Acute myeloid leukemia bearing t(7;11)(p15;p15) is a distinct cytogenetic entity with poor outcome and a distinct mutation profile: comparative analysis ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2009-07

AUTHORS

W-C Chou, C-Y Chen, H-A Hou, L-I Lin, J-L Tang, M Yao, W Tsay, B-S Ko, S-J Wu, S-Y Huang, S-C Hsu, Y-C Chen, Y-N Huang, M-H Tseng, C-F Huang, H-F Tien

ABSTRACT

Acute myeloid leukemia (AML) with t(7;11)(p15;p15), which results in a NUP98-HOXA9 fusion, is a distinct entity, but this subtype has not been characterized in detail. In a comprehensive study comparing 11 such patients with another 482 adult patients, we found that those with t(7;11) were younger (P=0.0076) and female (P=0.0111), with almost all having the M2-subtype of AML (P<0.0001). Even when those with low-risk karyotypes were excluded, patients with t(7;11) had poorer overall survival than the other AML group (median 13.5 and 20 months, respectively, P=0.045) and poorer relapse-free survival (median 6 and 12 months, respectively, P=0.003). The NUP98-HOXA9 fusion was strongly associated with KRAS and WT1 mutations (P=0.015 and P=0.0018, respectively). We characterized four varieties of this fusion, among which NUP98 exon 12/HOXA9 exon 1b was present in all 11 patients. We developed a highly sensitive and specific assay to quantify the abundance of leukemic cells, and found that the fusion remained detectable in morphological complete remission, even after allogeneic stem cell transplantation, suggesting that this disease was highly refractory to very intensive treatment. AML with NUP98-HOXA9 fusion therefore appears to have a distinct clinical and biological profile, and should be regarded as a poor prognostic group. More... »

PAGES

leu200925

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/leu.2009.25

DOI

http://dx.doi.org/10.1038/leu.2009.25

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1040146289

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19225539


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