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Molecular Mechanisms and Cell Biology of Pancreatic Diseases
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Molecular Mechanisms and Cell Biology of Pancreatic Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 March 2025) | Viewed by 1330

Special Issue Editor

Prof. Dr. Hirohito Ichii

E-Mail Website
Guest Editor
Department of Surgery, University of California, Irvine, CA 92697, USA
Interests: islet; pancreas; kidney transplantation; islet isolation; type I diabetes; memory T cell; immunosuppression

Special Issue Information

Dear Colleagues,

The pancreas, a crucial organ, regulates blood sugar levels and secretes digestive enzymes. Dysfunction can cause diverse diseases, impacting public health. Understanding pancreatic diseases at the cellular and molecular levels is key for effective diagnosis and treatment.

Research in this field has far-reaching applications. Genetic studies identify personalized medicine targets, enabling precision-based strategies. Animal models provide insights into disease mechanisms and novel drug evaluations. Cell signaling and transcription factor regulations pave the way for novel therapies.

We invite scholars in the field to contribute to this Special Issue by submitting their latest research on the molecular mechanisms, cell function, and disease progression of pancreatic diseases.

Prof. Dr. Hirohito Ichii
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • pancreatic diseases
  • pancreas
  • cell and molecular biology
  • pathogenesis
  • islet
  • therapeutic approaches

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Published Papers (1 paper)

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Research

18 pages, 3388 KiB  
Article
Gene Dysregulation and Islet Changes in PDAC-Associated Type 3c Diabetes
by Jessica L. E. Hill, Eliot Leonard, Dominique Parslow and David J. Hill
Int. J. Mol. Sci. 2025, 26(7), 3191; https://doi.org/10.3390/ijms26073191 - 29 Mar 2025
Viewed by 803
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy, often associated with new-onset diabetes. The relationship between PDAC and diabetes, particularly type 3c diabetes, remains poorly understood. This study investigates whether PDAC-associated diabetes represents a distinct subtype by integrating transcriptomic and histological analyses. [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy, often associated with new-onset diabetes. The relationship between PDAC and diabetes, particularly type 3c diabetes, remains poorly understood. This study investigates whether PDAC-associated diabetes represents a distinct subtype by integrating transcriptomic and histological analyses. Whole-tumour RNA sequencing data from The Cancer Genome Atlas (TCGA) were analysed to compare gene expression profiles between PDAC patients with and without diabetes. Cell-type Identification By Estimating Relative Subsets Of RNA Transcripts (CIBERSORT) deconvolution was employed to assess immune cell populations. Histopathological evaluations of pancreatic tissues were conducted to assess fibrosis and islet morphology. Histological analysis revealed perivascular fibrosis and islet basement membrane thickening in both PDAC cohorts. Transcriptomic data indicated significant downregulation of islet hormone genes insulin (INS) and glucagon (GCG) but not somatostatin (SST) in PDAC-associated diabetes, consistent with a type 3c diabetes phenotype. Contrary to previous reports, no distinct immunogenic signature was identified in PDAC with diabetes, as key immune checkpoint genes (Programmed Cell Death Protein 1 (PDCD1), Cytotoxic T-Lymphocyte Associated Protein 4 (CTLA4), Programmed Death-Ligand 1(PD-L1)) were not differentially expressed. The findings suggest that PDAC-associated diabetes arises through neoplastic alterations in islet physiology rather than immune-mediated mechanisms. The observed reductions in endocrine markers reinforce the concept of PDAC-driven β-cell dysfunction as a potential early indicator of malignancy. Given the poor response of PDAC to PD-L1 checkpoint inhibitors, further research is needed to elucidate alternative therapeutic strategies targeting tumour–islet interactions. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Cell Biology of Pancreatic Diseases)
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