Proto-Oncogene Proteins c-ret
"Proto-Oncogene Proteins c-ret" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
Receptor protein-tyrosine kinases involved in the signaling of GLIAL CELL-LINE DERIVED NEUROTROPHIC FACTOR ligands. They contain an extracellular cadherin domain and form a receptor complexes with GDNF RECEPTORS. Mutations in ret protein are responsible for HIRSCHSPRUNG DISEASE and MULTIPLE ENDOCRINE NEOPLASIA TYPE 2.
| Descriptor ID |
D051096
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| MeSH Number(s) |
D08.811.913.696.620.682.725.400.087 D12.776.395.550.200.188.500 D12.776.543.131.500 D12.776.543.750.630.217 D12.776.624.664.700.194
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| Concept/Terms |
Proto-Oncogene Proteins c-ret- Proto-Oncogene Proteins c-ret
- Proto Oncogene Proteins c ret
- c-ret, Proto-Oncogene Proteins
- Receptor Tyrosine Kinase RET
- ret Proto-Oncogene Proteins
- Proto-Oncogene Proteins, ret
- ret Proto Oncogene Proteins
- Proto-Oncogene Protein c-ret
- Proto Oncogene Protein c ret
- c-ret, Proto-Oncogene Protein
- c-ret Protein
- Proto-Oncogene Protein Ret
- Proto Oncogene Protein Ret
- Ret, Proto-Oncogene Protein
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Below are MeSH descriptors whose meaning is more general than "Proto-Oncogene Proteins c-ret".
Below are MeSH descriptors whose meaning is more specific than "Proto-Oncogene Proteins c-ret".
This graph shows the total number of publications written about "Proto-Oncogene Proteins c-ret" by people in this website by year, and whether "Proto-Oncogene Proteins c-ret" was a major or minor topic of these publications.
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| Year | Major Topic | Minor Topic | Total |
|---|
| 2015 | 1 | 0 | 1 |
| 2018 | 3 | 0 | 3 |
| 2019 | 1 | 0 | 1 |
| 2020 | 0 | 1 | 1 |
| 2021 | 1 | 1 | 2 |
| 2023 | 0 | 2 | 2 |
| 2024 | 1 | 0 | 1 |
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Below are the most recent publications written about "Proto-Oncogene Proteins c-ret" by people in Profiles.
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Targeting Oncogenic RET Kinase by Simultaneously Inhibiting Kinase Activity and Degrading the Protein. J Med Chem. 2025 Jan 09; 68(1):81-94.
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Efficacy and Safety of RET-Specific Kinase Inhibitors in RET-Altered Cancers: A Systematic Review. Cancer Invest. 2023 Sep; 41(8):739-749.
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The heterogeneous transition state of resistance to RET kinase inhibitors converges on ERK1/2-driven Aurora A/B kinases. Drug Resist Updat. 2023 May; 68:100958.
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Precision therapy for RET-altered cancers with RET inhibitors. Trends Cancer. 2021 12; 7(12):1074-1088.
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Patient-driven discovery and post-clinical validation of NTRK3 fusion as an acquired resistance mechanism to selpercatinib in RET fusion-positive lung cancer. Ann Oncol. 2021 06; 32(6):817-819.
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Structural basis of acquired resistance to selpercatinib and pralsetinib mediated by non-gatekeeper RET mutations. Ann Oncol. 2021 02; 32(2):261-268.
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Structural basis of resistance of mutant RET protein-tyrosine kinase to its inhibitors nintedanib and vandetanib. J Biol Chem. 2019 07 05; 294(27):10428-10437.
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S100 and CD34 positive spindle cell tumor with prominent perivascular hyalinization and a novel NCOA4-RET fusion. Genes Chromosomes Cancer. 2019 09; 58(9):680-685.
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Exploring the Potential of RET Kinase Inhibition for Irritable Bowel Syndrome: A Preclinical Investigation in Rodent Models of Colonic Hypersensitivity. J Pharmacol Exp Ther. 2019 02; 368(2):299-307.
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Enteric RET inhibition attenuates gastrointestinal secretion and motility via cholinergic signaling in rat colonic mucosal preparations. Neurogastroenterol Motil. 2019 04; 31(4):e13479.