Growth hormone, insulin-like growth factor system and carcinogenesis.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing preclinical mechanisms and clinical observational data without systematic review methodology.
PubMed 27387246 · doi:10.5603/EP.a2016.0053
What was done
This narrative review synthesized literature examining the role of the growth hormone (GH) and insulin-like growth factor (IGF) axis in cell cycle regulation, apoptosis, angiogenesis, and carcinogenesis. The authors consolidated findings from in vitro experiments, animal cancer models, epidemiological studies, and clinical data from populations with acromegaly, GH deficiency, or therapeutic GH administration.
What was found
The abstract reports no quantitative values or statistical metrics. It notes that while experimental in vitro and animal models provide substantial evidence that GH-IGF signaling promotes tumor progression and acts as a potential therapeutic target, the clinical evidence linking this system to cancer risk in patients with acromegaly, GH deficiency, or GH treatment is much weaker.
Why it matters
It highlights the gap between strong preclinical mechanistic models and inconclusive human clinical data regarding whether GH and IGF elevation translates directly into elevated cancer risk.
Limits
The abstract describes a narrative review without systematic search protocols or quantitative synthesis. The underlying human evidence is predominantly observational, subject to confounding, and does not establish causality.
Cited by
- supports IGF-1 acts as a major tumor promoter by stimulating cancer cell growth and overriding apoptosis pathways that eliminate damaged cells.