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Cancers
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Metastatic Pancreatic Ductal Adenocarcinoma
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Metastatic Pancreatic Ductal Adenocarcinoma

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (13 August 2021) | Viewed by 10812

Special Issue Editors

Prof. Dr. Maneesh Jain

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, College of Medicine, University of Nebraska Medical Center, Omaha, NE 68198, USA
Interests: pancreatic tumor microenvironment; targeted therapies; metastasis
Prof. Dr. Surinder K. Batra

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198-5870, USA
Interests: mucins; oncogenes; cancer stem cells; animal models

Special Issue Information

Dear Colleagues,

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers and is almost always associated with overt or occult metastasis at the time of clinical diagnosis. This malignancy is characterized by a highly complex and heterogeneous tumor microenvironment that contributes to therapy resistance and metastasis. The articles in this Special Issue will focus on various driver genes, signaling pathways, metabolic alterations, and cellular and acellular components that contribute to the metastatic fitness of pancreatic cancer cells. The issue will also focus on various aspects or organotropism and discuss how components of the immune system contribute to metastatic spread. Finally, the articles will also discuss various experimental models being employed to study pancreatic cancer metastasis and preclinical test experimental therapeutics targeting metastatic disease and provide an update on the clinical challenges in combating metastatic PDAC.

Prof. Dr. Maneesh Jain
Prof. Dr. Surinder K. Batra
Guest Editors

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 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 ductal adenocarcinoma
  • metastasis
  • metastatic fitness
  • tumor microenvironment
  • organotropism
  • metastatic niche
  • metabolomics
  • cancer stem cells
  • immune cells
  • animal models

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Published Papers (2 papers)

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Research

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18 pages, 40425 KiB  
Article
Pancreatic Lineage Specifier PDX1 Increases Adhesion and Decreases Motility of Cancer Cells
by Liya Kondratyeva, Igor Chernov, Eugene Kopantzev, Dmitry Didych, Alexey Kuzmich, Irina Alekseenko, Sergey Kostrov and Eugene Sverdlov
Cancers 2021, 13(17), 4390; https://doi.org/10.3390/cancers13174390 - 30 Aug 2021
Cited by 5 | Viewed by 2950
Abstract
Intercellular interactions involving adhesion factors are key operators in cancer progression. In particular, these factors are responsible for facilitating cell migration and metastasis. Strengthening of adhesion between tumor cells and surrounding cells or extracellular matrix (ECM), may provide a way to inhibit tumor [...] Read more.
Intercellular interactions involving adhesion factors are key operators in cancer progression. In particular, these factors are responsible for facilitating cell migration and metastasis. Strengthening of adhesion between tumor cells and surrounding cells or extracellular matrix (ECM), may provide a way to inhibit tumor cell migration. Recently, we demonstrated that PDX1 ectopic expression results in the reduction of pancreatic cancer line PANC-1 cell motility in vitro and in vivo, and we now provide experimental data confirming the hypothesis that suppression of migration may be related to the effect of PDX1 on cell adhesion. Cell migration analyses demonstrated decreased motility of pancreatic Colo357 and PANC-1 cell lines expressing PDX1. We observed decreased expression levels of genes associated with promoting cell migration and increased expression of genes negatively affecting cell motility. Expression of the EMT regulator genes was only mildly induced in cells expressing PDX1 during the simulation of the epithelial-mesenchymal transition (EMT) by the addition of TGFβ1 to the medium. PDX1-expressing cancer cell lines showed increased cell adhesion to collagen type I, fibronectin, and poly-lysine. We conclude that ectopic expression of PDX1 reduces the migration potential of cancer cells, by increasing the adhesive properties of cells and reducing the sensitivity to TGFβ1-induced EMT. Full article
(This article belongs to the Special Issue Metastatic Pancreatic Ductal Adenocarcinoma)
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Review

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18 pages, 6114 KiB  
Review
Stem Cells in the Exocrine Pancreas during Homeostasis, Injury, and Cancer
by Sophie C. Lodestijn, Sanne M. van Neerven, Louis Vermeulen and Maarten F. Bijlsma
Cancers 2021, 13(13), 3295; https://doi.org/10.3390/cancers13133295 - 30 Jun 2021
Cited by 6 | Viewed by 7146
Abstract
Cell generation and renewal are essential processes to develop, maintain, and regenerate tissues. New cells can be generated from immature cell types, such as stem-like cells, or originate from more differentiated pre-existing cells that self-renew or transdifferentiate. The adult pancreas is a dormant [...] Read more.
Cell generation and renewal are essential processes to develop, maintain, and regenerate tissues. New cells can be generated from immature cell types, such as stem-like cells, or originate from more differentiated pre-existing cells that self-renew or transdifferentiate. The adult pancreas is a dormant organ with limited regeneration capacity, which complicates studying these processes. As a result, there is still discussion about the existence of stem cells in the adult pancreas. Interestingly, in contrast to the classical stem cell concept, stem cell properties seem to be plastic, and, in circumstances of injury, differentiated cells can revert back to a more immature cellular state. Importantly, deregulation of the balance between cellular proliferation and differentiation can lead to disease initiation, in particular to cancer formation. Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with a 5-year survival rate of only ~9%. Unfortunately, metastasis formation often occurs prior to diagnosis, and most tumors are resistant to current treatment strategies. It has been proposed that a specific subpopulation of cells, i.e., cancer stem cells (CSCs), are responsible for tumor expansion, metastasis formation, and therapy resistance. Understanding the underlying mechanisms of pancreatic stem cells during homeostasis and injury might lead to new insights to understand the role of CSCs in PDAC. Therefore, in this review, we present an overview of the current literature regarding the stem cell dynamics in the pancreas during health and disease. Furthermore, we highlight the influence of the tumor microenvironment on the growth behavior of PDAC. Full article
(This article belongs to the Special Issue Metastatic Pancreatic Ductal Adenocarcinoma)
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