|
|
Previous Article | Table of Contents | Next Article 
Blood, Vol. 94 No. 5 (September 1), 1999:
pp. 1537-1544
Association of Chromosome Arm 9p Abnormalities With Adverse Risk in
Childhood Acute Lymphoblastic Leukemia: A Report From
the Children's Cancer Group
Nyla A. Heerema,
Harland N. Sather,
Martha G. Sensel,
Wen Liu-Mares,
Beverly J. Lange,
Bruce C. Bostrom,
James B. Nachman,
Peter
G. Steinherz,
Raymond Hutchinson,
Paul S. Gaynon,
Diane C. Arthur, and
Fatih M. Uckun
From the Department of Genetics, Hughes Institute, St Paul, MN; the
Department of Preventive Medicine, University of Southern California,
Los Angeles, CA; the Group Operations Center, Children's Cancer Group,
Arcadia, CA; the Division of Oncology, Children's Hospital of
Philadelphia, Philadelphia, PA; the Department of Hematology-Oncology,
Children's Hospitals and Clinics, Minneapolis, MN; the Department of
Pediatric Hematology-Oncology, University of Chicago, Chicago, IL; the
Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New
York, NY; the Department of Pediatric Hematology-Oncology, University
of Michigan, Ann Arbor, MI; the Department of Pediatric
Hematology-Oncology, Children's Hospital, Los Angeles, CA; Laboratory
of Pathology, National Cancer Institute, Bethesda, MD; the Children's
Cancer Group ALL Biology Reference Laboratory and Hughes Institute, St
Paul, MN.
Cytogenetic abnormalities of chromosome arm 9p occur frequently in
children with acute lymphoblastic leukemia (ALL). We analyzed 201 such
cases (11%) in 1,839 children with newly diagnosed ALL treated between
1989 and 1995 on risk-adjusted protocols of the Children's Cancer
Group (CCG). The majority of patients (131; 65%) with a 9p abnormality
were classified as higher risk. Nearly all patients had complex
karyotypes; most cases had deletions of 9p, add/der(9p), a dicentric
involving chromosome arm 9p, and/or balanced translocations and
inversions involving 9p. Event-free survival (EFS) estimates at 6 years
for patients with and without a 9p aberration were 61% (standard
deviation [SD] = 5%) and 76% (SD = 2%;
P < .0001). In addition, patients with a 9p abnormality had
an increased cumulative incidence of both marrow (P = .04) and central nervous system (P = .0001) relapses. Overall
survival also was significantly worse for patients with an abnormal 9p (P < .0001). These effects were most pronounced in
standard-risk patients (age 1 to 9 years with white blood cell count
<50,000/µL): 6-year EFS of 61% (SD = 9%) versus 80% (SD = 2%; P < .0001). Also, a 9p aberration was an adverse risk
factor for B-lineage, but not T-lineage patients. The effect of 9p
status on EFS was attenuated, but maintained in a multivariate analysis
of EFS after adjustment for Philadelphia chromosome status, age, white
blood cell (WBC) count, sex, race, and ploidy group (P
= .01). Thus, abnormalities of chromosome arm 9p identify a
subgroup of standard-risk patients with increased risk of treatment failure.

CiteULike Connotea Del.icio.us Digg Reddit Technorati What's this?
This article has been cited by other articles:

|
 |

|
 |
 
S. Sulong, A. V. Moorman, J. A. E. Irving, J. C. Strefford, Z. J. Konn, M. C. Case, L. Minto, K. E. Barber, H. Parker, S. L. Wright, et al.
A comprehensive analysis of the CDKN2A gene in childhood acute lymphoblastic leukemia reveals genomic deletion, copy number neutral loss of heterozygosity, and association with specific cytogenetic subgroups
Blood,
January 1, 2009;
113(1):
100 - 107.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
H. Nahi, H. Hagglund, T. Ahlgren, P. Bernell, M. Hardling, K. Karlsson, V. L. Lazarevic, M. Linderholm, B. Smedmyr, M. Astrom, et al.
An investigation into whether deletions in 9p reflect prognosis in adult precursor B-cell acute lymphoblastic leukemia: a multi-center study of 381 patients
Haematologica,
November 1, 2008;
93(11):
1734 - 1738.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. Mancini, D. Scappaticci, G. Cimino, M. Nanni, V. Derme, L. Elia, A. Tafuri, M. Vignetti, A. Vitale, A. Cuneo, et al.
A comprehensive genetic classification of adult acute lymphoblastic leukemia (ALL): analysis of the GIMEMA 0496 protocol
Blood,
May 1, 2005;
105(9):
3434 - 3441.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J. A.E. Irving, L. Bloodworth, N. P. Bown, M. C. Case, L. A. Hogarth, and A. G. Hall
Loss of Heterozygosity in Childhood Acute Lymphoblastic Leukemia Detected by Genome-Wide Microarray Single Nucleotide Polymorphism Analysis
Cancer Res.,
April 15, 2005;
65(8):
3053 - 3058.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
T. Itoyama, R. S. K. Chaganti, Y. Yamada, K. Tsukasaki, S. Atogami, H. Nakamura, M. Tomonaga, K. Ohshima, M. Kikuchi, and N. Sadamori
Cytogenetic analysis and clinical significance in adult T-cell leukemia/lymphoma: a study of 50 cases from the human T-cell leukemia virus type-1 endemic area, Nagasaki
Blood,
June 1, 2001;
97(11):
3612 - 3620.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
S. P. Whitman, M. P. Strout, G. Marcucci, A. G. Freud, L. L. Culley, N. J. Zeleznik-Le, K. Mrózek, K. S. Theil, U. R. Kees, C. D. Bloomfield, et al.
The Partial Nontandem Duplication of the MLL (ALL1) Gene Is a Novel Rearrangement That Generates Three Distinct Fusion Transcripts in B-Cell Acute Lymphoblastic Leukemia
Cancer Res.,
January 1, 2001;
61(1):
59 - 63.
[Abstract]
[Full Text]
|
 |
|
|
|