AIM: @entity2213 is a @entity4149 kinase inhibitor that has revolutionized the treatment of @entity1860 ( @entity1860 ). Despite its efficacy, about a third of @entity1 discontinue the treatment due to therapy failure or intolerance. The rational identification of @entity1 less likely to respond to @entity2213 would be of paramount clinical relevance. We have shown that transmembrane transporter @entity3871 genotyping predicts @entity2213 activity. In parallel, Polycomb group genes (PcGs) are epigenetic repressors implicated in @entity1860 progression and in therapy resistance. @entity1 _ METHODS: We measured the expression of eight PcGs in paired pre- and post- @entity2213 bone marrow samples from 30 @entity1860 @entity1 . RESULTS: @entity3752 , @entity68859 , @entity68860 and @entity28893 expression was significantly increased during @entity2213 treatment. Post-treatment levels of @entity68860 and @entity28893 predicted 3-month response rate. Measurement of post-treatment @entity3752 levels improved the predictive power of @entity3871 genotyping. CONCLUSION: These results suggest that the expression levels of PcGs might be useful for a more accurate risk stratification of @entity1860 @entity1 .

Polycomb genes are associated with response to XXXX in @entity1860 .

@entity1 :: ('9606', 'Species') :: ['patients', 'PATIENTS'] @entity3871 :: ('6580', 'Gene') :: ['hOCT1'] @entity3752 :: ('648', 'Gene') :: ['BMI1'] @entity68860 :: ('23466', 'Gene') :: ['CBX6'] @entity68859 :: ('80012', 'Gene') :: ['PHC3'] @entity28893 :: ('23492', 'Gene') :: ['CBX7'] @entity4149 :: ('D014443', 'Chemical') :: ['tyrosine'] @entity2213 :: ('MESH:C097613', 'Chemical') :: ['imatinib', 'Imatinib'] @entity1860 :: ('MESH:D015464', 'Disease') :: ['CML', 'chronic myeloid leukemia']
@entity2213 :: (MESH:C097613,Chemical) :: ['imatinib']
