FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2016279303> ?p ?o ?g. }

• W2016279303 abstract "Interferon α (IFNα) has been used for over 20 years to treat patients with MPN, recently it has been reported that IFNα leads to hematological remissions and a reduction of the JAK2V617F allele burden in most PV patients receiving this modality of therapy. In order to evaluate the cellular target by which IFNα affects hematopoietic progenitor cells in PV patients, CD34 + cells were isolated from cord blood, normal bone marrow and the peripheral blood of PV patients and were treated in vitro with each of the three commercially available forms of IFNα: Interferon α 2b (IFNα 2b), pegylated interferon α 2a (Peg-IFNα 2a) and pegylated interferon α 2b (Peg-IFNα 2b). Each form of IFNα was equally potent in suppressing hematopoietic colony formation by normal marrow CD34 + cells in a dose-dependent fashion, the IC50 of each of the three forms of IFNα as showed by inhibition of CFU-GM and BFU-E derived colony formation was 2000 units/ml. Interestedly, Peg-IFNα 2a and IFNα 2b were more effective than Peg-IFNα 2b in inhibiting BFU-E derived colony formation by PV CD34 + cells, at a concentration of 2000 units/ml, IFNα 2b and Peg-IFN 2a diminished CFU-GM derived colony by 80 % and BFU-E derived colony by 90%. The IC50 of IFN 2b and Peg-IFN 2a was 200 units/ml for PV CFU-GM and less than 100 units/ml for PV BFU-E, while the IC50 for Peg-IFN 2b exceeded 2000 units/ml for PV CFU-GM and was 500 units/ml for PV BFU-E. But CD34 + cells from cord blood were less sensitive to the treatment with each of three forms of IFN which was correlated with reduced expression of IFN receptor 1. In addition, exposure of PV CD34 + cells to equal doses of Peg-IFN 2a and IFN 2b resulted in a 38-40% reduction in the proportion of JAK2V617F-positive hematopoietic progenitor cells (HPC), while equivalent doses of Peg-IFN 2b did not reduce the number of malignant HPC. To further assess the cellular target of Peg-IFN 2a on JAK2V617F HPC, we performed similar studies on CD34 + cells from 12 additional PV patients. The numbers of JAK2V617F positive hematopoietic colonies were reduced in 11 of 12 cases treated with Peg-IFN 2a in vitro. Furthermore, in 7 of the 9 cases where JAK2V617F homozygous colonies were observed the addition of Peg-IFN 2a led to either the elimination of such homozygous colonies or a marked reduction in their numbers. In each of the 11 instances where Peg-IFN 2a reduced the number of colonies containing JAK2 mutated cells there was a concomitant increase in the numbers of colonies which contained exclusively WT JAK2. We further explored if IFN induces HPC growth inhibition and apoptosis through activation of the p38 MAP kinase pathway. Treatment with Peg-IFN 2a increased the phosphorylation/activition of p38 MAP kinase in PV CD34 + cells, while the p38-specific inhibitor SB203580 reversed the growth inhibition and apoptosis induced by Peg-IFN 2a. These data suggest that low doses of IFN selectively and directly suppress PV JAK2V617F HPC and that these agents act through the p38 MAP kinase pathway. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-54." @default.
• W2016279303 created "2016-06-24" @default.
• W2016279303 creator A5000837512 @default.
• W2016279303 creator A5006372952 @default.
• W2016279303 creator A5006812383 @default.
• W2016279303 creator A5014205411 @default.
• W2016279303 creator A5016397987 @default.
• W2016279303 creator A5033704013 @default.
• W2016279303 creator A5042483525 @default.
• W2016279303 creator A5087099599 @default.
• W2016279303 creator A5087689514 @default.
• W2016279303 creator A5088605815 @default.
• W2016279303 date "2010-04-15" @default.
• W2016279303 modified "2023-09-22" @default.
• W2016279303 title "Abstract LB-54: Interferon targets JAK2V617F positive hematopoietic progenitor cells and acts through the p38 MAP kinase pathway" @default.
• W2016279303 doi "https://doi.org/10.1158/1538-7445.am10-lb-54" @default.
• W2016279303 hasPublicationYear "2010" @default.
• W2016279303 type Work @default.
• W2016279303 sameAs 2016279303 @default.
• W2016279303 citedByCount "0" @default.
