| RRC ID |
52280
|
| 著者 |
Fukuhara S, Nomoto J, Kim SW, Taniguchi H, Miyagi Maeshima A, Tobinai K, Kobayashi Y.
|
| タイトル |
Partial deletion of the ALK gene in ALK-positive anaplastic large cell lymphoma.
|
| ジャーナル |
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.
|
| 巻・号 |
36(1)
|
| ページ |
150-158
|
| 公開日 |
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
|
| 引用数 |
3
|
| リソース情報 |
| ヒト・動物細胞 |
NH-12(RCB2108) |
