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• W2097337967 abstract "Summary Approximately one‐third of patients with chronic myeloid leukaemia will fail to achieve or maintain responses to imatinib. Changes in solute carrier family 22 (organic cation transporter), member 1 ( SLC 22 A 1, also termed OCT 1), the main transporter for imatinib, have been proposed as a possible predictive factor. We analysed SLC22A1 m RNA levels and single nucleotide polymorphisms ( SNP s) located in exon 7 in 153 diagnostic whole blood samples from two patient cohorts. The level of SLC22A1 expression did not significantly correlate with imatinib failure or achievement of molecular remission. The SNP 408V>M (g.1222G>A) was present in 65% of patients and was associated in all cases with an eight base‐pair insertion (8 + allele) at the 3′ end of exon 7. The latter generates an alternative splice site, leading to a premature stop codon. M 420del was found in 33% of patients and never in cis with 8 + (the 3 − allele). Significantly longer times to 1% and 0·1% molecular responses (by quantitative reverse transcription polymerase chain reaction) were seen in patients with 8 + 8 + or 8 + N compared to those with the remaining four genotypes (N = no insertion or deletion). Patients lacking 8 + and 3 − (NN, 18%) showed the best outcomes overall. Thus, while SLC 22 A 1 expression does not appear to affect response, alterations in its splicing or amino acid sequence may do so." @default.
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• W2097337967 date "2013-10-10" @default.
• W2097337967 modified "2023-10-15" @default.
• W2097337967 title "A common novel splice variant of<i>SLC22A1</i>(<i>OCT1)</i>is associated with impaired responses to imatinib in patients with chronic myeloid leukaemia" @default.
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• W2097337967 doi "https://doi.org/10.1111/bjh.12591" @default.
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