ArticlePloS one2012
ALK-activating homologous mutations in LTK induce cellular transformation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Current status and challenges of immunotherapy in ALK rearranged NSCLC.Frontiers in oncology · 2022Pooled it
- Mechanisms and Manifestations of Ligand Bias in Signaling: Focus on Receptor Tyrosine Kinases.Chemical reviews · 2026Review
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Spindle cell neoplasms with novel LTK fusion - Expanding the spectrum of kinase fusion-positive soft tissue tumors.Genes, chromosomes & cancer · 2024Article
- Molecular profiling and prognostic analysis in Chinese cholangiocarcinoma: an observational, retrospective single-center study.Investigational new drugs · 2024Observational
- Novel mutations in a second primary gastric cancer in a patient treated for primary colon cancer.World journal of surgical oncology · 2023Review
- RETRACTED: Tyrosine Kinase Inhibitors Target B Lymphocytes.Biomolecules · 2023Article
- Identification of Ultrasound-Sensitive Prognostic Markers of LAML and Construction of Prognostic Risk Model Based on WGCNA.Journal of oncology · 2023Article
- Molecular dissection of a hyper-aggressive CBFB-MYH11/FLT3-ITD-positive acute myeloid leukemia.Journal of translational medicine · 2022Article
- Article
- LTK fusions: A new target emerges in non-small cell lung cancer.Cancer cell · 2022Article
- Anaplastic lymphoma kinase (alk), a neuroblastoma associated gene, is expressed in neural crest domains during embryonic development of Xenopus.Gene expression patterns : GEP · 2021Article
- Knockdown of GSG2 inhibits prostate cancer progression in vitro and in vivo.International journal of oncology · 2020Article
- Review
- Bioinformatics Analysis Identifies Protein Tyrosine Kinase 7 (PTK7) as a Potential Prognostic and Therapeutic Biomarker in Stages I to IV Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Leukocyte receptor tyrosine kinase interacts with secreted midkine to promote survival of migrating neural crest cells.Development (Cambridge, England) · 2018Article
- ALKALs are in vivo ligands for ALK family receptor tyrosine kinases in the neural crest and derived cells.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Article
- Review
- Targeted therapies in development for non-small cell lung cancer.Journal of carcinogenesis · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leukocyte tyrosine kinase (LTK) is a receptor tyrosine kinase reported to be overexpressed in human leukemia. Though much regarding the function of LTK remains unknown, it shares a high degree of similarity with anaplastic lymphoma kinase (ALK), which is found mutated in human cancer. In order to determine if LTK has transforming potential, we created two LTK mutants, F568L and R669Q, that correspond to two well-characterized activating mutations of ALK (F1174L and R1275Q). LTK-F568L, but not wildtype LTK or LTK-R669Q, transformed hematopoietic cells to cytokine independence. LTK-F568L exhibited a stronger ability to induce loss of contact inhibition and anchorage-independent growth of epithelial cells compared to LTK-R669Q, while wildtype LTK was non-transforming in the same cells. Likewise, LTK-F568L induced greater neurite outgrowth of PC12 cells than R669Q, while wildtype LTK could not. Correlating with transforming activity, LTK-F568L displayed significantly enhanced tyrosine phosphorylation compared to wildtype LTK and LTK-R668Q and induced activation of various signaling proteins including Shc, ERK and the JAK/STAT pathway. Expression of wildtype LTK or LTK-R669Q generally led to weaker activation of signaling proteins than expression of LTK-F568L, or no activation at all. Thus, mutating LTK at residue F568, and to a lesser extent at R669, activates the receptor tyrosine kinase, inducing cell signaling that results in transforming properties. These studies suggest that aberrant activation of LTK may contribute to neoplastic cell growth.
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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.