ReviewTranslational lung cancer research2014
ALK and crizotinib: after the honeymoon…what else? Resistance mechanisms and new therapies to overcome it.
Review in Translational lung cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Efficacy and safety of ceritinib in anaplastic lymphoma kinase-rearranged non-small cell lung cancer: A systematic review and meta-analysis.Journal of clinical pharmacy and therapeutics · 2020Pooled it
- A Phase I Trial of the MET/OncoTargets and therapy · 2021Trial
- Molecular Anatomy of the EML4-ALK Fusion Protein for the Development of Novel Anticancer Drugs.International journal of molecular sciences · 2023Review
- Drugging Hijacked Kinase Pathways in Pediatric Oncology: Opportunities and Current Scenario.Pharmaceutics · 2023Review
- Clinical Profile, Practice Pattern, and Outcomes With First-Line Therapy in ALK-Positive Lung Cancer: Real-World Data From Resource-Constrained Settings.JTO clinical and research reports · 2023Article
- Efficacy of combination treatment using YHO-1701, an orally active STAT3 inhibitor, with molecular-targeted agents on cancer cell lines.Scientific reports · 2021Article
- EML4-ALK V3 oncogenic fusion proteins promote microtubule stabilization and accelerated migration through NEK9 and NEK7.Journal of cell science · 2020Article
- New generation anaplastic lymphoma kinase inhibitors.Translational lung cancer research · 2019Review
- Data driven polypharmacological drug design for lung cancer: analyses for targeting ALK, MET, and EGFR.Journal of cheminformatics · 2017Article
- Treating patients with ALK-rearranged non-small-cell lung cancer: mechanisms of resistance and strategies to overcome it.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017Review
- Down-regulation of E-cadherin enhances prostate cancer chemoresistance via Notch signaling.Chinese journal of cancer · 2017Article
- Development of a new choroidal metastasis in resistance to crizotinib therapy in anaplastic lymphoma kinase-rearranged non-small cell lung cancer.International journal of ophthalmology · 2017Article
- Article
- Nintedanib in NSCLC: evidence to date and place in therapy.Therapeutic advances in medical oncology · 2016Review
- Assessment ofOncology letters · 2016Article
- Molecular mechanisms that underpin EML4-ALK driven cancers and their response to targeted drugs.Cellular and molecular life sciences : CMLS · 2016Review
- Culture and Drug Profiling of Patient Derived Malignant Pleural Effusions for Personalized Cancer Medicine.PloS one · 2016Article
- Focus on Alectinib and Competitor Compounds for Second-Line Therapy inFrontiers in medicine · 2016Review
- Clinical potential of gene mutations in lung cancer.Clinical and translational medicine · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The last few decades have witnessed a silent revolution in the war against NSCLC, thanks to the discovery of "oncogenic drivers" and the subsequent development of targeted therapies. The discovery of the EML4-ALK fusion gene in a subgroup of patients with NSCLC and the subsequent clinical development of crizotinib has been an amazing success story in lung cancer translational-research, and its accelerated approval [only 4 years from the discovery of ALK rearrangement in NSCLC to the approval by the Food and Drug Administration (FDA)] marked the beginning of the new decade of targeted therapy. However, common to all targeted therapies, despite an initial benefit, patients inevitably experience tumor progression, due to the development of resistance. Several molecular mechanisms are responsible for acquired resistance, such as secondary mutations of ALK kinase domain or amplification of ALK fusion gene, or the activation of other oncogenic drivers, which may cause resistance independently of ALK genetic alterations. Pre-clinical data and early clinical trials showed the promising efficacy of a new class of ALK-inhibitors in overcoming acquired resistance. The inhibition of the molecular chaperone, HSP90, represents another promising strategy to overcome crizotinib resistance in ALK-rearranged NSCLC. Several molecules are currently under investigation in order to establish their specific role in the treatment of ALK-rearranged 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.