ArticleInternal medicine (Tokyo, Japan)2025
A CML Patient Carrying BCR::ABL1 Splicing Variants Did Not Experience Blast Crisis for 15 Years without Responding to Various TKIs.
Article in Internal medicine (Tokyo, Japan), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A 45-year-old man was diagnosed with CML in the chronic phase and therefore was sequentially treated with imatinib, dasatinib, nilotinib, and ponatinib. Neither ABL1 point mutations nor any additional chromosomal abnormalities were detected. The patient's best response was a partial cytogenetic response to nilotinib treatment. The deletion of amino acid residues 184-274 and a 35 bp insertion after nucleotide 1423 of ABL1 were detected before ponatinib administration. Two years after ponatinib administration, the patient died of a traumatic brain hemorrhage 15 years after the CML diagnosis. He did not progress to blast crisis, possibly because of the emergence of a loss-of-function ABL1 splicing variant.
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