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    GENE:

    RET (Ret Proto-Oncogene)

    i
    Other names: RET, Ret Proto-Oncogene, Proto-Oncogene Tyrosine-Protein Kinase Receptor Ret, Cadherin-Related Family Member 16, Rearranged During Transfection, RET Receptor Tyrosine Kinase, Cadherin Family Member 12, Proto-Oncogene C-Ret, CDHF12, CDHR16, PTC, Ret Proto-Oncogene (Multiple Endocrine Neoplasia And Medullary Thyroid Carcinoma 1, Hirschsprung Disease), Multiple Endocrine Neoplasia And Medullary Thyroid Carcinoma 1, Hirschsprung Disease 1, RET-ELE1, HSCR1, MEN2A, MEN2B, RET51, MTC1
    23h
    An Interpretable Machine Learning Model for Predicting Occult Central Lymph Node Metastasis in Papillary Thyroid Cancer. (PubMed, J Clin Endocrinol Metab)
    This is the first study to identify RET fusion positivity as an independent OLNM risk factor in cN0 PTC. The developed RF model demonstrates moderate predictive performance for OLNM risk and provides a framework for integrating clinical, sonographic, and molecular data, and is deployed as a web calculator (https://predictingoccultlymphnodemetastasis.shinyapps.io/web3/).
    Journal
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    BRAF (B-raf proto-oncogene) • RET (Ret Proto-Oncogene)
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    BRAF mutation • RET fusion
    1d
    KRAS-Wild Pancreatic Cancer-More Targets than Treatment Possibilities? (PubMed, Cancers (Basel))
    Currently, selpercatinib, larotrectinib, and repotrectinib are approved by the FDA for the treatment of certain solid tumors harboring specific gene fusions. Recent studies on zenocutuzumab resulted in the FDA-accelerated approval for NGR1 fusion-positive NSCLC and PDAC. Germline mutations may specifically increase responsiveness to poly(ADP-ribose) polymerase (PARP) inhibitors or platinum-based treatments. Comprehensive genomic profiling, incorporating fusion detection and germline testing, is essential to identify patients who may benefit from precision-based approaches.
    Review • Journal • PARP Biomarker
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    KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • RET (Ret Proto-Oncogene) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • FGFR (Fibroblast Growth Factor Receptor) • NRG1 (Neuregulin 1) • NTRK (Neurotrophic receptor tyrosine kinase)
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    KRAS mutation • KRAS wild-type • ALK fusion • RAS wild-type
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    Vitrakvi (larotrectinib) • Retevmo (selpercatinib) • Augtyro (repotrectinib) • Bizengri (zenocutuzumab-zbco)
    1d
    Accurate RET Fusion Detection in Solid Tumors Using RNA Sequencing Coverage Imbalance Analysis. (PubMed, Int J Mol Sci)
    Among the 18 RET fusion-positive samples, one was identified as an extremely rare case (RUFY3::RET), and two were determined to be novel fusions (FN1::RET, PPP1R21::RET). The findings of this study demonstrate that exon coverage imbalance analysis serves as a robust complement to computational RNA-seq analysis pipelines for the detection of clinically relevant RET fusions.
    Journal
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    RET (Ret Proto-Oncogene)
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    RET fusion • RET positive
    1d
    The shifting landscape of germline RET pathogenic variants with the introduction of panel testing. (PubMed, Surgery)
    RET pathogenic variants V804M, K666N, and C609Y were the most identified variants, particularly through broad panel testing, indicating increased incidental diagnosis of MEN2. The identification of previously unlisted variants underscores the need for dynamic guideline updates and ongoing curation to optimize clinical management of RET pathogenic variant carriers.
    Retrospective data • Journal
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    RET (Ret Proto-Oncogene)
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    RET C634* • RET V804* • RET positive
    6d
    Comparative genomic and clinicopathological analysis uncovers contrasting molecular profiles of canine and human thyroid carcinomas. (PubMed, Commun Biol)
    Thus, the genomic profile of canine FTC differs significantly from that of humans, with limited reliance on RAS/RAF signaling for oncogenic progression. Conversely, RET signaling likely underlies tumorigenesis in both canine and human MTC.
    Journal
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    HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • NRAS (Neuroblastoma RAS viral oncogene homolog) • RET (Ret Proto-Oncogene)
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    KRAS mutation • BRAF mutation • NRAS mutation • HER-2 expression • RET mutation • HER-2 elevation
    7d
    Chylous Ascites, a Rare Adverse Reaction to Selpercatinib. (PubMed, Cureus)
    Reducing the selpercatinib dose and implementing a low long-chain triglyceride diet led to symptom relief, stable ascites, and maintained tumor response. This case highlights effective management of tyrosine kinase inhibitor (TKI)-induced CA without compromising cancer control.