• W2016279303 crossrefType "proceedings-article" @default.
• W2016279303 hasAuthorship W2016279303A5000837512 @default.
• W2016279303 hasAuthorship W2016279303A5006372952 @default.
• W2016279303 hasAuthorship W2016279303A5006812383 @default.
• W2016279303 hasAuthorship W2016279303A5014205411 @default.
• W2016279303 hasAuthorship W2016279303A5016397987 @default.
• W2016279303 hasAuthorship W2016279303A5033704013 @default.
• W2016279303 hasAuthorship W2016279303A5042483525 @default.
• W2016279303 hasAuthorship W2016279303A5087099599 @default.
• W2016279303 hasAuthorship W2016279303A5087689514 @default.
• W2016279303 hasAuthorship W2016279303A5088605815 @default.
• W2016279303 hasConcept C10205521 @default.
• W2016279303 hasConcept C109159458 @default.
• W2016279303 hasConcept C153911025 @default.
• W2016279303 hasConcept C192285135 @default.
• W2016279303 hasConcept C201750760 @default.
• W2016279303 hasConcept C203014093 @default.
• W2016279303 hasConcept C2776178377 @default.
• W2016279303 hasConcept C2780007613 @default.
• W2016279303 hasConcept C28328180 @default.
• W2016279303 hasConcept C523546767 @default.
• W2016279303 hasConcept C54355233 @default.
• W2016279303 hasConcept C71924100 @default.
• W2016279303 hasConcept C86803240 @default.
• W2016279303 hasConcept C95444343 @default.
• W2016279303 hasConcept C98274493 @default.
• W2016279303 hasConceptScore W2016279303C10205521 @default.
• W2016279303 hasConceptScore W2016279303C109159458 @default.
• W2016279303 hasConceptScore W2016279303C153911025 @default.
• W2016279303 hasConceptScore W2016279303C192285135 @default.
• W2016279303 hasConceptScore W2016279303C201750760 @default.
• W2016279303 hasConceptScore W2016279303C203014093 @default.
• W2016279303 hasConceptScore W2016279303C2776178377 @default.
• W2016279303 hasConceptScore W2016279303C2780007613 @default.
• W2016279303 hasConceptScore W2016279303C28328180 @default.
• W2016279303 hasConceptScore W2016279303C523546767 @default.
• W2016279303 hasConceptScore W2016279303C54355233 @default.
• W2016279303 hasConceptScore W2016279303C71924100 @default.
• W2016279303 hasConceptScore W2016279303C86803240 @default.
• W2016279303 hasConceptScore W2016279303C95444343 @default.
• W2016279303 hasConceptScore W2016279303C98274493 @default.
• W2016279303 hasLocation W20162793031 @default.
• W2016279303 hasOpenAccess W2016279303 @default.
• W2016279303 hasPrimaryLocation W20162793031 @default.
• W2016279303 hasRelatedWork W1978228555 @default.
• W2016279303 hasRelatedWork W1984924774 @default.
• W2016279303 hasRelatedWork W1988221506 @default.
• W2016279303 hasRelatedWork W1991171923 @default.
• W2016279303 hasRelatedWork W1995433735 @default.
• W2016279303 hasRelatedWork W2031351523 @default.
• W2016279303 hasRelatedWork W2064055538 @default.
• W2016279303 hasRelatedWork W2072625217 @default.
• W2016279303 hasRelatedWork W2352332541 @default.
• W2016279303 hasRelatedWork W2376771180 @default.
• W2016279303 hasRelatedWork W2401558771 @default.
• W2016279303 hasRelatedWork W2417523607 @default.
• W2016279303 hasRelatedWork W2462395448 @default.
• W2016279303 hasRelatedWork W2496228640 @default.
• W2016279303 hasRelatedWork W2518069170 @default.
• W2016279303 hasRelatedWork W2559879605 @default.
• W2016279303 hasRelatedWork W2561242287 @default.
• W2016279303 hasRelatedWork W2584660382 @default.
• W2016279303 hasRelatedWork W2946423821 @default.
• W2016279303 hasRelatedWork W3100871656 @default.
• W2016279303 isParatext "false" @default.
• W2016279303 isRetracted "false" @default.
• W2016279303 magId "2016279303" @default.
• W2016279303 workType "article" @default.