ArticleProceedings of the National Academy of Sciences of the United States of America2016
Growth hormone is permissive for neoplastic colon growth.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT01261000 (Tissue Biomarker for Pegvisomant Action), which is not on this map. Cited by 64 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Tissue Biomarker for Pegvisomant Action
Who cites it
64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 97 citations in OpenAlex.
- Epithelial-Mesenchymal Transition in the Resistance to Somatostatin Receptor Ligands in Acromegaly.Frontiers in endocrinology · 2021Pooled it
- A permissive role of growth hormone (GH) in the development of second brain tumors after radiotherapy?Endocrine · 2017Pooled it
- Cancer risk in acromegaly: reassessing the evidence and impact of biochemical control.The Journal of clinical endocrinology and metabolism · 2026Article
- Local growth hormone promotes benign prostatic hyperplasia.JCI insight · 2026Article
- Impact of acromegaly subtypes on survival: results from a large multicenter cohort.Journal of the Endocrine Society · 2026Article
- Acromegaly and colorectal cancer risk: emerging roles of the gut microbiota.Frontiers in endocrinology · 2026Review
- Targeting Growth Hormone Receptor to Overcome Therapy Resistance in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2025Article
- Article
- Cancer screening in patients with acromegaly: a plea for a personalized approach and international registries.Reviews in endocrine & metabolic disorders · 2025Review
- Prevalence of Neoplasms in Patients with Acromegaly-A Single-Center Polish Study.Journal of clinical medicine · 2024Article
- Heterogeneity of tumor microenvironment cell groups in inflammatory and adenomatous polyposis coli mutant colorectal cancer based on single cell sequencing.Translational cancer research · 2024Article
- Non-pituitary growth hormone enables colon cell senescence evasion.Aging cell · 2024Article
- Excess endocrine growth hormone in acromegaly promotes the aggressiveness and metastasis of triple-negative breast cancer.iScience · 2024Article
- Growth Hormone Receptor Antagonist Markedly Improves Gemcitabine Response in a Mouse Xenograft Model of Human Pancreatic Cancer.International journal of molecular sciences · 2024Article
- Growth hormone and radiation therapy: friend, foe, or both?Endocrine-related cancer · 2024Review
- WIP1 is a novel specific target for growth hormone action.iScience · 2023Article
- Non-pituitary GH regulation of the tissue microenvironment.Endocrine-related cancer · 2023Article
- Role of Estrogen and Estrogen Receptor in GH-Secreting Adenomas.International journal of molecular sciences · 2023Review
- The frequency of dysplastic branching crypts in colorectal polypoid tubular adenomas.International journal of experimental pathology · 2023Article
- Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Growth hormone (GH) excess in acromegaly is associated with increased precancerous colon polyps and soft tissue adenomas, whereas short-stature humans harboring an inactivating GH receptor mutation do not develop cancer. We show that locally expressed colon GH is abundant in conditions predisposing to colon cancer and in colon adenocarcinoma-associated stromal fibroblasts. Administration of a GH receptor (GHR) blocker in acromegaly patients induced colon p53 and adenomatous polyposis coli (APC), reversing progrowth GH signals. p53 was also induced in skin fibroblasts derived from short-statured humans with mutant GHR. GH-deficient prophet of pituitary-specific positive transcription factor 1 (Prop1)(-/-) mice exhibited induced colon p53 levels, and cross-breeding them with Apc(min+/-) mice that normally develop intestinal and colon tumors resulted in GH-deficient double mutants with markedly decreased tumor number and size. We also demonstrate that GH suppresses p53 and reduces apoptosis in human colon cell lines as well as in induced human pluripotent stem cell-derived intestinal organoids, and confirm in vivo that GH suppresses colon mucosal p53/p21. GH excess leads to decreased colon cell phosphatase and tensin homolog deleted on chromosome 10 (PTEN), increased cell survival with down-regulated APC, nuclear β-catenin accumulation, and increased epithelial-mesenchymal transition factors and colon cell motility. We propose that GH is a molecular component of the "field change" milieu permissive for neoplastic colon growth.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.