ReviewJournal of medical genetics2000
Multiple endocrine neoplasia type 2 and RET: from neoplasia to neurogenesis.
Review in Journal of medical genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 241 citations in OpenAlex.
- Guideline
- Unveiling the Prevalence and Surgical Burden of Neurocristopathies: A Scoping Review and Statistical Analysis.Research square · 2026Article
- MEN2: surgical precision in the era of precision medicine.Endocrine-related cancer · 2025Review
- Article
- Coexisting RET/PTC and TERT Promoter Mutation Predict Poor Prognosis but Effective RET and MEK Targeting in Thyroid Cancer.The Journal of clinical endocrinology and metabolism · 2024Article
- Targeting the RET tyrosine kinase in neuroblastoma: A review and application of a novel selective drug design strategy.Biochemical pharmacology · 2023Review
- Cystic ovarian teratoma as a novel tumor and growth hormone deficiency as a new condition presenting in Multiple Endocrine Neoplasia type 2B: Case reports and review of the literature.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2022Review
- The Polycomb group geneFrontiers in neuroscience · 2022Article
- RMRP, RMST, FTX and IPW: novel potential long non-coding RNAs in medullary thyroid cancer.Orphanet journal of rare diseases · 2021Article
- RET overactivation leads to concurrent Hirschsprung disease and intestinal ganglioneuromas.Development (Cambridge, England) · 2020Article
- Disorders of neural crest derivates in oncoradiological practice.Translational cancer research · 2019Review
- A primer on the genetics of medullary thyroid cancer.Current oncology (Toronto, Ont.) · 2019Review
- Review
- [Imaging of medullary thyroid carcinoma].Der Radiologe · 2019Review
- Oncogenesis of Thyroid CancerAsian Pacific journal of cancer prevention : APJCP · 2017Article
- Hirschsprung's disease: clinical dysmorphology, genes, micro-RNAs, and future perspectives.Pediatric research · 2017Review
- On the Origin of Cells and Derivation of Thyroid Cancer: C Cell Story Revisited.European thyroid journal · 2016Review
- PTH and Vitamin D.Comprehensive Physiology · 2016Review
- Article
- Molecular approaches to thyroid cancer diagnosis.Endocrine-related cancer · 2014Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple endocrine neoplasia type 2 (MEN 2) is an inherited cancer syndrome characterised by medullary thyroid carcinoma (MTC), with or without phaeochromocytoma and hyperparathyroidism. MEN 2 is unusual among cancer syndromes as it is caused by activation of a cellular oncogene, RET. Germline mutations in the gene encoding the RET receptor tyrosine kinase are found in the vast majority of MEN 2 patients and somatic RET mutations are found in a subset of sporadic MTC. Further, there are strong associations of RET mutation genotype and disease phenotype in MEN 2 which have led to predictions of tissue specific requirements and sensitivities to RET activity. Our ability to identify genetically, with high accuracy, subjects with MEN 2 has revolutionised our ability to diagnose, predict, and manage this disease. In the past few years, studies of RET and its normal ligand and downstream interactions and the signalling pathways it activates have clarified our understanding of the roles played by RET in normal cell survival, proliferation, and differentiation, as well as in disease. Here, we review the current knowledge of the normal functions of RET and the effects of mutations of this gene in tumorigenesis and in normal development.
Indexed as
Identifiers
What OpenQuestion holds
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.