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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1996-7-10
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pubmed:abstractText |
We studied the fully banded chromosomes of 182 children with hyperdiploid (51-67) acute lymphoblastic leukemia (ALL) to better delineate the heterogeneity of this disease subtype. Forty-six percent of the cases had numerical changes exclusively, while the remainder had structural as well as numerical changes. Chromosome 21 was added most often (97% of cases), followed by chromosomes 6 (86%), X (81%), 14 (80%), 4 (76%), 18 (68%), 17 (68%), 10 (56%), 8 (34%) and 5 (26%). Chromosomal translocations, including the t(1;19)(q23;p13) and t(9;22)(q34;q11), were detected in only 20% of the cases, as compared with 50% in ALL in general. The most common structural alterations were duplication of the 1q arm and isochromosome of 17q, present in 25 (14%) and nine (5%) cases, respectively. The presence of absence of structural abnormalities in these cases did not influence event-free survival, as assessed in 168 patients enrolled in three successive protocols for children with newly diagnosed ALL. By contrast, patients with 51-55 chromosomes per leukemic cell (n=105) appeared to fare worse than the 56-67 subgroup (n=63) (5-year probability of event-free survival = 72 +/- 5% (s.e.) vs 86 +/- 5%; P=0.04 by the stratified log-rank test). The poorer prognosis of the 51-55 subgroup was partly due to the higher frequency of isochromosome of 17q; 6/7 patients with the isochromosome in this group have had an adverse event. Other unfavorable features within the hyperdiploid (51-55) ALL subgroup include a low prevalence of trisomies of chromosomes 4 and 10 and a higher proportion of patients with leukocyte counts greater than 50 X 10(9)/l when compared to hyperdiploid (56-67). Thus, ALL defined by 51-55 chromosomes appears to be a clinicobiologic entity quite distinct from cases with higher modal numbers.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0887-6924
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
213-24
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:8637229-Adolescent,
pubmed-meshheading:8637229-Chi-Square Distribution,
pubmed-meshheading:8637229-Child,
pubmed-meshheading:8637229-Child, Preschool,
pubmed-meshheading:8637229-Chromosome Aberrations,
pubmed-meshheading:8637229-Cohort Studies,
pubmed-meshheading:8637229-Diploidy,
pubmed-meshheading:8637229-Disease-Free Survival,
pubmed-meshheading:8637229-Female,
pubmed-meshheading:8637229-Humans,
pubmed-meshheading:8637229-Infant,
pubmed-meshheading:8637229-Karyotyping,
pubmed-meshheading:8637229-Male,
pubmed-meshheading:8637229-Precursor Cell Lymphoblastic Leukemia-Lymphoma,
pubmed-meshheading:8637229-Prognosis
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pubmed:year |
1996
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pubmed:articleTitle |
Heterogeneity of hyperdiploid (51-67) childhood acute lymphoblastic leukemia.
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pubmed:affiliation |
Departments of Pathology and Laboratory Medicine, St. Jude Children's Research Hospital, Memphis, TN, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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