rats treated with HPM, MWM or SASP, meanwhile, the current flow was reduced signifi-cantly, with values of 168.20 ± 6.14 vs 99.70 ± 3.13, 99.10 ± 4.28 and 120.30 ± 3.65 mA, respectively (P = 0.001). However, the HPM and MWM groups had higher current flow rates than the SASP group (99.70 ± 3.13, 99.10 ± 4.28 vs 120.30 ± 3.65 mA, P = 0.001). The number of the apoptotic colonic epithelial cells in HPM, MWM and SASP groups was largely reduced (61.5 ± 16.91 vs 15.5 ± 8.89, 14.8 ± 6.27 and 24.7 ± 9.68, respectively (P = 0.001); and the expression of occlu- din, claudin-1 and ZO-1 in the MWM and HPM groups was signifi cantly enhanced (0.48 ± 0.10, 0.64 ± 0.09 vs 0.18 ± 0.05 for occludin, 0.12 ± 0.02, 0.17 ± 0.03 vs 0.05 ± 0.01 for claudin-1, and 0.08 ± 0.01, 0.11 ± 0.01 vs 0.02 ± 0.01 for ZO-1). And in SASP group, the expression of occludin and ZO-1 was also signifi cantly increased (0.27 ± 0.04 vs 0.18 ± 0.05 for occludin and 0.05 ± 0.01 vs 0.02 ± 0.01 for ZO-1), but there was no significant difference for claudin-1. The HPM and MWM groups had higher expression of occludin, claudin-1 and ZO-1 than the SASP group. CONCLUSION: HPM and MWM treatment can down-regulate apoptosis of colonic epithelial cells, repair tight junctions and enhance colonic epithelial barrier function in rats with CD.

Epigenetic and metabolic regulation of breast cancer stem cells

Breast cancer has a relatively high mortality rate in women due to recurrence and metastasis. Increasing evidence has identified a rare population of cells with stem cell-like properties in breast cancer. These cells, termed cancer stem cells （CSCs）, which have the capacity for self-renewal and differentiation, contribute significantly to tumor progression, recurrence, drug resistance and metastasis. Clarifying the mechanisms regulating breast CSCs has important implications for our understanding of breast cancer progression and therapeutics. A strong connection has been found between breast CSCs and epithelial mesenchymal transition （EMT）. In addition, recent studies suggest that the maintenance of the breast CSC phenotype is associated with epigenetic and metabolic regulation. In this review, we focus on recent discoveries about the connection between EMT and CSC, and advances made in under- standing the roles and mechanisms of epigenetic and metabolic reprogramming in controlling breast CSC properties.