ReviewEndocrine pathology2007
RET signaling in endocrine tumors: delving deeper into molecular mechanisms.
Review in Endocrine pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 36 citations in OpenAlex.
- Neuroendocrine Neoplasms of the Lungs, Thyroid, and Thymus.Biomedicines · 2025Review
- Review
- Updates in the advances of sporadic medullary thyroid carcinoma: from the molecules to the clinic.Gland surgery · 2020Review
- Medullary Thyroid Carcinoma: Recent Advances Including MicroRNA Expression.Endocrine pathology · 2016Review
- Alternative splicing results in RET isoforms with distinct trafficking properties.Molecular biology of the cell · 2012Article
- The RET G691S polymorphism is a germline variant in desmoplastic malignant melanoma.Melanoma research · 2012Article
- Mammary gland morphological and gene expression changes underlying pregnancy protection of breast cancer tumorigenesis.Physiological genomics · 2012Article
- Determination of RET Sequence Variation in an MEN2 Unaffected Cohort Using Multiple-Sample Pooling and Next-Generation Sequencing.Journal of thyroid research · 2012Article
- Rap1GAP interacts with RET and suppresses GDNF-induced neurite outgrowth.Cell research · 2011Article
- Article
- Cancer driver mutations in protein kinase genes.Cancer letters · 2009Review
- Computational modeling of structurally conserved cancer mutations in the RET and MET kinases: the impact on protein structure, dynamics, and stability.Biophysical journal · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The rearranged during transfection (RET) proto-oncogene encodes a receptor tyrosine kinase that is implicated in the development of endocrine tumors of the thyroid and adrenal glands. In humans, activating RET mutations are found in the inherited cancer syndrome multiple endocrine neoplasia 2 and in sporadic medullary and papillary thyroid carcinomas. The specific type and location of RET mutations are strongly correlated with the disease phenotype and have both diagnostic and prognostic value. Recent advances in the molecular characterization of the RET receptor and its mutants have begun to define the mechanisms underlying the transforming ability of the different RET mutant forms. This information has revealed key functional features of these mutant proteins that distinguish the different clinically recognized mutations and provide clues as to the functional origins of the phenotypes associated with specific RET mutations. The elucidation of molecular mechanisms involved in RET-mediated transformation is a key step in the development of much needed therapeutics that target RET's oncogenic properties. Recent advances have begun to provide a deeper understanding of the receptor's function, and dysfunction, in human tumors that may guide this process.
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.