ReviewLung Cancer (Auckland, N.Z.)2019
Targeting RET-rearranged non-small-cell lung cancer: future prospects.
Review in Lung Cancer (Auckland, N.Z.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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.
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Who cites it
37 citing papers in PubMed, 62 citations in OpenAlex.
- Real-world evidence of RET fusion prevalence and testing in patients with metastatic non-small cell lung cancer.Translational oncology · 2026Article
- RET signaling as a mediator of estrogen receptor positive breast cancer brain metastasis.Communications biology · 2026Article
- Real-world FAERS safety analysis of Pralsetinib.Scientific reports · 2025Article
- Unraveling the molecular-pathological characteristics and cellular complexity of the tumor immune microenvironment in metastatic non-small cell lung cancer.Cell communication and signaling : CCS · 2025Review
- RNA splicing: Novel star in pulmonary diseases with a treatment perspective.Acta pharmaceutica Sinica. B · 2025Review
- The continually evolving landscape of novel therapies in oncogene-driven advanced non-small-cell lung cancer.Therapeutic advances in medical oncology · 2025Review
- Understanding the treatment response and resistance to targeted therapies in non-small cell lung cancer: clinical insights and perspectives.Frontiers in oncology · 2024Review
- The induction of ferroptosis by KLF11/NCOA4 axis: the inhibitory role in clear cell renal cell carcinoma.Human cell · 2023Article
- Expert consensus on the diagnosis and treatment of RET gene fusion non-small cell lung cancer in China.Thoracic cancer · 2023Article
- Updated Views in Targeted Therapy in the Patient with Non-Small Cell Lung Cancer.Journal of personalized medicine · 2023Review
- Recent Advances in Lung Cancer Therapy Based on Nanomaterials: A Review.Current medicinal chemistry · 2023Review
- Non-Small Cell Lung Cancer Targeted Therapy: Drugs and Mechanisms of Drug Resistance.International journal of molecular sciences · 2022Review
- Exploring histopathological and serum biomarkers in lung adenocarcinoma: Clinical applications and translational opportunities (Review).International journal of oncology · 2022Review
- New horizons for uncommon mutations in non-small cell lung cancer:World journal of clinical oncology · 2022Review
- Clinicopathologic characteristics and diagnostic methods ofTranslational lung cancer research · 2022Article
- Molecular Pathology of Lung Cancer.Cold Spring Harbor perspectives in medicine · 2022Review
- Liquid biopsy: Novel perspectives on the importance and spectrum ofMolecular and clinical oncology · 2022Article
- Research Progress on RET Fusion in Non-Small-Cell Lung Cancer.Frontiers in oncology · 2022Review
- Non-small-cell lung cancer: how to manageDrugs in context · 2022Review
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small-cell lung cancer (NSCLC) patients with mutated or rearranged oncogene drivers can be treated with upfront selective inhibitors achieving higher response rates and longer survival than chemotherapy. The RET gene can undergo chromosomal rearrangements in 1%-2% of all NSCLC patients, involving various upstream fusion partners such as KIF5B, CCDC6, NCOA4, and TRIM33. Many multikinase inhibitors are active against rearranged RET. Cabozantinib, vandetanib, sunitinib, lenvatinib, and nintedanib achieved tumor responses in about 30% of these patients in retrospective studies. Prospective phase II trials investigated the activity and toxicity of cabozantinib, vandetanib, sorafenib, and lenvatinib, and did not reach significantly higher response rates. VEGFR and EGFR inhibition represented the main ways of developing off-target toxicity. An intrinsic resistance emerged according to the type of RET fusion partners, as KIF5B-RET fusion is the most resistant. Also acquired mutations in rearranged RET oncogene developed as resistance to these multikinase inhibitors. Interestingly, RET fusions have been found as a resistance mechanism to EGFR-TKIs in EGFR-mutant NSCLC patients. The combination of EGFR and RET inhibition can overcome this resistance. The limitations in terms of activity and tolerability of the various multikinase inhibitors prompted the investigation of new highly selective RET inhibitors, such as RXDX-105, BLU-667, and LOXO-292. Some data emerged about intracranial antitumor activity of BLU-667 and LOXO-292. If these novel drugs will achieve high activity in RET rearranged NSCLC, also these oncogene-addicted tumors can undergo a significant survival improvement.
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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.