ReviewSeminars in cancer biology2017
ALK alterations and inhibition in lung cancer.
Review in Seminars in cancer biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed.
- Crizotinib versus observation or placebo for surgically resected early-stage ALK-positive non-small-cell lung cancer (Eastern Cooperative Oncology Group-American College of Radiology Imaging Network E4512): a phase 3 trial.The Lancet. Respiratory medicine · 2026Article
- Review
- Joint analysis of sQTL and Hi-C reveals spatial proximity between sQTLs and target genes in cancer tissues.Scientific reports · 2025Article
- Systematic review of lung cancer with breast metastasis.Journal of thoracic disease · 2025Review
- Immunotherapy for patients with advanced non-small cell lung cancer harboring oncogenic driver alterations other thanTranslational lung cancer research · 2024Article
- Real-World Data on Treatment Outcome of ALK-Positive Non-Small Cell Lung Cancer from an Indian Multicentric Cancer Registry.South Asian journal of cancer · 2024Article
- EML4-ALK fusion protein in Lung cancer cells enhances venous thrombogenicity through the pERK1/2-AP-1-tissue factor axis.Journal of thrombosis and thrombolysis · 2024Article
- Potential Ototoxicity of Insulin-like Growth Factor 1 Receptor Signaling Inhibitors: An In Silico Drug Repurposing Study of the Regenerating Cochlear Neuron Transcriptome.Journal of clinical medicine · 2023Article
- Association BetweenJTO clinical and research reports · 2022Article
- Is Elevation of Alkaline Phosphatase a Predictive Factor of Response to Alectinib in NSCLC?Current oncology (Toronto, Ont.) · 2021Article
- Oncogene addiction and tumor mutational burden in non-small-cell lung cancer: Clinical significance and limitations.Thoracic cancer · 2020Review
- Non-Coding RNA Networks in ALK-Positive Anaplastic-Large Cell Lymphoma.International journal of molecular sciences · 2019Review
- Review
- Review
- The value of cell block based on fine needle aspiration for lung cancer diagnosis.Journal of thoracic disease · 2017Article
- The second-generation ALK inhibitor alectinib effectively induces apoptosis in human neuroblastoma cells and inhibits tumor growth in a TH-MYCN transgenic neuroblastoma mouse model.Cancer letters · 2017Article
- Lung adenocarcinoma: from molecular basis to genome-guided therapy and immunotherapy.Journal of thoracic disease · 2017Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The advent of precision medicine in non-small cell lung cancer has remarkably altered the direction of research and improved clinical outcomes. The identification of molecular subsets with differential response to targeted therapies began with the identification of epidermal growth factor receptor mutated tumors in subsets of non-small cell lung cancer (NSCLC). Emboldened by unprecedented response rates to kinase inhibitors seen in that subset, the oncologic community searched for other molecular subsets featuring oncogene addiction. An early result of this search was the discovery of NSCLC driven by activating rearrangements of the anaplastic lymphoma kinase (ALK) gene. In an astoundingly brief period following the recognition of ALK-positive NSCLC, details of the biology, clinicopathologic features, development of targeted inhibitors, mechanisms of therapeutic resistance, and new generations of treatment were elucidated. This review summarizes the current understanding of the pathologic features, diagnostic approach, treatment options, resistance mechanisms, and future research areas for ALK-positive NSCLC.
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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.