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IRAK signalling in cancer

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

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资金

  1. Cincinnati Children's Hospital Research Foundation
  2. American Society of Hematology (ASH)
  3. National Institute of Health [RO1HL111103]
  4. Gabrielle's Angel Foundation
  5. Department of Defense grants

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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.

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