Literature DB >> 7772527

t(8;21) myelodysplasia, an early presentation of M2 AML.

A S Taj1, F M Ross, M Vickers, D N Choudhury, J F Harvey, J C Barber, C Barton, A G Smith.   

Abstract

The reciprocal translocation of genetic material between chromosomes 8 and 21, t(8;21), is usually restricted to cases of acute myeloid leukaemia (AML). Cases of AML with t(8;21) exhibit characteristic dysplastic features in myeloid and erythroid lineages with reduction in megakaryocytes. We report details of three patients presenting with myelodysplastic features; two had a typical t(8;21), and the third had a variant t(8;21) translocation. We discuss the significance of t(8;21) in the aetiology of myelodysplastic syndrome (MDS) and implications for the management of such patients.

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Year:  1995        PMID: 7772527     DOI: 10.1111/j.1365-2141.1995.tb08429.x

Source DB:  PubMed          Journal:  Br J Haematol        ISSN: 0007-1048            Impact factor:   6.998


  2 in total

1.  An activated receptor tyrosine kinase, TEL/PDGFbetaR, cooperates with AML1/ETO to induce acute myeloid leukemia in mice.

Authors:  Jay L Grisolano; Julie O'Neal; Jennifer Cain; Michael H Tomasson
Journal:  Proc Natl Acad Sci U S A       Date:  2003-07-24       Impact factor: 11.205

2.  The PEBP2betaMYH11 fusion created by Inv(16)(p13;q22) in myeloid leukemia impairs neutrophil maturation and contributes to granulocytic dysplasia.

Authors:  S C Kogan; E Lagasse; S Atwater; S C Bae; I Weissman; Y Ito; J M Bishop
Journal:  Proc Natl Acad Sci U S A       Date:  1998-09-29       Impact factor: 11.205

  2 in total

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