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Review
. 2022 Nov 1;32(6):594-597.
doi: 10.1097/MOU.0000000000001041. Epub 2022 Sep 8.

Metabolic syndrome, obesity and cancer risk

Federico Belladelli  1   2 , Francesco Montorsi  1   2 , Alberto Martini  3   4
Affiliations
Review

Metabolic syndrome, obesity and cancer risk

Federico Belladelli et al. Curr Opin Urol. .

Abstract

Purpose of review: This review aims to report the latest discoveries regarding the relationship between BMI, obesity, and cancer development and treatment.

Recent findings: Obesity and metabolic syndrome relationships with cancer have been deeply investigated in the literature but their association is still debated. Currently, it has been recorded an association between BMI and endometrial, colorectal, gastric, liver, bladder, and prostate cancer. The mechanisms behind this association have also been investigated. It has been hypothesized that chronic inflammation determined by obesity may concur to the development of tumors and that Insulin Resistance may enhance cell proliferation directly or indirectly. Moreover, different studies suggest that the relationship between higher BMI and cancer may include metabolic disturbances comparable to those linked to metabolic syndrome. However, greater weight has been linked to a better overall prognosis in patients with advanced disease, a concept called the obesity paradox. This paradox has been recently investigated in the context of urological malignancies, such as bladder, prostate, and kidney cancer.

Summary: Patients' metabolic and morphological status may impact their risk of developing different types of tumors and the response to systemic therapy. However, further research is necessary to better delineate the mechanisms behind these associations and how they could or should affect medical decision.

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References

    1. National Institute of Health. NHLBI obesity education initiative expert panel on the identification, evaluation, and treatment of overweight and obesity in adults. NHLBI Obes. Educ. Initiat. 2000. https://www.nhlbi.nih.gov/files/docs/guidelines/prctgd_c.pdf . Accessed May 2022.
    1. Lin WW, Karin M. A cytokine-mediated link between innate immunity, inflammation, and cancer. J Clin Invest 2007; 117:1175–1183.
    1. Comba A, Pasqualini ME. Primers on molecular pathways − lipoxygenases: their role as an oncogenic pathway in pancreatic cancer. Pancreatol 2009; 9:724–728.
    1. Aleksic T, Chitnis MM, Perestenko OV, et al. Type 1 insulin-like growth factor receptor translocates to the nucleus of human tumor cells. Cancer Res 2010; 70:6412–6419.
    1. Walker MP, Diaugustine RP, Zeringue E, et al. An IGF1/insulin receptor substrate-1 pathway stimulates a mitotic kinase (cdk1) in the uterine epithelium during the proliferative response to estradiol. J Endocrinol 2010; 207:225–235.