期刊
BRITISH JOURNAL OF CANCER
卷 112, 期 2, 页码 232-237出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/bjc.2014.513
关键词
IRAK; leukaemia; cancer; myelodysplasia; NF-kappa B
类别
资金
- Cincinnati Children's Hospital Research Foundation
- American Society of Hematology (ASH)
- National Institute of Health [RO1HL111103]
- Gabrielle's Angel Foundation
- Department of Defense grants
Innate immune signalling has an essential role in inflammation, and the dysregulation of signalling components of this pathway is increasingly being recognised as an important mediator in cancer initiation and progression. In some malignancies, dysregulation of inflammatory toll-like receptor (TLR) and interleukin-1 receptor (IL1R) signalling is typified by increased NF-kappa B activity, and it occurs through somatic mutations, chromosomal deletions, and/or transcriptional deregulation. Interleukin-1 receptor-associated kinase (IRAK) family members are mediators of TLR/IL1R superfamily signalling, and mounting evidence implicates these kinases as viable cancer targets. Although there have been previous efforts aimed at the development of IRAK kinase inhibitors, this is currently an area of renewed interest for cancer drug development.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据