guest ::
| Home > Publications database > Targeting IRAK4 disrupts inflammatory pathways and delays tumor development in chronic lymphocytic leukemia. > print |
| Home > Publications database > Targeting IRAK4 disrupts inflammatory pathways and delays tumor development in chronic lymphocytic leukemia. > print |
| 001 | 144013 | ||
| 005 | 20251110144758.0 | ||
| 024 | 7 | _ | |a 10.1038/s41375-019-0507-8 |2 doi |
| 024 | 7 | _ | |a pmid:31197259 |2 pmid |
| 024 | 7 | _ | |a 0887-6924 |2 ISSN |
| 024 | 7 | _ | |a 1476-5551 |2 ISSN |
| 024 | 7 | _ | |a altmetric:112716510 |2 altmetric |
| 037 | _ | _ | |a DKFZ-2019-01564 |
| 041 | _ | _ | |a eng |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Giménez, Neus |b 0 |
| 245 | _ | _ | |a Targeting IRAK4 disrupts inflammatory pathways and delays tumor development in chronic lymphocytic leukemia. |
| 260 | _ | _ | |a London |c 2020 |b Springer Nature |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1762782462_2549711 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 500 | _ | _ | |a 2020 Jan;34(1):100-114 / #EA:B060#LA:B060# / #DKFZ-MOST-Ca166# |
| 520 | _ | _ | |a Interleukin-1 receptor-associated kinase 4 (IRAK4) plays a critical role in Toll-like receptor (TLR) signal transduction and innate immune responses. Recruitment and subsequent activation of IRAK4 upon TLR stimulation is mediated by the myeloid differentiation primary response 88 (MYD88) adaptor protein. Around 3% of chronic lymphocytic leukemia (CLL) patients have activating mutations of MYD88, a driver mutation in this disease. Here, we studied the effects of TLR activation and the pharmacological inhibition of IRAK4 with ND2158, an IRAK4 competitive inhibitor, as a therapeutic approach in CLL. Our in vitro studies demonstrated that ND2158 preferentially killed CLL cells in a dose-dependent manner. We further observed a decrease in NF-κB and STAT3 signaling, cytokine secretion, proliferation and migration of primary CLL cells from MYD88-mutated and -unmutated cases. In the Eµ-TCL1 adoptive transfer mouse model of CLL, ND2158 delayed tumor progression and modulated the activity of myeloid and T cells. Our findings show the importance of TLR signaling in CLL development and suggest IRAK4 as a therapeutic target for this disease. |
| 536 | _ | _ | |a 312 - Functional and structural genomics (POF3-312) |0 G:(DE-HGF)POF3-312 |c POF3-312 |f POF III |x 0 |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, |
| 700 | 1 | _ | |a Schulz, Ralph |0 P:(DE-He78)cae043ee51d02e740b4c67196aa20afb |b 1 |e First author |
| 700 | 1 | _ | |a Higashi, Morihiro |b 2 |
| 700 | 1 | _ | |a Aymerich, Marta |b 3 |
| 700 | 1 | _ | |a Villamor, Neus |0 0000-0001-6538-4111 |b 4 |
| 700 | 1 | _ | |a Delgado, Julio |b 5 |
| 700 | 1 | _ | |a Juan, Manel |0 0000-0002-3064-1648 |b 6 |
| 700 | 1 | _ | |a López-Guerra, Mònica |b 7 |
| 700 | 1 | _ | |a Campo, Elias |b 8 |
| 700 | 1 | _ | |a Rosich, Laia |b 9 |
| 700 | 1 | _ | |a Seiffert, Martina |0 P:(DE-He78)e67f907703fcb2cf909f4d72d50268b5 |b 10 |e Last author |
| 700 | 1 | _ | |a Colomer, Dolors |0 0000-0001-7486-8484 |b 11 |
| 773 | _ | _ | |a 10.1038/s41375-019-0507-8 |0 PERI:(DE-600)2008023-2 |n 1 |p 100-114 |t Leukemia |v 34 |y 2020 |x 1476-5551 |
| 909 | C | O | |p VDB |o oai:inrepo02.dkfz.de:144013 |
| 910 | 1 | _ | |a Deutsches Krebsforschungszentrum |0 I:(DE-588b)2036810-0 |k DKFZ |b 1 |6 P:(DE-He78)cae043ee51d02e740b4c67196aa20afb |
| 910 | 1 | _ | |a Deutsches Krebsforschungszentrum |0 I:(DE-588b)2036810-0 |k DKFZ |b 10 |6 P:(DE-He78)e67f907703fcb2cf909f4d72d50268b5 |
| 913 | 1 | _ | |a DE-HGF |b Gesundheit |l Krebsforschung |1 G:(DE-HGF)POF3-310 |0 G:(DE-HGF)POF3-312 |3 G:(DE-HGF)POF3 |2 G:(DE-HGF)POF3-300 |4 G:(DE-HGF)POF |v Functional and structural genomics |x 0 |
| 914 | 1 | _ | |y 2020 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0300 |2 StatID |b Medline |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0310 |2 StatID |b NCBI Molecular Biology Database |
| 915 | _ | _ | |a JCR |0 StatID:(DE-HGF)0100 |2 StatID |b LEUKEMIA : 2017 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0200 |2 StatID |b SCOPUS |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0600 |2 StatID |b Ebsco Academic Search |
| 915 | _ | _ | |a Peer Review |0 StatID:(DE-HGF)0030 |2 StatID |b ASC |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0199 |2 StatID |b Clarivate Analytics Master Journal List |
| 915 | _ | _ | |a WoS |0 StatID:(DE-HGF)0110 |2 StatID |b Science Citation Index |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0150 |2 StatID |b Web of Science Core Collection |
| 915 | _ | _ | |a WoS |0 StatID:(DE-HGF)0111 |2 StatID |b Science Citation Index Expanded |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)1030 |2 StatID |b Current Contents - Life Sciences |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)1050 |2 StatID |b BIOSIS Previews |
| 915 | _ | _ | |a IF >= 10 |0 StatID:(DE-HGF)9910 |2 StatID |b LEUKEMIA : 2017 |
| 920 | 2 | _ | |0 I:(DE-He78)B060-20160331 |k B060 |l B060 Molekulare Genetik |x 0 |
| 920 | 1 | _ | |0 I:(DE-He78)B060-20160331 |k B060 |l B060 Molekulare Genetik |x 0 |
| 920 | 0 | _ | |0 I:(DE-He78)B060-20160331 |k B060 |l B060 Molekulare Genetik |x 0 |
| 980 | _ | _ | |a journal |
| 980 | _ | _ | |a VDB |
| 980 | _ | _ | |a I:(DE-He78)B060-20160331 |
| 980 | _ | _ | |a UNRESTRICTED |
| Library | Collection | CLSMajor | CLSMinor | Language | Author |
|---|