Résumé
Background: Colorectal adenoma is the precursor lesion of colorectal cancer, and diabetes mellitus is associated with an increased risk for colorectal cancer. Aims: To investigate the clinicopathological characteristics of colorectal adenoma in patients with type 2 diabetes mellitus (T2DM) and the risk factors for advanced adenoma. Methods: Seven hundred and eighty T2DM patients who underwent initial colonoscopy from January 2018 to December 2020 at the Second Affiliated Hospital of Zhejiang Chinese Medical University were enrolled retrospectively, including 227 patients with colorectal adenoma and 553 patients without colorectal polyps. Furthermore, 227 non-diabetic patients with colorectal adenoma who were 1:1 matched to T2DM-adenoma group for gender, age, body mass index (BMI) and smoking history were collected for a comparison study. The clinical and pathological characteristics of T2DM patients with colorectal adenoma were analyzed, and the risk factors for advanced adenoma were identified by univariate and multivariate analyses. Results: T2DM patients with colorectal adenoma were older than those without colorectal polyps, and male gender, tobacco smoking, and cholelithiasis/cholecystectomy were more frequently seen in T2DM-adenoma group (all P<0.05). The proportions of multiple adenomas and advanced adenoma in T2DM-adenoma group were greater than those in patients without T2DM (16.7% vs. 10.1%, and 21.6% vs. 14.1%, all P<0.05). Multivariate Logistic regression analysis identified that male gender (OR=1.299, 95% CI: 1.041-1.831, P=0.008), age (OR=1.129, 95% CI: 1.001-1.421, P=0.025), BMI (OR=1.118, 95% CI: 1.022-1.715, P=0.038) and T2DM (OR=1.408, 95% CI: 1.141-1.721, P=0.010) were the independent risk factors for advanced adenoma. Conclusions: Multiple colorectal adenomas and advanced adenoma are more likely to be detected in patients with T2DM. Male gender, age, BMI and T2DM are associated with the risk of advanced adenoma.
Résumé
Background: Studies showed that aberrant activation of JAK/STAT3 signaling pathway promoted the tumorigenesis and progression of hepatocellular carcinoma (HCC), and transforming growth factor-β1 (TGF-β1) has either tumor-suppressing or tumor-promoting effect in regulation of tumor progression.Aims: To investigate the effect of specific inhibition of JAK/STAT3 signaling pathway on HCC and whether TGF-β1 signaling pathway is involved in this process or not.Methods: Thirty Wistar rats were randomly divided into three groups: control group, HCC group, and HCC+AG490 group.In the latter two groups, diethylnitrosamine was administered in drinking water to induce HCC model, and in HCC+AG490 group, AG490, a specific inhibitor of JAK was injected intraperitoneally in the first week of model establishment.At the end of the 16th week, all rats were sacrificed.The maximum diameter of tumor nodules in the liver was recorded and the number of tumors with maximum diameter greater than 1 cm was counted.Expression and distribution of STAT3 and TGF-β1 in liver tissue were determined by real-time PCR, immunohistochemistry, and immunofluorescence.Results: Compared with the control group, expressions of STAT3 and TGF-β1 mRNA in liver tissue were significantly increased in HCC group (P<0.05).Phosphorylated STAT3 (p-STAT3) and TGF-β1 proteins were absent in liver tissue in control group, and both were up-regulated and co-expressed in HCC group.While in HCC+AG490 group, expressions of STAT3 and TGF-β1 mRNA were significantly lower than those in HCC group (P<0.05);the liver tissue was weakly positive for p-STAT3 and TGF-β1 proteins, and the number of tumor nodules greater than 1 cm and the maximum diameter were markedly reduced when compared with the HCC group [1.20±1.03 and (1.14±0.18) cm vs.4.30±1.06 and (1.78±0.27) cm, P all<0.05].Conclusions: Specific inhibition of JAK/STAT3 signaling pathway may restrain the tumorigenesis and progression of HCC partially by interfering TGF-β1 signaling pathway.
Résumé
Epithelial-mesenchymal transition (EMT) is a process by which epithelial cells lose their own features and become mesenchymal cells, and more and more studies have shown that EMT plays an important role in the invasion and metastasis of hepatocellular carcinoma (HCC). This article reviews the signaling pathways involved in the progression of HCC and molecules involved in the regulation of EMT, in order to provide a new direction for the treatment of HCC.