Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.8
4.4
Journals
Cancers
Special Issues
Insulin Resistance, Diabetes, and Cancer: An Overview of the Pathogenetic...
cancers-logo
Submit to Special Issue Submit Abstract to Special Issue Review for Cancers Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Insulin Resistance, Diabetes, and Cancer: An Overview of the Pathogenetic Mechanisms

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

Deadline for manuscript submissions: 31 May 2026 | Viewed by 1611

Special Issue Editors

Dr. Kumar Ganesan

E-Mail Website
Guest Editor
School of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, 3, Sassoon Road, Hong Kong 999077, China
Interests: breast cancer; diabetes; signaling pathways; phytopharmacology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Kunka Mohanram Ramkumar

E-Mail Website
Guest Editor
Department of Biotechnology, School of Bioengineering, SRM Institute of Science and Technology, Kattankulathur, India
Interests: diabetes; cellular signaling; apoptosis; angiogenesis; epigenetics; natural products; redox biology; Nrf2

Special Issue Information

Dear Colleagues,

Epidemiological studies have consistently established a strong link between metabolic disorders—specifically insulin resistance and type 2 diabetes (T2D)—and an increased risk for the development and progression of various cancers, including liver, pancreatic, breast, endometrial, and colorectal cancer. This association also correlates with worse prognosis and higher cancer-related mortality. While hyperglycemia and hyperinsulinemia are considered central to this relationship, the exact molecular and cellular mechanisms driving this pathological crosstalk remain complex and multifactorial.

This Special Issue aims to provide a comprehensive overview of the pathogenetic mechanisms bridging insulin resistance, diabetes, and oncogenesis. We invite the submission of original research articles, reviews, and systematic reviews that elucidate the intricate biological pathways involved. Topics of interest include, but are not limited to, the following:

  • The role of hyperinsulinemia and insulin-like growth factor (IGF-1) signaling in promoting tumor proliferation and survival;
  • The impact of chronic inflammation and oxidative stress in the diabetic microenvironment on cancer initiation and progression;
  • Dysregulated metabolic pathways (e.g., in glucose, lipid, and amino acid metabolism) in cancer cells under diabetic conditions;
  • The involvement of adipose tissue dysfunction, adipokines, and cytokines in linking obesity, diabetes, and cancer;
  • The gut microbiome as a potential modulator of insulin resistance and cancer risk.
  • The effect of antidiabetic medications (e.g., metformin, SGLT2 inhibitors, insulin) on cancer risk and outcomes;
  • Novel biomarkers and preclinical models for studying the diabetes–cancer axis.

We hope this collection of articles will enhance our understanding of these shared pathogenic mechanisms and inspire new strategies for cancer prevention and therapy in this high-risk patient population.

Dr. Kumar Ganesan
Prof. Dr. Kunka Mohanram Ramkumar
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 250 words) can be sent to the Editorial Office for assessment.

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

  • insulin resistance
  • type 2 diabetes
  • hyperinsulinemia
  • IGF-1 signaling
  • tumor microenvironment
  • metabolic inflammation
  • adipokines
  • antidiabetic drugs
  • cancer metabolism
  • phytocompounds
  • bioactive molecules
  • hormone regulation
  • intracellular signalling pathways

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

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:

