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Mechanisms linking excess adiposity and carcinogenesis promotion
Ana I Pérez-Hernández1, Victoria Catalán2, Javier Gómez-Ambrosi2
1Metabolic Research Laboratory, Clínica Universidad de Navarra , Pamplona , Spain.
Frontiers in Endocrinology
|May 16, 2014
Summary
Obesity is linked to increased cancer risk, potentially causing 15-20% of cancer deaths. This review explores how obesity-related inflammation, insulin resistance, and adipose tissue hypoxia drive cancer development.
Area of Science:
- Metabolic diseases
- Oncology
- Public health
Background:
- Obesity is a major metabolic disease linked to insulin resistance and cardiovascular risk.
- A strong association exists between obesity and various cancers, including breast, colorectal, and prostate cancer.
- Obesity is estimated to contribute to 15-20% of all cancer-related deaths globally.
Purpose of the Study:
- To review the key mechanisms linking obesity to cancer development.
- To examine the role of inflammatory changes, insulin resistance, and adipose tissue hypoxia in obesity-associated tumorigenesis.
- To highlight the public health significance of understanding the obesity-cancer relationship.
Main Methods:
- Literature review focusing on the interplay between obesity and cancer.
- Analysis of three primary pathways: inflammation, insulin resistance, and adipose tissue hypoxia.
- Examination of signaling pathways and microenvironmental interactions in tumor growth.
Main Results:
- Obesity promotes cancer development through dysfunctional adipose tissue and altered signaling.
- Inflammatory changes, including macrophage polarization and altered adipokine profiles, are implicated.
- Insulin resistance and adipose tissue hypoxia are identified as critical contributing factors.
Conclusions:
- Obesity significantly increases cancer risk and mortality.
- Understanding the mechanistic links is crucial for improving cancer prevention and management strategies.
- Further research is needed to elucidate the complex interactions between obesity and cancer progression.
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