Associated Papers
Clonal architecture of FLT3-ITD and acquired 13q uniparental disomy define prognostic heterogeneity and therapeutic vulnerabilities in acute myeloid leukemia.
Lai A et al.
Neoplasia (new York, N.y.), 2025
41411742 (PubMed )
Supplement: mmc2.xlsx › Sheet1
Next-Generation Sequencing Improves Diagnosis, Prognosis and Clinical Management of Myeloid Neoplasms.
Carbonell D et al.
Cancers, 2019
31540291 (PubMed )
Supplement: cancers-11-01364-s001.zip › cancers-588721-SI.pdf
appreci8: a pipeline for precise variant calling integrating 8 tools.
Sandmann S et al.
Bioinformatics (oxford, England), 2018
29945233 (PubMed )
Supplement: bty518_supplementary_data_s4.xlsx › TP_Mutations
Persistence of pre-leukemic clones during first remission and risk of relapse in acute myeloid leukemia.
Rothenberg-Thurley M et al.
Leukemia, 2018
29472724 (PubMed )
Supplement: 41375_2018_34_MOESM2_ESM.xlsx › Supplemental_Table_3
Gene conversion (655G splicing mutation) and the founder effect (Gln318Stop) contribute to the most frequent severe point mutations in congenital adrenal hyperplasia (21-hydroxylase deficiency) in the Spanish population.
Ezquieta B et al.
Clinical Genetics, 2002
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