Review

24 pages, 1653 KB  
Review
Diabetes-Driven Post-Translational Remodeling in Pancreatic Ductal Adenocarcinoma
by Srikanth Kavyashree, Kannan Harithpriya, Kumar Ganesan and Kunka Mohanram Ramkumar
Cancers 2026, 18(10), 1657; https://doi.org/10.3390/cancers18101657 - 20 May 2026
Viewed by 194
Abstract
Diabetes mellitus (DM), particularly Type 2 DM (T2DM), is increasingly recognized as both a risk factor and an early manifestation of pancreatic ductal adenocarcinoma (PDAC), yet the molecular mechanisms bridging these conditions remain poorly understood. There is growing evidence that chronic metabolic stress [...] Read more.
Diabetes mellitus (DM), particularly Type 2 DM (T2DM), is increasingly recognized as both a risk factor and an early manifestation of pancreatic ductal adenocarcinoma (PDAC), yet the molecular mechanisms bridging these conditions remain poorly understood. There is growing evidence that chronic metabolic stress in diabetes induces persistent cellular reprogramming and metabolic memory through stable post-translational and epigenetic alterations, independent of conventional insulin resistance, obesity, and inflammatory pathways. We aim to elucidate how hyperglycaemia and metabolic overload contribute to the accumulation of major intermediates, such as acetyl-CoA, Uridine diphosphate N-acetylglucosamine (UDP-GlcNAc), and reactive oxygen species, which induce broad changes in post-translational modifications in diabetes-induced PDAC. A comprehensive literature search was conducted using electronic databases, including PubMed, Scopus, and Web of Science databases, to retrieve studies published between 2005 and 2025. This review synthesizes current understanding of post-translational modifications (PTM) dynamics in diabetes-associated PDAC, with emphasis on their role in modulating oncogenic pathways such as KRAS-MAPK and PI3K-AKT. We introduce the concept of PTM remodeling, wherein transient metabolic perturbations become persistently stabilized, contributing to metabolic memory and tumor initiation. In addition, we examine how PTM-driven alterations influence the pancreatic tumor microenvironment, including stromal activation, immune evasion, and metabolic crosstalk, reinforcing a bidirectional link between tumor progression and systemic metabolic dysfunction. Furthermore, emerging therapeutic strategies targeting PTM-regulating enzymes, metabolic substrates, and signaling nodes are discussed as potential approaches to disrupt this axis. Collectively, precision targeting of PTM-mediated metabolic reprogramming represents a promising framework for early intervention and therapeutic development in PDAC associated with diabetes. Full article
(This article belongs to the Special Issue Insulin Resistance, Diabetes, and Cancer: An Overview of the Pathogenetic Mechanisms)
►▼ Show Figures

Figure 1

48 pages, 2926 KB  
Review
Beyond Insulin Resistance: Exploring the Centrality of the Gut–Liver Axis in Mediating Immunometabolic Dysregulation Driving Hepatocellular Carcinoma in MASLD and Diabetes
by Mario Romeo, Claudio Basile, Giuseppina Martinelli, Fiammetta Di Nardo, Carmine Napolitano, Alessia De Gregorio, Paolo Vaia, Luigi Di Puorto, Mattia Indipendente, Alessandro Federico and Marcello Dallio
Cancers 2026, 18(8), 1316; https://doi.org/10.3390/cancers18081316 - 21 Apr 2026
Viewed by 864
Abstract
Hepatocellular carcinoma (HCC) represents a major global health challenge and the third leading cause of cancer-related mortality worldwide. Its epidemiological burden is rapidly increasing, largely driven by the rising prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD), which is now recognized as the [...] Read more.
Hepatocellular carcinoma (HCC) represents a major global health challenge and the third leading cause of cancer-related mortality worldwide. Its epidemiological burden is rapidly increasing, largely driven by the rising prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD), which is now recognized as the most common chronic liver disease globally. Notably, MASLD frequently coexists with type 2 diabetes mellitus (T2DM), sharing several features, including the interplay of common genetic, metabolic, and environmental factors, thus contributing to a complex multifactorial pathogenesis. Relevantly, patients affected by both conditions represent a subgroup at particularly high risk of liver disease progression and hepatocarcinogenesis. In this population, metabolic and inflammatory disturbances act synergistically to create a pro-tumorigenic hepatic environment where insulin resistance (IR) plays a crucial role, by driving hepatic lipotoxicity, mitochondrial dysfunction, and inflammatory signaling with oxidative stress, thereby establishing a permissive environment for worsening steatosis and malignant transformation. Increasing evidence supports the concept of MASLD as a multisystem disorder reflecting the systemic nature of metabolic dysfunction. Within this framework, beyond IR, extrahepatic factors have also emerged as important contributors to steatosis progression, worsening of T2DM, and modulation of HCC risk. In particular, the gut–liver axis has gained recognition as a key regulator of hepatic homeostasis, integrating signals from the intestinal microbiota, immune responses, and metabolic pathways. Dysregulation of this crosstalk promotes systemic inflammation and metabolic imbalance, exacerbating IR and fostering a pro-oncogenic hepatic environment. This review examines the interconnected metabolic and immune mechanisms linking IR and gut–liver axis dysfunction to HCC development in patients with MASLD and T2DM, highlighting their implications for risk stratification and precision-based therapeutic strategies. Full article
(This article belongs to the Special Issue Insulin Resistance, Diabetes, and Cancer: An Overview of the Pathogenetic Mechanisms)
►▼ 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