Does Growth Hormone Cause Cancer?

P. J. Jenkins; A. Mukherjee; S. M. Shalet


Clin Endocrinol. 2006;64(2):115-121. 

In This Article


Convincing experimental data suggest that the GH/IGF-1 axis plays an important role in cancer development and behaviour. Epidemiological studies have supported an association with cancer, but not with tumour induction per se, although this is a distinction that is important mechanistically but not clinically. Acromegaly is associated with an increased risk of colorectal cancer; the magnitude of the risk is controversial but appears linked to elevated GH/IGF-1 levels. The relevance to physiological replacement in patients with GHD is uncertain. Extensive study of cancer survivors treated with GH has failed to demonstrate an increase in tumour recurrence and de novo cancers but a small increase in second malignant neoplasms. One long-term follow-up study of children treated with human pituitary GH suggested an increase in colorectal cancer and lymphoma,[31] but surveillance data from many thousands of children and adults treated with GH have not shown any increase in cancer risk.[32] However, it is prudent for further long-term surveillance to continue. Existing experimental data have shown the proliferative and antiapoptotic effects of IGF-1, which would provide an environment that favours survival of genetically damaged cells. Even if such an environment had only a small influence on survival of such damaged cells, exposure to a large number of 'at risk' cells over many years, although not inducing cancer, could serve to accelerate carcinogenesis.

Finally, even if GH/IGF-1 therapy does result in a small increase in cancer risk compared with untreated patients with GH deficiency, it is likely that the eventual risk will be the same as the general population. Such a restoration to normality will need to be balanced against the known increased morbidity of untreated GH deficiency. However, these in vitro effects countenance strongly against the use of rGH or rhIGF-I as an 'elixir of youth' in adults with an intact GH/IGF-I axis.

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