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Review
. 2014 Jan;7(1):38-50.
doi: 10.1177/1756283X13501786.

The role of obesity in gastrointestinal cancer: evidence and opinion

Affiliations
Review

The role of obesity in gastrointestinal cancer: evidence and opinion

Claire L Donohoe et al. Therap Adv Gastroenterol. 2014 Jan.

Abstract

There is increasing recognition of the impact of being overweight and obese on the development of cancers at diverse sites including the gastrointestinal tract. Large epidemiological studies indicate that up to 14% of tumours may be related to obesity. Pathophysiological mechanisms underpinning this association are not well understood and so are discussed in this review.

Keywords: adipose tissue, carcinogenesis; inflammation; signalling pathways; visceral adiposity.

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Conflict of interest statement

Conflicting of interest statement: The authors have no conflicts of interest to declare.

Figures

Figure 1.
Figure 1.
Excess visceral adipose tissue results in systemic inflammation. The expanded adipose tissue mass in patients who are viscerally obese is infiltrated with macrophages and activated T cells. These cells, as well as the increased number of adipose cells, produce factors which result in a state of systemic inflammation which is thought to increase tumourigenesis.
Figure 2.
Figure 2.
The obese state of systemic inflammation upregulates intracellular pathways which promote functional aspects of cancer cell. Cancers which develop within an obese environment may become selectively altered to signal via specific pathways. Many of the factors upregulated systemically in the obese state including leptin, interleukin(IL)-6, insulin, tumour necrosis factor and insulin-like growth factor (IGF)-1 all signal via similar candidate pathways include the phosphoinositide 3-kinase (PI3K), mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription 3 (STAT3) pathways. Activation of these pathways leads to multiple downstream effects including cell proliferation and cell survival. Illustration courtesy of Alessandro Baliani © 2013.

References

    1. Adams T., Stroup A., Gress R., Adams K., Calle E., Smith S., et al. (2009) Cancer incidence and mortality after gastric bypass surgery. Obesity (Silver Spring) 17: 796–802 - PMC - PubMed
    1. Aggarwal B., Kunnumakkara A., Harikumar K., Gupta S., Tharakan S., Koca C., et al. (2009) Signal Transducer and Activator of Transcription-3, Inflammation, and Cancer. Ann NY Acad Sci 1171(1): 59–76 - PMC - PubMed
    1. Akiyama T., Yoneda M., Inamori M., Iida H., Endo H., Hosono K., et al. (2009) Visceral obesity and the risk of Barrett’s esophagus in Japanese patients with non-alcoholic fatty liver disease. BMC Gastroenterol 9: 56. - PMC - PubMed
    1. Algire C., Amrein L., Zakikhani M., Panasci L., Pollak M. (2010) Metformin blocks the stimulative effect of a high-energy diet on colon carcinoma growth in vivo and is associated with reduced expression of fatty acid synthase. Endocrine-Related Cancer 17: 351–360 - PubMed
    1. Bassols J., Ortega F., Moreno-Navarrete J., Peral B., Ricart W., Fernandez-Real J. (2009) Study of the proinflammatory role of human differentiated omental adipocytes. J Cell Biochem 107: 1107–1117 - PubMed

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