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Related Experiment Video

Updated: May 22, 2026

Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line

Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line

Published on: April 11, 2025

Chronic inflammation in cancer development.

Gabriele Multhoff¹, Michael Molls, Jürgen Radons

¹Department of Radiation Oncology, Klinikum rechts der Isar, Technische Universität München Munich, Germany. gabriele.multhoff@lrz.tu-muenchen.de

Frontiers in Immunology

|May 9, 2012

Summary

This summary is machine-generated.

Chronic inflammation drives cancer development by promoting tumor growth and spread, while also activating immune responses. Key mediators like NF-κB and STAT-3 fuel this process, influencing tumor progression and immune suppression.

Keywords:

IL-1 NF-κB STAT-3 carcinogenesis heat shock proteins inflammation tumorigenic factors

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A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

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A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

Published on: August 8, 2014

Area of Science:

Oncology
Immunology
Molecular Biology

Background:

Chronic inflammation plays a dual role in cancer, both promoting and potentially inhibiting tumor development.
Intrinsic and extrinsic pathways link cancer and inflammation, activating key transcription factors.

Purpose of the Study:

To review the critical role of pro-inflammatory mediators in inflammation-driven carcinogenesis.
To outline the molecular mechanisms of IL-1 signaling in tumors.
To elucidate the dual roles of stress proteins in anti-cancer immunity and apoptosis.

Main Methods:

Review of existing literature on inflammation, carcinogenesis, and immune response.
Analysis of molecular mechanisms involving transcription factors (NF-κB, STAT-3, HIF-1) and cytokines (IL-1, IL-6, TNF).

Main Results:

Inflammation promotes carcinogenesis, tumor growth, invasion, and metastasis.
Activated transcription factors (NF-κB, STAT-3) and mediators (IL-1, IL-6, TNF, PGHS-2) drive tumor-associated inflammation and suppress anti-tumor immunity.
Stress proteins exhibit dual roles in anti-cancer immunity and anti-apoptotic functions.

Conclusions:

Pro-inflammatory mediators are crucial in inflammation-driven carcinogenesis.
Understanding IL-1 signaling and stress protein functions is key to developing anti-cancer strategies.