Reference - Detail
| RRC ID | 52280 |
|---|---|
| Author | Fukuhara S, Nomoto J, Kim SW, Taniguchi H, Miyagi Maeshima A, Tobinai K, Kobayashi Y. |
| Title | Partial deletion of the ALK gene in ALK-positive anaplastic large cell lymphoma. |
| Journal | Hematol Oncol |
| Abstract |
Anaplastic lymphoma kinase (ALK) protein is an orphan receptor tyrosine kinase that is constitutively activated by aberrant translocations of the ALK gene in anaplastic large cell lymphoma, ALK-positive and several other cancers. Additionally, aberrant mutation and amplification of the ALK gene, resulting in ALK kinase activation, were detected mainly in neuroblastoma. Recently, truncated ALK protein was also reported in neuroblastoma. Here, we describe a novel truncated form of the ALK transcript with in-frame skipping through exons 2 to 17 (ALKΔ2-17) in anaplastic large cell lymphoma, ALK-positive. The ALKΔ2-17 showed ligand-independent deregulated phosphorylation that initiated strong STAT3 signalling in NIH3T3 cells. The ALKΔ2-17-transduced NIH3T3 cells showed oncogenic potential in a colony formation assay. Our data indicate that the aberrant deletion of the ALK gene might be oncogenic, providing a novel insight into the oncogenic role of the ALK pathway. |
| Volume | 36(1) |
| Pages | 150-158 |
| Published | 2018-2-1 |
| DOI | 10.1002/hon.2455 |
| PMID | 28665006 |
| MeSH | Anaplastic Lymphoma Kinase Animals Cell Line, Tumor Humans Lymphoma, Large-Cell, Anaplastic / enzymology Lymphoma, Large-Cell, Anaplastic / genetics* Mice Middle Aged Mutation NIH 3T3 Cells Receptor Protein-Tyrosine Kinases / metabolism* |
| IF | 3.193 |
| Times Cited | 3 |
| Altmetric score |
オルトメトリクス指標項目
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| The most frequently cited source | Patent(IFI CLAIMS) |
| Total number of mentions | 4 |
| Altmetric score changes over past 6months | 3.0 |
| Resource | |
| Human and Animal Cells | NH-12(RCB2108) |