Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Molecular Research on Microenvironment and Pancreatic Tumorigenesis

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 13670

Share This Special Issue

Special Issue Editor

Dr. Richard Tomasini

E-Mail Website
Guest Editor

Cancer Research Center of Marseille, Institut Paoli-Calmettes, CNRS, UMR7258, Institut National de la Santé et de la Recherche Médicale (INSERM), U1068, University Aix-Marseille, 13009 Marseille, France
Interests: pancreatic cancer; microenvironment; extracellular vesicles; intercellular communication; macrophages; cancer-associated fibroblasts; monocyte; neural remodeling; peri-neural invasion

Special Issue Information

Dear Colleagues,

While being a growing field of research to improve pancreatic cancer therapies and patient care, the role of non-tumoral cells composing the intra-tumoral microenvironment still needs to be better understood. Indeed, known to impact tumor cells’ proliferation, metabolism, cell death and resistance to therapies among others, the translational potential of studies to deepen the impact of this microenvironmental network on pancreatic cancer failed to significantly improve patients’ survival.

Composed mainly of vascular, nervous and immune cells that are embedded in a cancer-associated fibroblast-driven extracellular matrix, understanding the complex and multiscale connection shaping this intra-tumoral microenvironment, and the consequent crosstalk with tumor cells, should open new avenues to target both cellular and acellular active components of such aggressive tumors.

This Special Issue intends to deepen, at the molecular level, the impact of the intratumoral microenvironment on pancreatic cancer development and spreading, as well as its ability to avoid immune surveillance and favor therapeutic resistance.

Dr. Richard Tomasini
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

Cancer-associated fibroblasts
Adipocytes
Immune system
Endothelial cells
Nervous system
Extracellular matrix
Secreted factors
Extracellular vesicles
Biomarkers
Therapeutic resistance
Metabolism

Published Papers (3 papers)

Download All Papers

Research

Jump to: Review

17 pages, 5973 KiB

Open AccessArticle

ANXA1 Contained in EVs Regulates Macrophage Polarization in Tumor Microenvironment and Promotes Pancreatic Cancer Progression and Metastasis

by Nunzia Novizio, Raffaella Belvedere, Emanuela Pessolano, Silvana Morello, Alessandra Tosco, Pietro Campiglia, Amelia Filippelli and Antonello Petrella

Int. J. Mol. Sci. 2021, 22(20), 11018; https://doi.org/10.3390/ijms222011018 - 13 Oct 2021

Cited by 24 | Viewed by 2757

Abstract

The tumor microenvironment (TME) is a dynamic system where nontumor and cancer cells intercommunicate through soluble factors and extracellular vesicles (EVs). The TME in pancreatic cancer (PC) is critical for its aggressiveness and the annexin A1 (ANXA1) has been identified as one of the oncogenic elements. Previously, we demonstrated that the autocrine/paracrine activities of extracellular ANXA1 depend on its presence in EVs. Here, we show that the complex ANXA1/EVs modulates the macrophage polarization further contributing to cancer progression. The EVs isolated from wild type (WT) and ANXA1 knock-out MIA PaCa-2 cells have been administrated to THP-1 macrophages finding that ANXA1 is crucial for the acquisition of a protumor M2 phenotype. The M2 macrophages activate endothelial cells and fibroblasts to induce angiogenesis and matrix degradation, respectively. We have also found a significantly increased presence of M2 macrophage in mice tumor and liver metastasis sections previously obtained by orthotopic xenografts with WT cells. Taken together, our data interestingly suggest the relevance of ANXA1 as potential diagnostic/prognostic and/or therapeutic PC marker. Full article

(This article belongs to the Special Issue Molecular Research on Microenvironment and Pancreatic Tumorigenesis)

► Show Figures

Figure 1

Review

Jump to: Research

21 pages, 2105 KiB

Open AccessReview

Pancreatic Cancer and Cellular Senescence: Tumor Microenvironment under the Spotlight

by Michela Cortesi, Michele Zanoni, Francesca Pirini, Maria Maddalena Tumedei, Sara Ravaioli, Ilario Giovanni Rapposelli, Giovanni Luca Frassineti and Sara Bravaccini

Int. J. Mol. Sci. 2022, 23(1), 254; https://doi.org/10.3390/ijms23010254 - 27 Dec 2021

Cited by 30 | Viewed by 5989

Abstract

Pancreatic ductal adenocarcinoma (PDAC) has one of the most dismal prognoses of all cancers due to its late manifestation and resistance to current therapies. Accumulating evidence has suggested that the malignant behavior of this cancer is mainly influenced by the associated strongly immunosuppressive, desmoplastic microenvironment and by the relatively low mutational burden. PDAC develops and progresses through a multi-step process. Early in tumorigenesis, cancer cells must evade the effects of cellular senescence, which slows proliferation and promotes the immune-mediated elimination of pre-malignant cells. The role of senescence as a tumor suppressor has been well-established; however, recent evidence has revealed novel pro-tumorigenic paracrine functions of senescent cells towards their microenvironment. Understanding the interactions between tumors and their microenvironment is a growing research field, with evidence having been provided that non-tumoral cells composing the tumor microenvironment (TME) influence tumor proliferation, metabolism, cell death, and therapeutic resistance. Simultaneously, cancer cells shape a tumor-supportive and immunosuppressive environment, influencing both non-tumoral neighboring and distant cells. The overall intention of this review is to provide an overview of the interplay that occurs between senescent and non-senescent cell types and to describe how such interplay may have an impact on PDAC progression. Specifically, the effects and the molecular changes occurring in non-cancerous cells during senescence, and how these may contribute to a tumor-permissive microenvironment, will be discussed. Finally, senescence targeting strategies will be briefly introduced, highlighting their potential in the treatment of PDAC. Full article

(This article belongs to the Special Issue Molecular Research on Microenvironment and Pancreatic Tumorigenesis)

► Show Figures

Figure 1

17 pages, 1137 KiB

Open AccessReview

Highlights on the Role of KRAS Mutations in Reshaping the Microenvironment of Pancreatic Adenocarcinoma

by Shirin Hafezi, Maha Saber-Ayad and Wael M. Abdel-Rahman

Int. J. Mol. Sci. 2021, 22(19), 10219; https://doi.org/10.3390/ijms221910219 - 23 Sep 2021

Cited by 15 | Viewed by 4060

Abstract

The most frequent mutated oncogene family in the history of human cancer is the RAS gene family, including NRAS, HRAS, and, most importantly, KRAS. A hallmark of pancreatic cancer, recalcitrant cancer with a very low survival rate, is the prevalence of oncogenic mutations in the KRAS gene. Due to this fact, studying the function of KRAS and the impact of its mutations on the tumor microenvironment (TME) is a priority for understanding pancreatic cancer progression and designing novel therapeutic strategies for the treatment of the dismal disease. Despite some recent enlightening studies, there is still a wide gap in our knowledge regarding the impact of KRAS mutations on different components of the pancreatic TME. In this review, we will present an updated summary of mutant KRAS role in the initiation, progression, and modulation of the TME of pancreatic ductal adenocarcinoma (PDAC). This review will highlight the intriguing link between diabetes mellitus and PDAC, as well as vitamin D as an adjuvant effective therapy via TME modulation of PDAC. We will also discuss different ongoing clinical trials that use KRAS oncogene signaling network as therapeutic targets. Full article

(This article belongs to the Special Issue Molecular Research on Microenvironment and Pancreatic Tumorigenesis)

► Show Figures