dc.contributor.author | Diab, A | |
dc.contributor.author | Zickl, L | |
dc.contributor.author | Abdel-Wahab, O | |
dc.contributor.author | Jhanwar, S | |
dc.contributor.author | Gulam, MA | |
dc.contributor.author | Panageas, KS | |
dc.contributor.author | Patel, JP | |
dc.contributor.author | Jurcic, J | |
dc.contributor.author | Maslak, P | |
dc.contributor.author | Paietta, E | |
dc.contributor.author | Mangan, JK | |
dc.contributor.author | Carroll, M | |
dc.contributor.author | Fernandez, HF | |
dc.contributor.author | Teruya-Feldstein, J | |
dc.contributor.author | Luger, SM | |
dc.contributor.author | Douer, D | |
dc.contributor.author | Litzow, MR, | |
dc.contributor.author | Lazarus, HM | |
dc.contributor.author | Rowe, JM | |
dc.contributor.author | Levine, RL | |
dc.contributor.author | Tallman, MS | |
dc.date.accessioned | 2013-10-28T12:23:21Z | |
dc.date.available | 2013-10-28T12:23:21Z | |
dc.date.issued | 2013 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/pubmed/23102703 | |
dc.identifier.uri | http://erepository.uonbi.ac.ke:8080/xmlui/handle/123456789/57955 | |
dc.description.abstract | Previous small series have suggested that acute myeloid leukemia with t(8;16) is a distinct morphologic and clinical entity associated with poor prognosis. We describe 18 patients with t(8;16) AML, including their clinical, cytomorphologic, immunophenotypic and cytogenetic features. Half of the patients had extramedullary disease, most commonly leukemia cutis, which often preceded bone marrow involvement and six had therapy-related AML. Patients with t(8;16) AML commonly present with clinical and pathological features that mimic APL, with promyelocytes and promyeloblast-like cells and coagulopathy in most patients. Several patients also presented with marrow histiocytes with hemophagocytosis and erythrophagocytosis. Comprehensive molecular analysis for co-occurring genetic alterations revealed a somatic mutation in RUNX1 in 1 of 6 t(8;16) patients with no known AML mutation in the remaining five t(8;16) patients. This suggests that the t(8;16) translocation could be sufficient to induce hematopoietic cell transformation to AML without acquiring other genetic alteration. These data further support classifying t(8;16) AML as a clinically and molecularly defined subtype of AML marked by characteristic clinical and cytomorphologic features that mimic APL, and is associated with very poor survival | en |
dc.language.iso | en | en |
dc.title | Acute myeloid leukemia with translocation t(8;16) presents with features which mimic acute promyelocytic leukemia and is associated with poor prognosis | en |
dc.type | Article | en |
local.publisher | College of Biological and Physical Sciences ,Department of physics | en |