ReviewCancer science2018
Drug resistance in anaplastic lymphoma kinase-rearranged lung cancer.
Review in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Comparative efficacy and safety of first-line treatments for advanced non-small cell lung cancer with ALK-rearranged: a meta-analysis of clinical trials.BMC cancer · 2021Pooled it
- Virtual screening and MD simulation-guided discovery of CDK12-IN-3, a potent ALK inhibitor suppressing neuroblastoma growthFrontiers in chemistry · 2026Article
- ALK-Targeted Therapy: Resistance Mechanisms and Emerging Precision Strategies.Current issues in molecular biology · 2025Review
- Cancer-associated fibroblasts promote drug resistance in ALK-driven lung adenocarcinoma cells by upregulating lipid biosynthesis.Cancer & metabolism · 2025Article
- Exploring the Genetic Orchestra of Cancer: The Interplay Between Oncogenes and Tumor-Suppressor Genes.Cancers · 2025Review
- Intratumoral heterogeneity and drug resistance in cancer.Cancer cell international · 2025Review
- LTK mutations responsible for resistance to lorlatinib in non-small cell lung cancer harboring CLIP1-LTK fusion.Communications biology · 2024Article
- Recent advances in molecular targeted therapy of lung cancer: Possible application in translation medicine.Iranian journal of basic medical sciences · 2024Review
- Chromatographic analysis of ponatinib and its impurities: method development, validation, and identification of new degradation product.Frontiers in chemistry · 2024Article
- ALK-rearranged and EGFR wild-type lung adenocarcinoma transformed to small cell lung cancer: a case report.Frontiers in oncology · 2024Article
- Review
- Drugging Hijacked Kinase Pathways in Pediatric Oncology: Opportunities and Current Scenario.Pharmaceutics · 2023Review
- MET Amplification as a Resistance Driver to TKI Therapies in Lung Cancer: Clinical Challenges and Opportunities.Cancers · 2023Review
- Fibroblast growth factor receptor 3 overexpression mediates ALK inhibitor resistance in ALK-rearranged non-small cell lung cancer.Cancer science · 2022Article
- Review
- An insight into lung cancer: a comprehensive review exploring ALK TKI and mechanisms of resistance.Bosnian journal of basic medical sciences · 2022Review
- HER3 activation contributes toward the emergence of ALK inhibitor-tolerant cells in ALK-rearranged lung cancer with mesenchymal features.NPJ precision oncology · 2022Article
- Clinical outcome, long-term survival and tolerability of sequential therapy of first-line crizotinib followed by alectinib in advanced ALK+NSCLC: A multicenter retrospective analysis in China.Thoracic cancer · 2022Article
- A narrative review of tumor heterogeneity and challenges to tumor drug therapy.Annals of translational medicine · 2021Review
- Head to head evaluation of second generation ALK inhibitors brigatinib and alectinib as first-line treatment for ALK+ NSCLC using anOncotarget · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anaplastic lymphoma kinase (ALK) gene encodes a receptor tyrosine kinase, and many kinds of ALK fusion genes have been found in a variety of carcinomas. There is almost no detectable expression of ALK in adults. However, through ALK gene rearrangement, the resultant ALK fusion protein is aberrantly overexpressed and dimerized through the oligomerization domains, such as the coiled-coil domain, in the fusion partner that induces abnormal constitutive activation of ALK tyrosine kinase. This results in dysregulated cell proliferation. ALK gene rearrangement has been observed in 3%-5% of non-small-cell lung cancers, and multiple ALK inhibitors have been developed for the treatment of ALK-positive lung cancer. Among those inhibitors, in Japan, 3 (4 in the USA) ALK tyrosine kinase inhibitors (TKIs) have been approved and are currently used in clinics. All of the currently approved ALK-TKIs have been shown to induce marked tumor regression in ALK-rearranged non-small-cell lung cancer; however, tumors inevitably relapse because of acquired resistance within a few years. This review focuses on ALK-TKIs, their resistance mechanisms, and the potential therapeutic strategies to overcome resistance.
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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.