Ontology type: schema:ScholarlyArticle Open Access: True
2012-02
AUTHORSD Marin, I H Gabriel, S Ahmad, L Foroni, H de Lavallade, R Clark, S O'Brien, R Sergeant, C Hedgley, D Milojkovic, J S Khorashad, M Bua, A Alsuliman, A Khoder, K Stringaris, N Cooper, J Davis, J M Goldman, J F Apperley, K Rezvani
ABSTRACTNatural killer (NK) cells are expanded in chronic myeloid leukemia (CML) patients on tyrosine kinase inhibitors (TKI) and exert cytotoxicity. The inherited repertoire of killer immunoglobulin-like receptors (KIR) may influence response to TKI. We investigated the impact of KIR-genotype on outcome in 166 chronic phase CML patients on first-line imatinib treatment. We validated our findings in an independent patient group. On multivariate analysis, KIR2DS1 genotype (RR=1.51, P=0.03) and Sokal risk score (low-risk RR=1, intermediate-risk RR=1.53, P=0.04, high-risk RR=1.69, P=0.034) were the only independent predictors for failure to achieve complete cytogenetic response (CCyR). Furthermore, KIR2DS1 was the only factor predicting shorter progression-free (PFS) (RR=3.1, P=0.03) and overall survival (OS) (RR=2.6, P=0.04). The association between KIR2DS1 and CCyR, PFS and OS was validated by KIR genotyping in 174 CML patients on first-line imatinib in the UK multi-center SPIRIT-1 trial; in this cohort, KIR2DS1(+) patients had significantly lower 2-year probabilities of achieving CCyR (76.9 vs 87.9%, P=0.003), PFS (85.3 vs 98.1%, P=0.007) and OS (94.4 vs 100%, P=0.015) than KIR2DS1(-) patients. The impact of KIR2DS1 on CCyR was greatest when the ligand for the corresponding inhibitory receptor, KIR2DL1, was absent (P=0.00006). Our data suggest a novel role for KIR-HLA immunogenetics in CML patients on TKI. More... »
PAGESleu2011180
http://scigraph.springernature.com/pub.10.1038/leu.2011.180
DOIhttp://dx.doi.org/10.1038/leu.2011.180
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PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/21844874
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