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The p53/Adipose-Tissue/Cancer Nexus
Kevin Zwezdaryk1, Deborah Sullivan1, Zubaida Saifudeen2
1Department of Microbiology and Immunology, Tulane University School of Medicine, New Orleans, LA, United States.
Frontiers in Endocrinology
|August 31, 2018
Summary
Obesity promotes cancer by altering metabolism and inflammation. Adipose tissue in the tumor microenvironment, influenced by p53, fuels cancer growth and progression.
Area of Science:
- Oncology
- Metabolic Syndrome
- Molecular Biology
Background:
- Obesity is linked to increased cancer risk and progression.
- Adipose tissue within the tumor microenvironment (TME) promotes malignancy.
- Obesity-induced systemic metabolic disturbances contribute to cancer.
Purpose of the Study:
- To review the role of p53, cellular metabolism, and adipose tissue dysfunction in obesity-related cancers.
- To elucidate the mechanisms by which adipose tissue in the TME influences cancer progression.
Main Methods:
- Literature review of studies investigating obesity, metabolism, p53, and cancer.
- Analysis of signaling pathways involving adipose tissue, p53, and tumor cell metabolism.
- Examination of inflammatory mechanisms in the TME related to obesity.
Main Results:
- Obesity exacerbates cancer risk through systemic metabolic changes and TME inflammation.
- Elevated p53 levels in obesity amplify inflammatory cytokine release, promoting cancer.
- Adipose tissue in the TME dysregulates tumor cell metabolism via paracrine signaling and direct interactions.
Conclusions:
- p53, cellular metabolism, and adipose tissue dysfunction are key interconnected factors in obesity-associated cancer.
- Targeting these pathways may offer novel therapeutic strategies for cancer in obese individuals.
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