Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
4.0
4.2
Journals
Biology
Special Issues
Examining the Biology of Mesothelin in Normal Physiology, Cancer and...
share announcement

Examining the Biology of Mesothelin in Normal Physiology, Cancer and Therapeutic Development

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cancer Biology".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 4024

Special Issue Editor

Dr. Christine Alewine

E-Mail Website
Guest Editor
NCI Center for Cancer Research, Bethesda, MD, USA
Interests: pancreatic cancer; mesothelin; immunotoxin

Special Issue Information

Dear Colleagues,

Mesothelin (MSLN) was first cloned and characterized from a screen for surface antigens highly expressed in cancer cells but lacking in normal cells. After a quarter century of studying MSLN as a target for anti-cancer therapeutics and clinical diagnostics, our understanding of this unusual protein has grown tremendously, however, this knowledge has yet to yield a drug or clinical diagnostics approval.

We propose in this Special Issue to examine the biology of MSLN in the growth and metastasis of various cancers, to appreciate the role of MSLN in physiologic processes outside of cancer, and to investigate novel strategies utilizing our present knowledge of MSLN biology to bring improved clinical diagnostics and therapeutics to patients. A successful quest for beneficial clinical end products relies on an enhanced understanding of the structure, expression, modifications, processing, localization, signaling and interactions of MSLN, and an appreciation for how these impact drug design, safety, distribution, delivery, efficacy, resistance, and immune response as well as the clinical performance of diagnostics. Further, the field requires novel pre-clinical models to investigate these developments, and novel clinical trial designs to test them in patients. Advances will require the convergence of research from clinical, translational, and basic scientists. This Special Issue provides a forum for integrating MSLN research from these various disciplines to stimulate continued innovation in the field.

Dr. Christine Alewine
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. Biology is an international peer-reviewed open access monthly 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 2700 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

  • mesothelin
  • mesothelioma
  • pancreatic cancer
  • ovarian cancer
  • liver fibrosis
  • megakaryocyte potentiating factor
  • immunotherapy
  • antibody conjugates
  • glycosylation
  • serum marker
  • MUC16
  • serum mesothelin-related protein

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

12 pages, 785 KiB  
Article
Mesothelin Gene Variants Affect Soluble Mesothelin-Related Protein Levels in the Plasma of Asbestos-Exposed Males and Mesothelioma Patients from Germany
by Hans-Peter Rihs, Swaantje Casjens, Irina Raiko, Jens Kollmeier, Martin Lehnert, Kerstin Nöfer, Kerstin May-Taube, Nina Kaiser, Dirk Taeger, Thomas Behrens, Thomas Brüning and Georg Johnen
Biology 2022, 11(12), 1826; https://doi.org/10.3390/biology11121826 - 14 Dec 2022
Cited by 1 | Viewed by 1464
Abstract
Malignant mesothelioma (MM) is a severe disease mostly caused by asbestos exposure. Today, one of the best available biomarkers is the soluble mesothelin-related protein (SMRP), also known as mesothelin. Recent studies have shown that mesothelin levels are influenced by individual genetic variability. This [...] Read more.
Malignant mesothelioma (MM) is a severe disease mostly caused by asbestos exposure. Today, one of the best available biomarkers is the soluble mesothelin-related protein (SMRP), also known as mesothelin. Recent studies have shown that mesothelin levels are influenced by individual genetic variability. This study aimed to investigate the influence of three mesothelin (MSLN) gene variants (SNPs) in the 5′-untranslated promoter region (5′-UTR), MSLN rs2235503 C > A, rs3764246 A > G, rs3764247 A > C, and one (rs1057147 G > A) in the 3′-untranslated region (3′-UTR) of the MSLN gene on plasma concentrations of mesothelin in 410 asbestos-exposed males without cancer and 43 males with prediagnostic MM (i.e., with MM diagnosed later on) from the prospective MoMar study, as well as 59 males with manifest MM from Germany. The mesothelin concentration differed significantly between the different groups (p < 0.0001), but not between the prediagnostic and manifest MM groups (p = 0.502). Five to eight mutations of the four SNP variants studied were associated with increased mesothelin concentrations (p = 0.001). The highest mesothelin concentrations were observed for homozygous variants of the three promotor SNPs in the 5′-UTR (p < 0.001), and the highest odds ratio for an elevated mesothelin concentration was observed for MSLN rs2235503 C > A. The four studied SNPs had a clear influence on the mesothelin concentration in plasma. Hence, the analysis of these SNPs may help to elucidate the diagnostic background of patients displaying increased mesothelin levels and might help to reduce false-positive results when using mesothelin for MM screening in high-risk groups. Full article
(This article belongs to the Special Issue Examining the Biology of Mesothelin in Normal Physiology, Cancer and Therapeutic Development)
►▼ Show Figures

Figure 1

Review

Jump to: Research

17 pages, 1473 KiB  
Review
The Role of Mesothelin in Activation of Portal Fibroblasts in Cholestatic Liver Injury
by Takahiro Nishio, Yukinori Koyama, Hiroaki Fuji, Kei Ishizuka, Keiko Iwaisako, Kojiro Taura, Etsuro Hatano, David A. Brenner and Tatiana Kisseleva
Biology 2022, 11(11), 1589; https://doi.org/10.3390/biology11111589 - 28 Oct 2022
Cited by 1 | Viewed by 2104
Abstract
Fibrosis is a common consequence of abnormal wound healing, which is characterized by infiltration of myofibroblasts and formation of fibrous scar. In liver fibrosis, activated Hepatic Stellate Cells (aHSCs) and activated Portal Fibroblasts (aPFs) are the major contributors to the origin of hepatic [...] Read more.
Fibrosis is a common consequence of abnormal wound healing, which is characterized by infiltration of myofibroblasts and formation of fibrous scar. In liver fibrosis, activated Hepatic Stellate Cells (aHSCs) and activated Portal Fibroblasts (aPFs) are the major contributors to the origin of hepatic myofibroblasts. aPFs are significantly involved in the pathogenesis of cholestatic fibrosis, suggesting that aPFs may be a primary target for anti-fibrotic therapy in cholestatic injury. aPFs are distinguishable from aHSCs by specific markers including mesothelin (Msln), Mucin 16 (Muc16), and Thymus cell antigen 1 (Thy1, CD90) as well as fibulin 2, elastin, Gremlin 1, ecto-ATPase nucleoside triphosphate diphosphohydrolase 2. Msln plays a critical role in activation of PFs, via formation of Msln-Muc16-Thy1 complex that regulates TGFβ1/TGFβRI-mediated fibrogenic signaling. The opposing pro- and anti-fibrogenic effects of Msln and Thy1 are key components of the TGFβ1-induced activation pathway in aPFs. In addition, aPFs and activated lung and kidney fibroblasts share similarities across different organs with expression of common markers and activation cascade including Msln-Thy1 interaction. Here, we summarize the potential function of Msln in activation of PFs and development of cholestatic fibrosis, offering a novel perspective for anti-fibrotic therapy targeting Msln. Full article
(This article belongs to the Special Issue Examining the Biology of Mesothelin in Normal Physiology, Cancer and Therapeutic Development)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop