Obesity-Induced Inflammation and Cancer Risk

Obesity is characterised by the expansion of adipose tissue and a state of chronic low-grade inflammation that alters systemic metabolism and promotes oncogenesis. Enlarged and dysfunctional adipocytes secrete elevated levels of pro-inflammatory cytokines, adipokines and growth factors, which activate signalling pathways such as PI3K/Akt/mTOR, JAK/STAT and NF-κB, driving DNA damage, cell proliferation and survival. Concomitantly, insulin resistance and dyslipidaemia engender hormonal imbalances and increased bioavailability of fatty acids, further fuelling tumour growth. The resulting crosstalk between inflamed adipose depots and emerging neoplastic cells underlies the heightened incidence and poorer outcomes seen in obesity-associated cancers—including endometrial, colorectal, postmenopausal breast and pancreatic malignancies. Globally, understanding these mechanisms informs public health strategies centred on weight management, lifestyle intervention and the development of anti-inflammatory or metabolic-targeted therapies to mitigate cancer risk.

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Obesity-Induced Inflammation and Cancer Risk publication trend

The graph below shows the total number of articles in obesity-induced inflammation and cancer risk across all publications each year (not limited to Nature Index journals).

Technical terms

Autophagy: A regulated intracellular process of self-digestion that maintains cellular homeostasis by degrading and recycling damaged organelles and macromolecules.

Adipokines: Bioactive molecules—including leptin, adiponectin and resistin—secreted by adipose tissue that modulate inflammation, metabolism and cell signalling.

Cytokines: Small secreted proteins, such as interleukins and tumour necrosis factor, that mediate and regulate immune and inflammatory responses.

Tumour microenvironment: The surrounding milieu of stromal cells, immune cells, extracellular matrix and soluble factors that interact with cancer cells to influence tumour initiation and progression.

Insulin resistance: A metabolic condition in which cells exhibit diminished responsiveness to insulin, leading to compensatory hyperinsulinaemia and dysregulated glucose and lipid metabolism.

References

1. The obesity-autophagy-cancer axis: Mechanistic insights and therapeutic perspectives. Seminars in Cancer Biology (2024).
2. New insights into the role of adipocytes in pancreatic cancer progression: paving the way towards novel therapeutic targets. Theranostics (2023).
3. Obesity-Induced Adipose Tissue Inflammation as a Strong Promotional Factor for Pancreatic Ductal Adenocarcinoma. Cells (2019).
4. Obesity, metabolic dysregulation, and cancer: a growing concern and an inflammatory (and microenvironmental) issue. Annals of the New York Academy of Sciences (2012).