Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
2.4
3.1
Journals
CIMB
Special Issues
New Sight: Molecular Research in Pancreatic Cancer
cimb-logo
Submit to CIMB Review for CIMB Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

New Sight: Molecular Research in Pancreatic Cancer

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 5439

Special Issue Editor

Dr. Ada Aita

E-Mail
Guest Editor
Department of Medicine, DIMED University of Padova, Padua, Italy
Interests: molecular biology; pancreatica cancer; SARS-CoV-2; quality assurance; quality indicators; laboratory medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pancreatic cancer is one of the most common causes of cancer death in the world, with the highest mortality rates in Europe and North America. It remains one of the most dismal diseases with poor prognosis and a 5‑year survival rate of only 5%. The vast majority of patients are diagnosed with advanced metastatic disease, and due to the high heterogeneity, metabolic reprogramming, and dense stromal environment, currently available treatments are of only limited efficacy. Recent insight into the biology and genetics of pancreatic cancer has supported its molecular classification in different subgroups with potential subtype-specific therapeutic vulnerabilities, providing the opportunity to define a de novo clinically applicable molecular taxonomy. In particular, genomic analysis of 456 pancreatic ductal adenocarcinomas identified 32 recurrently mutated genes that aggregate into 10 pathways: KRAS, TGF-β, WNT, NOTCH, ROBO/SLIT signaling, G1/S transition, SWI-SNF, chromatin modification, DNA repair, and RNA processing. Expression analysis defined 4 subtypes: (1) squamous, (2) pancreatic progenitor, (3) immunogenic, and (4) aberrantly differentiated endocrine exocrine that correlate with histopathological characteristics. To date, much research is directed at elucidating fundamental molecular mechanisms underlying the biology of pancreatic cancer to translate into clinically applicable strategies for early detection, prediction of prognosis, and effective therapies for patients diagnosed with pancreatic cancer. The purpose of this Special Issue is to publish original research papers and/or relevant updates of literature data on current knowledge concerning the molecular subtyping of pancreatic cancer and explores future strategies for using a molecular taxonomy to guide therapeutic development and ultimately routine therapy with the overall goal of improving outcomes for this disease.

Dr. Ada Aita
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. Current Issues in Molecular 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 2200 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

  • molecular subgroups
  • pancreatic cancer
  • squamous subtype
  • pancreatic progenitor subtype
  • immunogenic subtype
  • aberrantly differentiated endocrine exocrine subtype

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

16 pages, 3821 KiB  
Article
Mutant K-Ras in Pancreatic Cancer: An Insight on the Role of Wild-Type N-Ras and K-Ras-Dependent Cell Cycle Regulation
by Robert Ferguson, Karen Aughton, Anthony Evans, Victoria Shaw, Jane Armstrong, Adam Ware, Laura Bennett, Eithne Costello and William Greenhalf
Curr. Issues Mol. Biol. 2023, 45(3), 2505-2520; https://doi.org/10.3390/cimb45030164 - 17 Mar 2023
Cited by 2 | Viewed by 1659
Abstract
The development of K-Ras independence may explain the failure of targeted therapy for pancreatic cancer (PC). In this paper, active N as well as K-Ras was shown in all human cell lines tested. In a cell line dependent on mutant K-Ras, it was [...] Read more.
The development of K-Ras independence may explain the failure of targeted therapy for pancreatic cancer (PC). In this paper, active N as well as K-Ras was shown in all human cell lines tested. In a cell line dependent on mutant K-Ras, it was shown that depleting K-Ras reduced total Ras activity, while cell lines described as independent had no significant decline in total Ras activity. The knockdown of N-Ras showed it had an important role in controlling the relative level of oxidative metabolism, but only K-Ras depletion caused a decrease in G2 cyclins. Proteasome inhibition reversed this, and other targets of APC/c were also decreased by K-Ras depletion. K-Ras depletion did not cause an increase in ubiquitinated G2 cyclins but instead caused exit from the G2 phase to slow relative to completion of the S-phase, suggesting that the mutant K-Ras may inhibit APC/c prior to anaphase and stabilise G2 cyclins independently of this. We propose that, during tumorigenesis, cancer cells expressing wild-type N-Ras protein are selected because the protein protects cancer cells from the deleterious effects of the cell cycle-independent induction of cyclins by mutant K-Ras. Mutation independence results when N-Ras activity becomes adequate to drive cell division, even in cells where K-Ras is inhibited. Full article
(This article belongs to the Special Issue New Sight: Molecular Research in Pancreatic Cancer)
►▼ Show Figures

Figure 1

Review

Jump to: Research

36 pages, 16792 KiB  
Review
Molecular Research in Pancreatic Cancer: Small Molecule Inhibitors, Their Mechanistic Pathways and Beyond
by Shaila A. Shetu, Nneoma James, Gildardo Rivera and Debasish Bandyopadhyay
Curr. Issues Mol. Biol. 2023, 45(3), 1914-1949; https://doi.org/10.3390/cimb45030124 - 27 Feb 2023
Cited by 2 | Viewed by 3230
Abstract
Pancreatic enzymes assist metabolic digestion, and hormones like insulin and glucagon play a critical role in maintaining our blood sugar levels. A malignant pancreas is incapable of doing its regular functions, which results in a health catastrophe. To date, there is no effective [...] Read more.
Pancreatic enzymes assist metabolic digestion, and hormones like insulin and glucagon play a critical role in maintaining our blood sugar levels. A malignant pancreas is incapable of doing its regular functions, which results in a health catastrophe. To date, there is no effective biomarker to detect early-stage pancreatic cancer, which makes pancreatic cancer the cancer with the highest mortality rate of all cancer types. Primarily, mutations of the KRAS, CDKN2A, TP53, and SMAD4 genes are responsible for pancreatic cancer, of which mutations of the KRAS gene are present in more than 80% of pancreatic cancer cases. Accordingly, there is a desperate need to develop effective inhibitors of the proteins that are responsible for the proliferation, propagation, regulation, invasion, angiogenesis, and metastasis of pancreatic cancer. This article discusses the effectiveness and mode of action at the molecular level of a wide range of small molecule inhibitors that include pharmaceutically privileged molecules, compounds under clinical trials, and commercial drugs. Both natural and synthetic small molecule inhibitors have been counted. Anti-pancreatic cancer activity and related benefits of using single and combined therapy have been discussed separately. This article sheds light on the scenario, constraints, and future aspects of various small molecule inhibitors for treating pancreatic cancer—the most dreadful cancer so far. Full article
(This article belongs to the Special Issue New Sight: Molecular Research in Pancreatic Cancer)
►▼ 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