ArticleNeoplasia (New York, N.Y.)2011
Identification of oncogenic point mutations and hyperphosphorylation of anaplastic lymphoma kinase in lung cancer.
Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 55 citations in OpenAlex.
- A novel secondary ALK gene mutation which resistant to second-generation TKIs: a case report and literature review.Frontiers in oncology · 2024Article
- Case report: ALK D1225N missense mutation in lung adenocarcinoma responds to tyrosine kinase inhibitors.Frontiers in pharmacology · 2023Article
- A novel HIF1α-STIL-FOXM1 axis regulates tumor metastasis.Journal of biomedical science · 2022Article
- Analysis of M6A associated lncRNAs in prognosis and immune response of NSCLC patients.American journal of translational research · 2022Article
- Prognostic comparative genes predict targets for sorafenib combination therapies in hepatocellular carcinoma.Computational and structural biotechnology journal · 2022Article
- Article
- Alectinib treatment improves photodynamic therapy in cancer cell lines of different origin.BMC cancer · 2021Article
- Whole-exome mutational landscape of neuroendocrine carcinomas of the gallbladder.Signal transduction and targeted therapy · 2021Article
- ALK is frequently phosphorylated in Merkel cell carcinoma and associates with longer survival.PloS one · 2021Article
- Panomicon: A web-based environment for interactive, visual analysis of multi-omics data.Heliyon · 2020Article
- Correlation between combiningEuropean journal of nuclear medicine and molecular imaging · 2020Article
- Infantile inflammatory myofibroblastic tumors: clinicopathological and molecular characterization of 12 cases.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Integrative analyses of noncoding RNAs reveal the potential mechanisms augmenting tumor malignancy in lung adenocarcinoma.Nucleic acids research · 2020Article
- Targeting anaplastic lymphoma kinase in neuroblastoma.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2019Review
- Genomic heterogeneity of ALK fusion breakpoints in non-small-cell lung cancer.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018Article
- Synergistic Effects of NOTCH/γ-Secretase Inhibition and Standard of Care Treatment Modalities in Non-small Cell Lung Cancer Cells.Frontiers in oncology · 2018Article
- Genetic susceptibility to neuroblastoma.Current opinion in genetics & development · 2017Review
- ALK: a tyrosine kinase target for cancer therapy.Cold Spring Harbor molecular case studies · 2017Review
- Co-targeting ALK and EGFR parallel signaling in oral squamous cell carcinoma.Oral oncology · 2016Article
- Therapeutically Targetable ALK Mutations in Leukemia.Cancer research · 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
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oncogenic property of anaplastic lymphoma kinase (ALK) plays an essential role in the pathogenesis of various cancers and serves as an important therapeutic target. In this study, we identified frequent intragenic loss of heterozygosity and six novel driver mutations within ALK in lung adenocarcinomas. Overexpression of H694R or E1384K mutant ALK leads to hyperphosphorylation of ALK, and activation of its downstream mediators STAT3, AKT, and ERK resulted in enhanced cell proliferation, colony formation, cell migration, and tumor growth in xenograft models. Furthermore, the activated phospho-Y1604 ALK was increasingly detected in 13 human lung cancer cell lines and 263 lung cancer specimens regardless of tumor stages and types. Treatment of two different ALK inhibitors, WHI-P154 and NVP-TAE684, resulted in the down-regulation of aberrant ALK signaling, shrinkage of tumor, and suppression of metastasis and significantly improved survival of ALK mutant-bearing mice. Together, we identified that novel ALK point mutations possessed tumorigenic effects mainly through hyperphosphorylation of Y1604 and activation of downstream oncogenic signaling. The upregulated phospho-Y1604 ALK could serve as a diagnostic biomarker for lung cancer. Furthermore, targeting oncogenic mutant ALKs with inhibitors could be a promising strategy to improve the therapeutic efficacy of fatal lung cancers.
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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.