ArticleDiscover oncology2024
Essential thrombocytosis transformed AML with TP53 mutations and its clinical implications.
Article in Discover oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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1 citing paper in PubMed.
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6 authors.
Funding
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Abstract
Essential thrombocytosis (ET) is a chronic myeloproliferative neoplasm. There is a rare possibility of its transformation from ET into acute myeloid leukemia (AML). While the TP53 mutation is a well-known risk factor for AML, limited research exists regarding ET patients who develop AML with TP53 mutations. Among three ET transformed AML patients, two exhibited TP53 mutations, with an increased number of AML cells. Conversely, the third ET patient who transformed to AML without TP53 mutations had a lower burden of AML cells. The patients with TP53 mutations had shorter survival times compared to that without mutations, in response to decitabine treatment. In contrast, the patient with ET transformed AML without TP53 mutations showed a better response to decitabine. The ET transformed AML without TP53 mutations patient exhibited a survival period exceeding 20 months. ET patients who develop AML with a high allelic burden of TP53 mutations may experience a more aggressive disease progression and severe complications compared to AML patient without TP53 mutations. Our report sheds light on the distinct clinical presentations of ET patients who develop AML, characterized by different TP53 mutations and varying therapeutic outcomes when treated with decitabine. However, further studies that include a larger quantity of samples are needed to elucidate the precise underlying molecular mechanisms involved in this process.
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