NDLI: Identification of novel cluster groups in pediatric high-risk B-precursor acute lymphoblastic leukemia with gene expression profiling: correlation with genome-wide DNA copy number alterations, clinical characteristics, and outcome

Content Provider	PubMed Central
Author	Harvey, Richard C. Mullighan, Charles G. Wang, Xuefei Dobbin, Kevin K. Davidson, George S. Bedrick, Edward J. Chen, I-ming Atlas, Susan R. Kang, Huining Kerem, Ar Wilson, Carla S. Wharton, Walker Murphy, Maurice Meenakshi, Devidas Carroll, Andrew J. Borowitz, Michael J. Bowman, W. Paul Downing, James R. Mary, Relling Yang, Jun Bhojwani, Deepa Carroll, William L. Bruce, Camitta Reaman, Gregory H. Smith, Malcolm Hunger, Stephen P. Willman, Cheryl L.
Copyright Year	2010
Abstract	To resolve the genetic heterogeneity within pediatric high-risk B-precursor acute lymphoblastic leukemia (ALL), a clinically defined poor-risk group with few known recurring cytogenetic abnormalities, we performed gene expression profiling in a cohort of 207 uniformly treated children with high-risk ALL. Expression profiles were correlated with genome-wide DNA copy number abnormalities and clinical and outcome features. Unsupervised clustering of gene expression profiling data revealed 8 unique cluster groups within these high-risk ALL patients, 2 of which were associated with known chromosomal translocations (t(1;19)(TCF3-PBX1) or MLL), and 6 of which lacked any previously known cytogenetic lesion. One unique cluster was characterized by high expression of distinct outlier genes AGAP1, CCNJ, CHST2/7, CLEC12A/B, and PTPRM; ERG DNA deletions; and 4-year relapse-free survival of 94.7% ± 5.1%, compared with 63.5% ± 3.7% for the cohort (P = .01). A second cluster, characterized by high expression of BMPR1B, CRLF2, GPR110, and MUC4; frequent deletion of EBF1, IKZF1, RAG1-2, and IL3RA-CSF2RA; JAK mutations and CRLF2 rearrangements (P < .0001); and Hispanic ethnicity (P < .001) had a very poor 4-year relapse-free survival (21.0% ± 9.5%; P < .001). These studies reveal striking clinical and genetic heterogeneity in high-risk ALL and point to novel genes that may serve as new targets for diagnosis, risk classification, and therapy.
Related Links	http://dx.doi.org/10.1182/blood-2009-08-239681
Starting Page	4874
File Format	PDF
ISSN	15280020
e-ISSN	15280020
Journal	Blood
Issue Number	23
Volume Number	116
Language	English
Publisher	American Society of Hematology
Publisher Date	2010-12-02
Access Restriction	Open
Rights Holder	American Society of Hematology
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Hematology Biochemistry Immunology

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