ArticleJournal of thyroid research2011
How to Treat a Signal? Current Basis for RET-Genotype-Oriented Choice of Kinase Inhibitors for the Treatment of Medullary Thyroid Cancer.
Article in Journal of thyroid research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Molecular Mechanisms of FAT Atypical Cadherin 1 (FAT1), the Hippo Pathway, and the Yes-Associated Protein (YAP) Signaling Pathways in Some Cancers.Asian Pacific journal of cancer prevention : APJCP · 2026Review
- The diverse functions of FAT1 in cancer progression: good, bad, or ugly?Journal of experimental & clinical cancer research : CR · 2022Review
- Clinical features and signaling effects of RET D631Y variant multiple endocrine neoplasia type 2 (MEN2).The Korean journal of internal medicine · 2022Article
- Practical Considerations Relating to Routine Clinical Biomarker Testing for Non-small Cell Lung Cancer: Focus on Testing forFrontiers in medicine · 2020Review
- Corrigendum to "How to Treat a Signal? Current Basis for RET-Genotype-Oriented Choice of Kinase Inhibitors for the Treatment of Medullary Thyroid Cancer".Journal of thyroid research · 2016Article
- Quantitative analysis of receptor tyrosine kinase-effector coupling at functionally relevant stimulus levels.The Journal of biological chemistry · 2015Article
- MK-2206 causes growth suppression and reduces neuroendocrine tumor marker production in medullary thyroid cancer through Akt inhibition.Annals of surgical oncology · 2013Article
- Profile of cabozantinib and its potential in the treatment of advanced medullary thyroid cancer.OncoTargets and therapy · 2013Article
- Evolving paradigms for successful molecular imaging of medullary thyroid carcinoma.European journal of nuclear medicine and molecular imaging · 2012Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The significance of RET in thyroid cancer comes from solid evidence that, when inherited, an RET activating mutation primes C-cells to transform into medullary carcinomas. Moreover, environmental exposure to radiation also induces rearranged transforming RET "isoforms" that are found in papillary thyroid cancer. The RET gene codes for a tyrosine kinase receptor that targets a diverse set of intracellular signaling pathways. The nature of RET point mutations predicts differences in the mechanisms by which the receptor becomes activated and correlates with different forms of clinical presentation, age of onset, and biological aggressiveness. A number of RET-targeting Tyrosine Kinase Inhibitors (TKIs) are currently undergoing clinical trials to evaluate their effectiveness in the treatment of thyroid cancer, and it is conceivable that the RET genotype may also influence response to these compounds. The question that now emerges is whether, in the future, the rational for treatment of refractory thyroid cancer will be based on the management of an abnormal RET signal. In this paper we address the RET-targeting TKIs and review studies about the signaling properties of distinct RET mutants as a means to predict response and design combinatorial therapies for the soon to be available TKIs.
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.