ArticleOncogene2013
RET is a potential tumor suppressor gene in colorectal cancer.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02328677 (ColoCare Transdisciplinary Research in Colorectal Cancer Prognosis), which is not on this map. Cited by 58 papers.
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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.
ColoCare Transdisciplinary Research in Colorectal Cancer Prognosis
Who cites it
58 citing papers in PubMed, 105 citations in OpenAlex.
- RET Signaling Pathway in Human Cancer: Oncogenic Mechanisms, Selective Inhibitors, and Emerging Resistance Strategies.International journal of molecular sciences · 2026Review
- mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- IGSF10 is a RET antagonist regulating Ewing sarcoma growth and GnRH neuron migration.Cell reports · 2025Article
- Agnostic Biomarkers and Molecular Signatures in Colorectal Cancer-Guiding Chemotherapy and Predicting Response.Biomedicines · 2025Review
- Olink Profiling of Intestinal Tissue Identifies Novel Biomarkers For Colorectal Cancer.Journal of proteome research · 2025Article
- Review
- Review
- RET is a sex-biased regulator of intestinal tumorigenesis.Frontiers in gastroenterology (Lausanne, Switzerland) · 2023Article
- Proteomic quantification of receptor tyrosine kinases involved in the development and progression of colorectal cancer liver metastasis.Frontiers in oncology · 2023Article
- Article
- Non-thyroidal second primary malignancy in papillary thyroid cancer patients.European thyroid journal · 2022Article
- Case of Recurrent Primary Hyperparathyroidism, Congenital Granular Cell Tumor, and Aggressive Colorectal Cancer.Journal of the Endocrine Society · 2022Article
- Epigenetic silencing and tumor suppressor gene of HAND2 by targeting ERK signaling in colorectal cancer.Cell communication and signaling : CCS · 2022Article
- Comprehensive profiling of 1015 patients' exomes reveals genomic-clinical associations in colorectal cancer.Nature communications · 2022Article
- Modular and mechanistic changes across stages of colorectal cancer.BMC cancer · 2022Article
- Multi-Omic Approaches in Colorectal Cancer beyond Genomic Data.Journal of personalized medicine · 2022Review
- RET signaling pathway and RET inhibitors in human cancer.Frontiers in oncology · 2022Review
- Candidate targets of copy number deletion events across 17 cancer types.Frontiers in genetics · 2022Article
- Genomic profiles of Indonesian colorectal cancer patients.F1000Research · 2022Article
- Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 5 countries.
Funding
Abstract
Cancer arises as the consequence of mutations and epigenetic alterations that activate oncogenes and inactivate tumor suppressor genes. Through a genome-wide screen for methylated genes in colon neoplasms, we identified aberrantly methylated RET in colorectal cancer. RET, a transmembrane receptor tyrosine kinase and a receptor for the glial cell-derived neurotrophic factor family ligands, was one of the first oncogenes to be identified, and has been shown to be an oncogene in thyroid cancer and pheochromocytoma. However, unexpectedly, we found RET is methylated in 27% of colon adenomas and in 63% of colorectal cancers, and now provide evidence that RET has tumor suppressor activity in colon cancer. The aberrant methylation of RET correlates with decreased RET expression, whereas the restoration of RET in colorectal cancer cell lines results in apoptosis. Furthermore, in support of a tumor suppressor function of RET, mutant RET has also been found in primary colorectal cancer. We now show that these mutations inactivate RET, which is consistent with RET being a tumor suppressor gene in the colon. These findings suggest that the aberrant methylation of RET and the mutational inactivation of RET promote colorectal cancer formation, and that RET can serve as a tumor suppressor gene in the colon. Moreover, the increased frequency of methylated RET in colon cancers compared with adenomas suggests RET inactivation is involved in the progression of colon adenomas to cancer.
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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.