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Review Open Access

Obesity, chronic breast inflammation and carcinogenesis: Molecular pathways and clinical implications (Review)

  • Authors:
    • Fangying Li
    • Zhenhua Gao
  • View Affiliations / Copyright

    Affiliations: First Clinical Medical College of Gansu University of Chinese Medicine, Lanzhou, Gansu 730000, P.R. China, Department of General Surgery, The First People's Hospital of Baiyin, Baiyin, Gansu 730900, P.R. China
    Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 12
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    Published online on: November 27, 2025
       https://doi.org/10.3892/ijo.2025.5825
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Abstract

Obesity is a global epidemic strongly associated with increased breast cancer (BC) risk and mortality, particularly in postmenopausal women. Obesity‑induced chronic breast inflammation drives carcinogenesis via dysregulated adipokine signaling (leptin and adiponectin), insulin resistance, hyperinsulinemia and pro‑inflammatory cytokines (TNF‑α and IL‑6). These factors activate oncogenic pathways (NF‑κB and PI3K/AKT/mTOR pathways), which promote DNA damage, cell proliferation and immunosuppression. Clinically, obesity is associated with advanced tumor presentation, reduced treatment efficacy and poorer survival compared with those of normal‑weight patients with BC. Despite progress, the molecular interactions between obesity‑related inflammation and BC remain incompletely understood, and diagnostic/prognostic tools for obese patients require refinement. The present review synthesizes current evidence on obesity‑BC mechanisms and their clinical translation to inform prevention and precision oncology strategies.
View Figures

Figure 1

Obesity-induced molecular events and
chronic breast inflammation. By Figdraw (https://www.figdraw.com/static/index.html#/; 2.0
version; ID: RSAYO3b3b5). AMPK, AMP-activated protein kinase; CLS,
crown-like structures; COX-2, cyclooxygenase-2; ECM, extracellular
matrix; EMT, epithelial-mesenchymal transition; FFA, free fatty
acids; IGF-1, insulin-like growth factor-1; IGF1R, IGF-1 receptor;
IR, insulin receptor; JAK2, Janus kinase 2; MCP-1, monocyte
chemoattractant protein-1; MyD88, myeloid differentiation primary
response 88; PGE2, prostaglandin E2; ROS, reactive oxygen species;
TLR4, toll-like receptor 4.

Figure 2

Time-resolved crosstalk in the obese
breast microenvironment during early carcinogenesis. By Figdraw
(https://www.figdraw.com/static/index.html#/; 2.0
version; ID: UAAWW758ae). The depicted adipocyte-immune
interactions and epigenetic reprogramming events are primarily
derived from high-fat diet-fed, ovariectomized (postmenopausal)
murine mammary tissue models and ex vivo explants from obese
postmenopausal women. γH2AX, phosphorylated histone H2AX; CCL2, C-C
motif chemokine ligand 2; CLS, crown-like structures; ERα, estrogen
receptor α; FFA, free fatty acids; G-CSF, granulocyte-colony
stimulating factor; H3K27ac, histone H3 lysine 27 acetylation;
Ly6C, lymphocyte antigen 6C; SASP, senescence-associated secretory
phenotype.

Figure 3

Clinical translation: Risk
stratification, intervention and monitoring in obese patients with
breast cancer. By Figdraw (https://www.figdraw.com/static/index.html#/; 2.0
version; ID: POWPUb1704). AMPK, AMP-activated protein kinase; CLS,
crown-like structures; HOTAIR, HOX transcript antisense RNA;
lncRNA, long non-coding RNA; SCD1, stearoyl-CoA desaturase-1; TLR4,
toll-like receptor 4.
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Copy and paste a formatted citation
Spandidos Publications style
Li F and Gao Z: Obesity, chronic breast inflammation and carcinogenesis: Molecular pathways and clinical implications (Review). Int J Oncol 68: 12, 2026.
APA
Li, F., & Gao, Z. (2026). Obesity, chronic breast inflammation and carcinogenesis: Molecular pathways and clinical implications (Review). International Journal of Oncology, 68, 12. https://doi.org/10.3892/ijo.2025.5825
MLA
Li, F., Gao, Z."Obesity, chronic breast inflammation and carcinogenesis: Molecular pathways and clinical implications (Review)". International Journal of Oncology 68.1 (2026): 12.
Chicago
Li, F., Gao, Z."Obesity, chronic breast inflammation and carcinogenesis: Molecular pathways and clinical implications (Review)". International Journal of Oncology 68, no. 1 (2026): 12. https://doi.org/10.3892/ijo.2025.5825
Copy and paste a formatted citation
x
Spandidos Publications style
Li F and Gao Z: Obesity, chronic breast inflammation and carcinogenesis: Molecular pathways and clinical implications (Review). Int J Oncol 68: 12, 2026.
APA
Li, F., & Gao, Z. (2026). Obesity, chronic breast inflammation and carcinogenesis: Molecular pathways and clinical implications (Review). International Journal of Oncology, 68, 12. https://doi.org/10.3892/ijo.2025.5825
MLA
Li, F., Gao, Z."Obesity, chronic breast inflammation and carcinogenesis: Molecular pathways and clinical implications (Review)". International Journal of Oncology 68.1 (2026): 12.
Chicago
Li, F., Gao, Z."Obesity, chronic breast inflammation and carcinogenesis: Molecular pathways and clinical implications (Review)". International Journal of Oncology 68, no. 1 (2026): 12. https://doi.org/10.3892/ijo.2025.5825
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