Background And Aim: A comparison was made between pancreatic ductal adenocarcinoma (PDAC), pancreatic intraepithelial neoplasia (PanIN) and intraductal papillary mucinous carcinoma (IPMC) in order to understand the association between several markers and malignant potential.
Patients And Methods: Fifteen surgically resected PDACs and four IPMCs were subjected to immunohistochemistry with primary antibodies to Ki-67, p53, MUC2, Gli-1, and Claudin-18 (CLDN18).
Results: Ki-67, P53, MUC2, Gli-1 and CLDN18 were positive in 6 (50%), 10 (66.6%), 0 (0%), 4 (26.6%), and 6 (40%) of the 15 PDACs, respectively. Low- to high-grade PanIN complexes were found in 2 out of the 15 PDACs. Gli-1 was continuously expressed in low- and high-grade PanINs. CLDN18 was specifically expressed in high-grade PanINs, whereas the corresponding invasive tubules did not express CLDN18. P53 was positively stained in one of the 4 IPMCs in which minimally invasive tubular type carcinomas were observed. Ki-67 and CLDN18 were positively stained in all 4 IPMCs. CLDN18 was specifically expressed in intestinal-type components of IPMCs.
Conclusion: CLDN18 is involved in intestinal-type epithelial differentiation in the progression of IPMCs, contradicting the previous knowledge of its specificity in gastric epithelial differentiation.
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Nat Rev Gastroenterol Hepatol
January 2025
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Ministerio de Sanidad, Madrid, Spain.
Two main stages are differentiated in patients with advanced chronic liver disease (ACLD), one compensated (cACLD) with an excellent prognosis, and the other decompensated (dACLD), defined by the appearance of complications (ascites, variceal bleeding and hepatic encephalopathy) and associated with high mortality. Preventing the progression to dACLD might dramatically improve prognosis and reduce the burden of care associated with ACLD. Portal hypertension is a major driver of the transition from cACLD to dACLD, and a portal pressure of ≥10 mmHg defines clinically significant portal hypertension (CSPH) as the threshold from which decompensating events may occur.
View Article and Find Full Text PDFJ Immunother Cancer
January 2025
Department of Oncology, Taipei Veterans General Hospital, Taipei, Taiwan
Background: Cholangiocarcinoma is a challenging malignancy with limited responses to conventional therapies, particularly immune checkpoint inhibitor therapy. Tumor-infiltrating lymphocytes (TILs) and tertiary lymphoid structures (TLSs) are key components of the tumor microenvironment (TME) and have been implicated in the immune response to cancer. However, the role and difference of TLSs and TILs in patients with cholangiocarcinoma remains unclear.
View Article and Find Full Text PDFJ Adv Res
January 2025
Department of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan 250012 China; Shandong Engineering Research Center of Biomarker and Artificial Intelligence Application, Jinan 250012 China. Electronic address:
Introduction: Pancreatic cancer (PC) cannot currently be completely cured and has a poor prognosis. Necroptosis is a distinct form of regulated cell death that differs from both necrosis and apoptosis. Understanding the role of necroptosis during PC progression would open new avenues for targeted therapy.
View Article and Find Full Text PDFBiochim Biophys Acta Gen Subj
January 2025
School of Health and Life Sciences, University of Health and Rehabilitation, Sciences, Qingdao 266071, China. Electronic address:
Aberrant glycosylation has been implicated in promoting the progression and metastasis of pancreatic ductal adenocarcinoma (PDAC). However, the contribution of different glycosylation-related genes in PDAC remains to be clarified. In this study, we performed a differential analysis of RNA-Seq data from TCGA and GTEx and found GALNT5 as the most significant upregulated glycosylation-related gene in PDAC.
View Article and Find Full Text PDFPLoS Pathog
January 2025
Department of Cancer and Genomic Sciences, College of Medicine and Health, University of Birmingham, Birmingham, United Kingdom.
Upon infection, human papillomavirus (HPV) manipulates host cell gene expression to create an environment that is supportive of a productive and persistent infection. The virus-induced changes to the host cell's transcriptome are thought to contribute to carcinogenesis. Here, we show by RNA-sequencing that oncogenic HPV18 episome replication in primary human foreskin keratinocytes (HFKs) drives host transcriptional changes that are consistent between multiple HFK donors.
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