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Obesity and risk of digestive cancer |
Hépato-Gastro. Volume 19, Number 2, 73-6, Février 2012, Mini-revue
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 Résumé
Texte intégral
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Author(s) : Patrick Hillon, Samia Hamza |
Summary : More than 70 000 cases of cancer (5% of cancers) diagnosed yearly in the European Community are exclusively due to overweight. Many epidemiological studies support a correlation between metabolic disorders induced by obesity and risk of renal, thyroid and digestive cancer (oesophageal adenocarcinoma, colorectal, pancreatic, and gallbladder cancer) in both genders, gynaecological cancer (endometrium, post menopausal breast cancer) in women, and liver cancer in men. Mechanisms involved in overweight carcinogenesis are abnormalities in adipokin secretion, and insulin resistance. Among these factors, experimental and epidemiological evidences suggest that insulin resistance plays a predominant role. Increased level of insulin and non-protein banded IGF-1 in type 2 diabetes patients, stimulates cellular growth and inhibits apoptosis. Abnormalities in adipokin secretion by the visceral adipose tissue play a role at different stages of obesity-induced carcinogenesis. Excess of leptin and plasminogène activator inhibitor-1 (PA-1), associated with a decrease in adiponectin secretion in obese people, contributes to insulin resistance and carcinogenesis through cellular growth and angiogenesis stimulation. Remodelling of the extracellular matrix due to metalloproteinase stimulation by PAI-1 is also able to promote cell migration. Obesity not only increases cancer frequency\; it is also liable to modify the prognosis and the response to antiangiogenic therapy of digestive cancers. This data suggests the need for clinicians to take into account overweight in cancer risk evaluation and to consider obesity and metabolic disorders as confounding factors in designing therapeutic studies. |
Keywords : obesity, insulin resistance, adipokins, risk of cancer, prognosis, treatment |
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