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Endocrine Abstracts (2012) 29 S7.3

University of Manchester, Manchester, UK.


By 2008, we1 and others had established that excess body mass index (BMI), as an approximation of general body adiposity and excess calorie intake, is associated with increased risk of several cancer types. These associations exist for both common (colon, endometrial, post-menopausal breast cancers, oesophageal adenocarcinoma) and less common malignancies (thyroid cancer, non-Hodgkin lymphoma). Given the plausibility of the biological explanations (including insulin/IGF-I; sex steroids; and adipokines/inflammatory cytokines), the consistency of associations, the sufficiently long latency times between BMI measurement and cancer occurrence, and the recent demonstrations of risk reversibility in morbidly obese cohorts undergoing bariatric surgery, many of these associations are probably causal. Approximately 124 000 new cancer cases may be attributable to excess BMI in Europe (2008). Since 2008, it has become clear that associations between BMI and cancer risk may be modified in the presence of other risk factors. For example, in users of hormonal replacement therapy, the associations between BMI and endometrial and post-menopausal breast cancers are attenuated. In turn, these observations point to a strong influence of oestrogen as an intermediary between obesity and cancer development in these cancer groups. Two areas of recent research will be highlighted: (i) it is hypothesised that approximations of central adiposity, such as waist circumference (WC), may better describe associations between adiposity and increased cancer risk, but updated standardised analyses do not fully support this, suggesting a refinement to the proposed mechanistic role of insulin resistance in carcinogenesis; and (ii) studies of the impact of BMI on cancer-specific mortality in patients with a diagnosis of an obesity-related cancer do not necessarily mirror relationships seen for incident risk. These observations suggest that obesity may act through pathways, which in turn, are prognostic pathways for certain cancers. Better understanding of these associations will facilitate refinements of approaches to prevent obesity-related cancers.

1. Renehan et al. Lancet 2008 371 (9612) 569–78.

Declaration of interest: The authors declare that there is a conflict of interest.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

Volume 29

15th International & 14th European Congress of Endocrinology

European Society of Endocrinology 

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Obesity and cancer (<1 min ago)