期刊
CANCER SCIENCE
卷 108, 期 10, 页码 1913-1920出版社
WILEY
DOI: 10.1111/cas.13333
关键词
ALK cancer; anaplastic large-cell lymphoma; inflammatory myofibroblastic tumor; neuroblastoma
类别
资金
- Japan Society for the Promotion of Science [26293242]
- Japan Health Sciences Foundation
- Japan Science and Technology Agency
- P-CREATE Japan Agency for Medical Research and Development (AMED) (Japan) [16cm0106509h001]
- KAKENHI [17H04224]
- Grants-in-Aid for Scientific Research [17H04224, 26293242] Funding Source: KAKEN
The anaplastic lymphoma kinase (ALK) gene was initially identified as a fusion partner of the nucleophosmin gene in anaplastic large-cell lymphoma with t(2;5)(p23;q35) translocation, and then described with different genetic abnormalities in a number of tumors. Although ALK is known to be involved in the pathogenesis of neuroblastoma through activating mutations or gene amplification, its role in the pathogenesis of other pediatric cancers is still elusive. In addition to neuroblastoma, the high-grade amplification of ALK has been described in a subset of rhabdomyosarcoma cases. Normal ALK protein expression is restricted to the nervous systems of adult mammals, but the aberrant expression of ALK has been observed in a variety of pediatric cancers, including glioma and Ewing sarcoma. The discovery of oncogenic activation of ALK in neuroblastoma suggests that this cancer could be potentially treated with an ALK inhibitor, as could other cancers, such as non-small-cell lung cancer and anaplastic large-cell lymphoma. However, cellular responses to mutant ALK are complex when compared to rearranged ALK, and treatment remains a challenge. This review focuses on the biology of ALK in pediatric cancers and possible therapeutic strategies for ALK-associated tumors.
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