SynthesisTechnology in cancer research & treatment
EML4-ALK in Non-small Cell Lung Cancer: Molecular Mechanisms and Targeted Therapies.
Synthesis in Technology in cancer research & treatment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is a malignancy characterized by high global incidence and mortality rates, with approximately 85% of cases classified as non-small cell lung cancer (NSCLC). Advances in molecular biology and targeted therapeutic agents have ushered NSCLC into the era of precision medicine. The echinoderm microtubule-associated protein-like 4 (EML4) and anaplastic lymphoma kinase (ALK) fusion gene represents a pivotal target for personalized treatment in NSCLC. Although ALK inhibitors exhibit significant efficacy against EML4-ALK-positive tumors, addressing drug resistance remains a major challenge. Identifying novel therapeutic targets and implementing combination therapies are essential for optimizing subsequent treatment strategies and improving overall prognosis. In the management of patients with EML4-ALK gene fusion, continuous monitoring of tumor progression and timely adjustment of treatment regimens based on disease status are critical to achieving long-term clinical benefits. This review comprehensively summarizes recent advances in the clinicopathological features, targeted drug development, resistance mechanisms, and potential therapeutic targets associated with the EML4-ALK fusion gene.
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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.