Title of article :
Classification, subtype discovery, and prediction of outcome in pediatric acute lymphoblastic leukemia by gene expression profiling
Author/Authors :
Yeoh، نويسنده , , Eng-Juh and Ross، نويسنده , , Mary E and Shurtleff، نويسنده , , Sheila A and Williams، نويسنده , , W.Kent and Patel، نويسنده , , Divyen and Mahfouz، نويسنده , , Rami and Behm، نويسنده , , Fred G and Raimondi، نويسنده , , Susana C and Relling، نويسنده , , Mary V and Patel، نويسنده , , Anami and Cheng، نويسنده , , Cheng and Campana، نويسنده , , Dario and Wilkins، نويسنده , , Dawn and Zhou، نويسنده , , Xiaodong and Li، نويسنده , , Jinyan and Liu، نويسنده , , Huiqing and Pui، نويسنده , , Ching-Hon and Evans، نويسنده , , William E and Naeve، نويسنده , , Clayton and Wong، نويسنده , , Limsoon and Downing، نويسنده , , James R، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2002
Pages :
11
From page :
133
To page :
143
Abstract :
Treatment of pediatric acute lymphoblastic leukemia (ALL) is based on the concept of tailoring the intensity of therapy to a patientʹs risk of relapse. To determine whether gene expression profiling could enhance risk assignment, we used oligonucleotide microarrays to analyze the pattern of genes expressed in leukemic blasts from 360 pediatric ALL patients. Distinct expression profiles identified each of the prognostically important leukemia subtypes, including T-ALL, E2A-PBX1, BCR-ABL, TEL-AML1, MLL rearrangement, and hyperdiploid >50 chromosomes. In addition, another ALL subgroup was identified based on its unique expression profile. Examination of the genes comprising the expression signatures provided important insights into the biology of these leukemia subgroups. Further, within some genetic subgroups, expression profiles identified those patients that would eventually fail therapy. Thus, the single platform of expression profiling should enhance the accurate risk stratification of pediatric ALL patients.
Journal title :
Cancer Cell
Serial Year :
2002
Journal title :
Cancer Cell
Record number :
1334835
Link To Document :
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