ReviewClinics (Sao Paulo, Brazil)2012
Molecular mechanisms of RET receptor-mediated oncogenesis in multiple endocrine neoplasia 2.
Review in Clinics (Sao Paulo, Brazil), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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
24 citing papers in PubMed, 48 citations in OpenAlex.
- Pralsetinib for patients with advanced or metastatic RET-altered thyroid cancer (ARROW): a multi-cohort, open-label, registrational, phase 1/2 study.The lancet. Diabetes & endocrinology · 2021Trial
- Article
- Genomic and transcriptomic landscapes of metastatic neuroendocrine neoplasms from distinct primary sites and their clinical implications.Scientific reports · 2025Article
- Kinome profiling reveals pathogenic variant specific protein signalling networks in MEN2 children with Medullary Thyroid Cancer.NPJ precision oncology · 2025Article
- Variability in proliferative and migratory defects in Hirschsprung disease-associated RET pathogenic variants.American journal of human genetics · 2025Article
- Variability in proliferative and migratory defects in Hirschsprung disease-associatedbioRxiv : the preprint server for biology · 2024Article
- Childhood Multiple Endocrine Neoplasia (MEN) Syndromes: Genetics, Clinical Heterogeneity and Modifying Genes.Journal of clinical medicine · 2024Review
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Clinical characteristics of a large familial cohort with Medullary thyroid cancer and germline Cys618ArgFrontiers in endocrinology · 2023Article
- Review
- RET signaling pathway and RET inhibitors in human cancer.Frontiers in oncology · 2022Review
- A novel germline variant in RET gene resulting in an additional cysteine in a family with familial medullary thyroid carcinoma.Familial cancer · 2021Article
- ARTEMIN Promotes Oncogenicity and Resistance to 5-Fluorouracil in Colorectal Carcinoma by p44/42 MAPK Dependent Expression of CDH2.Frontiers in oncology · 2021Article
- Unexpected Pathogenic RET p.V804M Variant Leads to the Clinical Diagnosis and Management of Medullary Thyroid Carcinoma.The American journal of case reports · 2020Article
- Rodent models of pheochromocytoma, parallels in rodent and human tumorigenesis.Cell and tissue research · 2018Review
- Dermal Hyperneury and Multiple Sclerotic Fibromas in Multiple Endocrine Neoplasia Type 2A Syndrome.JAMA dermatology · 2017Article
- A Brief Review on The Molecular Basis of Medullary Thyroid Carcinoma.Cell journal · 2017Review
- Identification and characterization of two novel germline RET variants associated with medullary thyroid carcinoma.Endocrine · 2015Article
- The rare intracellular RET mutation p.S891A in a Chinese Han family with familial medullary thyroid carcinoma.Journal of biosciences · 2014Article
- Haplotype Frequency of G691S/S904S in the RET Proto-Onco-gene in Patients with Medullary Thyroid Carcinoma.Iranian journal of public health · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple endocrine neoplasia type 2 is an inherited cancer syndrome characterized by tumors of thyroid and adrenal tissues. Germline mutations of the REarranged during Transfection (RET) proto-oncogene, leading to its unregulated activation, are the underlying cause of this disease. Multiple endocrine neoplasia type 2 has been a model in clinical cancer genetics, demonstrating how knowledge of the genetic basis can shape the diagnosis and treatment of the disease. Here, we discuss the nature and effects of the most common recurrent mutations of RET found in multiple endocrine neoplasia type 2. Current understanding of the molecular mechanisms of RET mutations and how they alter the structure and function of the RET protein leading to its aberrant activation, and the effects on RET localization and signaling are described.
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.