    Journal
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    RET (Ret Proto-Oncogene)
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    RET fusion • RET positive
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    Retevmo (selpercatinib)
    15d
    Comprehensive Molecular Diagnostic Tests in Non-Small Cell Lung Cancer: Frequency of ALK, ROS1, RET, and Other Gene Fusions/Rearrangements in a Romanian Cohort. (PubMed, Cancers (Basel))
    These alterations were mutually exclusive with common drivers such as EGFR or KRAS. Detection of rare fusions highlights the therapeutic potential of comprehensive NGS profiling in Romanian NSCLC patients.
    Journal
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    EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • RET (Ret Proto-Oncogene) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK1 (Neurotrophic tyrosine kinase, receptor, type 1) • NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • FGFR3 (Fibroblast growth factor receptor 3) • EML4 (EMAP Like 4) • NTRK2 (Neurotrophic tyrosine kinase, receptor, type 2) • CD74 (CD74 Molecule) • TACC3 (Transforming acidic coiled-coil containing protein 3) • ETV6 (ETS Variant Transcription Factor 6) • PTPRZ1 (Protein Tyrosine Phosphatase Receptor Type Z1)
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    EGFR mutation • EGFR L858R • ALK positive • RET fusion • ALK fusion • ROS1 fusion
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    Oncomine Focus Assay
    16d
    Selpercatinib-induced Acalculous Cholecystitis in an Elderly Patient with RET Fusion-positive Non-small Cell Lung Cancer: A Case Report. (PubMed, Intern Med)
    This is the first reported case of selpercatinib-induced acalculous cholecystitis in a patient. The report highlighted the potential efficacy of selpercatinib in elderly patients while underscoring the risk of severe adverse events and emphasizing monitoring and personalized dose management.
    Journal
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    RET (Ret Proto-Oncogene) • KIF5B (Kinesin Family Member 5B)
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    RET fusion • RET positive
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    Retevmo (selpercatinib)
    16d
    Cytotoxic Effects of Sorafenib, Lapatinib, and Bevacizumab, Alone and in Combination, on Medullary Thyroid Carcinoma Cells. (PubMed, Curr Oncol)
    The Lapatinib-Bevacizumab combination produced the most potent inhibition of cell viability, comparable to high-dose monotherapy. These findings suggest that combining kinase inhibitors with Bevacizumab may enhance antitumor activity, allow the use of lower drug doses, and overcome resistance, representing a promising therapeutic strategy for medullary thyroid carcinoma that warrants further investigation in clinical settings.
    Journal
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    RET (Ret Proto-Oncogene)
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    RET mutation
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    Avastin (bevacizumab) • sorafenib • lapatinib
    17d
    Discovery of a Proteolysis Targeting Chimera for TRKA and RET-derived oncoproteins. (PubMed, Sci Rep)
    Mechanistically, TPM3-TRKA degradation by compound 9 was dependent on CRBN-mediated polyubiquitination and proteasomal degradation; accordingly, it was hindered by inhibitors of the proteasome (MG132) or Cullins (MLN4924), by dominant negative Cullin 4A mutant, and by free pomalidomide. Finally, a compound 9 derivative, compound 20, induced in vivo degradation of TMP3-TRKA in KM12 cells mouse xenografts. In conclusion, our study indicated that PROTAC-mediated degradation is an efficient strategy to intercept RET and TRKA oncogenic signaling.
    Journal
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    RET (Ret Proto-Oncogene) • CCDC6 (Coiled-Coil Domain Containing 6) • CRBN (Cereblon) • TPM3 (Tropomyosin 3) • CUL4A (Cullin 4A)
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    pomalidomide • pevonedistat (MLN4924) • MG132
    18d
    Precision medicine advances in pancreatic cancer driven by genomic and molecular alterations. (PubMed, World J Gastrointest Oncol)
    Cross-cancer analyses underscore the necessity of PDAC-specific strategies despite shared genomic drivers. Collectively, these insights support routine germline and somatic testing, enrollment in biomarker-matched trials, and rational combination strategies, establishing molecular profiling as central to advancing precision treatment in pancreatic cancer.
    Review • Journal • Tumor mutational burden • IO biomarker
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    KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • RET (Ret Proto-Oncogene) • FGFR2 (Fibroblast growth factor receptor 2) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • SMAD4 (SMAD family member 4)
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    TP53 mutation • TMB-H • BRAF V600 • RET fusion • FGFR2 fusion
    18d
    RET Receptor Tyrosine Kinase Promotes Breast Cancer Metastasis to the Brain and RET Inhibitors Pralsetinib and Selpercatinib Suppress Breast Cancer Brain Metastases. (PubMed, bioRxiv)
    Using two mouse studies that model multi-organ metastases and breast tumor formation in the brain, we observed that RET inhibition significantly prevented the circulating tumor cells from forming brain metastases and suppressed the growth of intracranially implanted tumor cells, but did not significantly inhibit the progression of well-established brain metastases. Together, our findings demonstrated that RET is highly activated in BCBM and functioning as a novel mediator of BCBM, and that RET plays a new role as a viable therapeutic target for BCBM.
    Journal
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    HER-2 (Human epidermal growth factor receptor 2) • RET (Ret Proto-Oncogene)
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    Retevmo (selpercatinib) • Gavreto (pralsetinib)