Understanding the Interplay Between Obesity and Cancer - From Mechanisms to Therapeutic Opportunities

Sep 23, 2026

Uploaded by Pentious

Obesity has become a central global public health challenge, strongly linked to multiple chronic diseases and intensified scientific interest due to its complex association with cancer. This review explains how obesity shapes tumorigenesis, progression, metastasis, and treatment efficacy through molecular mechanisms. It highlights obesity-driven remodeling of the tumor microenvironment, metabolic pathway disruption, and pro-tumor inflammation, which together enable cancer development while diminishing therapeutic responses. The article also aims to support identification of therapeutic strategies for obesity-related cancers.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages22

Reading Time55 min

AccessFree to download

Simple Summary

Abstract

Keywords

1. Introduction

Obesity definition and metabolic/inflammatory consequences

Hallmarks of cancer influenced by obesity

Metaflammation as a bridging concept

Global prevalence and health impact

Obesity–cancer relationship and clinical outcomes

Review Understanding the Interplay Between Obesity and Cancer: From Mechanisms to Therapeutic Opportunities Sunsook Hwang 1,2, Byungjoo Kim 1,2, Seungyeon Yang 3,4 and Seung Min Jeong 3,4, * Academic Editor: Edward Sauter Received: 21 April 2026 Revised: 13 May 2026 Accepted: 15 May 2026 Published: 17 May 2026 Copyright: © 2026 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license. 1 Department of Immunology, School of Medicine, Konkuk University, Chungju 27478, Republic of Korea; [sunhwang@kku.ac.kr](sunhwang@kku.ac.kr) (S.H.) 2 Research Institute of Medical Science, KU Open Innovation Center, Chungju 27478, Republic of Korea 3 Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea 4 Institute for Aging and Metabolic Diseases, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea * Correspondence: [smjeong@catholic.ac.kr](smjeong@catholic.ac.kr); Tel.: +82-2-3147-8336 Simple Summary Obesity is a growing global health problem that affects not only general health but also cancer risk and treatment outcomes. People with obesity are more likely to develop certain cancers, and their tumors often respond less effectively to therapy. This is partly because excess body fat alters the microenvironment around tumors, changes how cancer cells use energy, and alters abnormal adipose tissue-derived signals that promote tumor growth. In this review, we summarize how these obesity-related changes contribute to cancer progression and treatment resistance, and we discuss potential strategies to improve therapy. A better understanding of these mechanisms may support the development of more effective treatments for patients with obesity-related cancers. Abstract Obesity has risen to the forefront of global public health challenges, particularly due to its association with several chronic diseases. Its association with cancer has attracted significant research interest. The relationship between obesity and cancer is complex and profoundly influences tumorigenesis, cancer progression, metastasis, and therapeutic efficacy. This review provides the molecular basis of these interactions, elucidating how obesity triggers changes in the tumor microenvironment, disrupts metabolic pathways, and promotes inflammation. These factors facilitate cancer development and reduce the efficacy of treatments. By unraveling these mechanisms, we aim to identify therapeutic strategies that could mitigate obesity’s detrimental effects on cancer outcomes and contribute to the development of more effective strategies for managing obesity-related cancers. Keywords: obesity; tumor progression; therapy resistance; tumor microenvironment; inflammation; metabolic reprogramming 1. Introduction Obesity is defined by the World Health Organization (WHO) as abnormal or excessive fat accumulation that presents a risk to health, conventionally assessed by a body mass index (BMI) ≥ 30 kg/m2. This definition emphasizes excessive adipose tissue accumulation—particularly visceral fat—as the central pathophysiological feature linking obesity to its downstream metabolic and inflammatory consequences, which are discussed in subsequent sections. Conceptually, obesity contributes to cancer through many of the established hallmarksof cancer [1,2] . The hallmarks most strongly affected by obesity include sustaining proliferative signaling and resisting cell death, driven by chronic activation of insulin/IGF-1 and adipokine-mediated pathways; deregulating cellular energetics, through systemic and local metabolic reprogramming; tumor-promoting inflammation, mediated by adipose tissue-derived cytokines; genome instability, due to oxidative stress and impaired DNA repair; and avoiding immune destruction, through obesity-driven immunosu

FAQs

How does obesity affect cancer risk and outcomes?

Obesity is associated with higher likelihood of developing certain cancers and with increased recurrence and mortality among cancer survivors. The review links these effects to changes in cellular and molecular pathways.

What mechanisms connect obesity to cancer progression?

The review explains that obesity alters the tumor microenvironment, disrupts metabolic pathways, and promotes inflammation. It also discusses chronic immune and metabolic interactions that support tumor-promoting processes.

What is metaflammation in the context of obesity and cancer?

Metaflammation refers to chronic, low-grade, metabolically driven inflammation characteristic of obesity. The review positions it as a bridge between obesity-related metabolic dysregulation and tumor-promoting inflammation.

Sep 23, 2026

Uploaded by Pentious