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Dear Colleagues,

I am pleased to invite you to contribute to the Special Issue entitled “The Study of Molecular Pathogenesis and Therapeutic Strategies of Pancreatic Cancer”. Pancreatic cancer is an aggressive form of cancer characterised by poor prognosis and survival rate. Despite rapid progress in this field, and the fact that the core genetic mutations associated with pancreatic cancer are well known, their role in pancreatic cancer pathogenesis and progression is yet to be explored. The genomic complexity of pancreatic cancer is defined by high mutational burden and intratumoral heterogeneity. This tumour heterogeneity is closely related to the failure of therapeutic intervention strategies in pancreatic cancer. Henceforth, delineating the heterogeneous molecular pathology of this cancer will facilitate the identification of new molecular targets for personalised therapeutic options.

This Special Issue aims to discuss recent advancements in our understanding of new molecular targets, multifocal neoplasia associated with precancerous lesions, dysregulation/upregulation of cell signalling networks, pathophysiology of the complex tumour microenvironment and innovative therapeutic intervention in pancreatic cancer.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following: original research articles and reviews.

I look forward to receiving your contributions.

Prof. Dr. Marco Falasca
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. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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 cancer
pancreatic ductal adenocarcinoma
molecular pathogenesis
chemotherapy
metastasis
tumour microenvironment
neoadjuvant therapy
immunotherapy
chemoresistance
novel therapeutics

Published Papers (2 papers)

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Research

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15 pages, 3070 KiB

Open AccessArticle

TWEAK/Fn14 Signalling Regulates the Tissue Microenvironment in Chronic Pancreatitis

by N. Dianah B. Abu Bakar, Rodrigo Carlessi, Jully Gogoi-Tiwari, Julia Köhn-Gaone, Vincent Williams, Marco Falasca, John K. Olynyk, Grant A. Ramm and Janina E. E. Tirnitz-Parker

Cancers 2023, 15(6), 1807; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers15061807 - 16 Mar 2023

Cited by 1 | Viewed by 1644

Abstract

Chronic pancreatitis increases the risk of developing pancreatic cancer through the upregulation of pathways favouring proliferation, fibrosis, and sustained inflammation. We established in previous studies that the ligand tumour necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) signals through its cognate receptor fibroblast growth factor-inducible 14 (Fn14) to regulate these underlying cellular processes in the chronic liver injury niche. However, the role of the TWEAK/Fn14 signalling pathway in pancreatic disease is entirely unknown. An analysis of publicly available datasets demonstrated that the TWEAK receptor Fn14 is upregulated in pancreatitis and pancreatic adenocarcinoma, with single cell RNA sequencing revealing pancreatic ductal cells as the main Fn14 producers. We then used choline-deficient, ethionine-supplemented (CDE) diet feeding of wildtype C57BL/6J and Fn14 knockout littermates to (a) confirm CDE treatment as a suitable model of chronic pancreatitis and (b) to investigate the role of the TWEAK/Fn14 signalling pathway in pancreatic ductal proliferation, as well as fibrotic and inflammatory cell dynamics. Our time course data obtained at three days, three months, and six months of CDE treatment reveal that a lack of TWEAK/Fn14 signalling significantly inhibits the establishment and progression of the tissue microenvironment in CDE-induced chronic pancreatitis, thus proposing the TWEAK/Fn14 pathway as a novel therapeutic target. Full article

(This article belongs to the Special Issue The Study of Molecular Pathogenesis and Therapeutic Strategies of Pancreatic Cancer)

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Review

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22 pages, 1925 KiB

Open AccessReview

Perineural Invasion in Pancreatic Ductal Adenocarcinoma: From Molecules towards Drugs of Clinical Relevance

by Federico Selvaggi, Eugenia Melchiorre, Ilaria Casari, Sebastiano Cinalli, Massimiliano Cinalli, Gitana Maria Aceto, Roberto Cotellese, Ingrid Garajova and Marco Falasca

Cancers 2022, 14(23), 5793; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14235793 - 24 Nov 2022

Cited by 10 | Viewed by 2677

Abstract

Pancreatic ductal adenocarcinoma is one of the most threatening solid malignancies. Molecular and cellular mediators that activate paracrine signalling also regulate the dynamic interaction between pancreatic cancer cells and nerves. This reciprocal interface leads to perineural invasion (PNI), defined as the ability of cancer cells to invade nerves, similar to vascular and lymphatic metastatic cascade. Targeting PNI in pancreatic cancer might help ameliorate prognosis and pain relief. In this review, the modern knowledge of PNI in pancreatic cancer has been analysed and critically presented. We focused on molecular pathways promoting cancer progression, with particular emphasis on neuropathic pain generation, and we reviewed the current knowledge of pharmacological inhibitors of the PNI axis. PNI represents a common hallmark of PDAC and correlates with recurrence, poor prognosis and pain in pancreatic cancer patients. The interaction among pancreatic cancer cells, immune cells and nerves is biologically relevant in each stage of the disease and stimulates great interest, but the real impact of the administration of novel agents in clinical practice is limited. It is still early days for PNI-targeted treatments, and further advanced studies are needed to understand whether they could be effective tools in the clinical setting. Full article

(This article belongs to the Special Issue The Study of Molecular Pathogenesis and Therapeutic Strategies of Pancreatic Cancer)

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