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Related Experiment Video

Updated: Jul 5, 2026

Techniques to Induce and Quantify Cellular Senescence

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

AGE-RAGE system and carcinogenesis.

Riichiro Abe¹, Sho-ichi Yamagishi

¹Department of Dermatology, Hokkaido University Graduate School of Medicine, N 15 W 7, Kita-ku, Sapporo 060-8638, Japan. aberi@med.hokudai.ac.jp

Current Pharmaceutical Design

|May 14, 2008

Summary

Diabetes increases cancer risk due to hyperglycemia-induced oxidative stress. The advanced glycation end products (AGE)-receptor for AGE (RAGE) system creates a feedback loop, elevating cancer development in diabetic patients.

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Published on: September 19, 2025

Area of Science:

Oncology
Endocrinology
Molecular Biology

Background:

Diabetes mellitus is linked to increased cancer incidence.
Hyperglycemia in diabetes elevates oxidative stress, leading to DNA damage and potentially carcinogenesis.
Advanced glycation end products (AGE) and their receptor (RAGE) are implicated in cancer development.

Purpose of the Study:

To review the current understanding of the AGE-RAGE system's role in cancer development.
To explore the interplay between AGE-RAGE, oxidative stress, and cancer in diabetic patients.

Main Methods:

Literature review of clinical studies and scientific evidence.
Analysis of the molecular mechanisms linking diabetes, oxidative stress, AGE-RAGE, and carcinogenesis.

Main Results:

Hyperglycemia drives oxidative stress and DNA damage, initiating cancer.
The AGE-RAGE system promotes oxidative stress and vice versa, forming a positive feedback loop.
This feedback loop exacerbates cancer risk in individuals with diabetes.

Conclusions:

The AGE-RAGE system and oxidative stress crosstalk significantly contributes to cancer development in diabetes.
Targeting the AGE-RAGE pathway may offer therapeutic strategies for cancer prevention in diabetic populations.