Format

Send to

Choose Destination
See comment in PubMed Commons below
J Clin Oncol. 2002 May 1;20(9):2302-9.

Favorable impact of the t(9;11) in childhood acute myeloid leukemia.

Author information

1
Department of Hematology-Oncology, St Jude Children's Research Hospital, Memphis, TN 38105-2794, USA.

Abstract

PURPOSE:

To determine the impact of MLL rearrangements on the outcome of children with acute myeloid leukemia (AML).

PATIENTS AND METHODS:

We analyzed the clinical and biologic features of 298 infants and children with primary AML treated on four consecutive institutional clinical trials. The Kaplan-Meier method was used in survival analysis and the Cox proportional-hazards model was used to analyze the effect of potential prognostic factors on event-free survival (+/- 1 SE).

RESULTS:

Molecular studies of 152 cases detected 42 with MLL rearrangements. The karyotypes of these 42 revealed the t(9;11) (15 cases), abnormalities of chromosomes 10 and 11 (nine cases), the t(11;19) (four cases), other abnormalities of 11q23 (seven cases), and miscellaneous rearrangements (seven cases). Among these 42 patients, the 15 whose leukemic cells carried the t(9;11) had a better outcome (66% +/- 15%) than the other 27 (25.9% +/- 11.2%; P =.004). Cases with the t(9;11) were also characterized by M5 AML morphology (21 of 23 cases). Of the 63 patients with M5 AML, the 21 whose leukemic cells demonstrated the t(9;11) had a better outcome (71.1% +/- 11%) than the other 42 (25.8% +/- 7.9%; P =.0004). The only independent factors indicating a favorable prognosis were presenting leukocyte count less than 50 x 10(9)/L (relative risk of relapse, 0.73; 95% confidence interval, 0.55 to 0.97; P =.03) and the t(9;11) (relative risk of relapse, 0.32; 95% confidence interval, 0.16 to 0.64; P =.002).

CONCLUSION:

We conclude that the t(9;11) is the most favorable genetic factor for patients with AML treated at our institution.

PMID:
11981001
DOI:
10.1200/JCO.2002.08.023
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Atypon
    Loading ...
    Support Center