DBTC joint Ethanol drinking can induce chronic pancreatitis in accordance with the pathophysiological modification of human. DBTC joint Ethanol-induced pancreatitis in mice is an effective and handy experimental method. The model is suitable to study the mechanism of pancreatic fibrosis in chronic pancreatitis.

As a family of G protein-coupled receptors (GPCRs) with a seven-span transmembrane structure, frizzled class receptors (FZDs) play crucial roles in regulating multiple biological functions. However, their transcriptional expression profile and prognostic significance in acute myeloid leukemia (AML) are unclear. In AML, the role of FZDs was explored by performing the comprehensive analysis on the relationship between clinical characteristics and mRNA expression profiles from public databases including cBioPortal for Cancer Genomics, Gene Expression Profile Interactive Analysis (GEPIA), and Cancer Cell Line Encyclopedia (CCLE). We identified that in the majority of 27 AML cell lines, frizzled class receptor 6 (FZD6) was high-expressed. A significantly higher expression of FZD6 in AML patients was observed when compared to normal controls ( P < 0.01 ). Compared with intermediate and poor/adverse risk group patients, FZD6 expressed much lower in cytogenetic favorable risk group patients ( P < 0.0001 ). Patients with higher-expressed FZD6 were associated with shorter overall survival (OS) ( P = 0.0089 ) rather than progression-free survival (PFS). However, the predictive effect of FZD6 on OS could be reversed by hematopoietic stem cell transplantation (HSCT). The data of gene set enrichment analysis (GSEA) demonstrated that 4 gene sets, including MYC targets, HEME metabolism, E2F targets, and UV response, were differentially enriched in the high-expression FZD6 group. To conclude, the study suggested that high expression of FZD6 might be a novel poor prognostic biomarker for AML treatment.

Pancreatic ductal metaplasia (PDM) is the stepwise replacement of differentiated somatic cells with ductal or ductallike cells in the pancreas. PDM is usually triggered by cellular and environmental insults. PDM development may involve all cell lineages of the pancreas, and acinar cells with the highest plasticity are the major source of PDM. Pancreatic progenitor cells are also involved as cells of origin or transitional intermediates. PDM is heterogeneous at the histological, cellular, and molecular levels and only certain subsets of PDM develop further into pancreatic intraepithelial neoplasia (PanIN) and then pancreatic ductal adenocarcinoma (PDAC). The formation and evolution of PDM is regulated at the cellular and molecular levels through a complex network of signaling pathways. The key molecular mechanisms that drive PDM formation and its progression into PanIN/PDAC remain unclear, but represent key targets for reversing or inhibiting PDM. Alternatively, PDM could be a source of pancreas regeneration, including both exocrine and endocrine components. Cellular aging and apoptosis are obstacles to PDM-to-PanIN progression or pancreas regeneration. Functional identification of the cellular and molecular events driving senescence and apoptosis in PDM and its progression would help not only to restrict the development of PDM into PanIN/PDAC, but may also facilitate pancreatic regeneration. This review systematically assesses recent advances in the understanding of PDM physiology and pathology, with a focus on its implications for enhancing regeneration and prevention of cancer.

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