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 Previous Article | Table of Contents | Next Article 
Blood, Vol. 91 No. 2 (January 15), 1998:
pp. 608-615
Distinctive Demography, Biology, and Outcome of Acute
Myeloid Leukemia and Myelodysplastic Syndrome in Children With Down
Syndrome: Children's Cancer Group Studies 2861 and 2891
By
Beverly J. Lange,
Nathan Kobrinsky,
Dorothy R. Barnard,
Diane C. Arthur,
Jonathan D. Buckley,
William B. Howells,
Stuart Gold,
Jean Sanders,
Steven Neudorf,
Franklin O. Smith, and
William G. Woods
From The Children's Hospital of Philadelphia and the University of
Pennsylvania School of Medicine, Philadelphia PA; the Children's
Cancer Group, Arcadia, CA; Roger Maris Cancer Center, Fargo, ND; Izaak
W. Killam Hospital for Children, Halifax, Nova Scotia, Canada;
University of Minnesota, Minneapolis, MN; University of Southern
California School of Medicine, Los Angeles, CA; University of North
Carolina, Chapel Hill, NC; Fred Hutchinson Cancer Research Center,
Seattle, WA; Children's Hospital of Pittsburgh, Pittsburgh, PA; and
Riley Hospital for Children, Indianapolis, IN.
 |
ABSTRACT |
In recent pediatric trials of acute myeloid leukemia (AML), children
with Down syndrome (DS) have had significantly more megakaryoblastic leukemia and have experienced better outcome than other children. To
further characterize AML in DS, Children's Cancer Group Studies 2861 and 2891 prospectively studied demography, biology, and response in AML
and myelodysplastic syndrome (MDS) of children with and without DS.
These studies evaluated timing of induction therapy and compared
postremission chemotherapy with marrow transplantation in 1,206 children. One-hundred eighteen (9.8%) had DS, a fourfold increase in
20 years. DS patients were younger, had lower white blood cell and
platelet counts, more antecedent MDS, acute megakaryoblastic leukemia
or undifferentiated AML, and an under-representation of chromosomal
translocations (P < .001 for each variable). Four-year event-free survival in DS was 69% versus 35% in others (P < .001). Intensively timed induction conferred significantly higher
mortality in DS patients; bone marrow transplantation offered no
advantage. Conventional induction followed by chemotherapy achieved an
88%, 4-year, disease-free survival in DS patients versus
42% in others (P < .001). Megakaryoblastic
leukemia was unfavorable in others but prognostically neutral in DS.
AML in DS is demographically and biologically distinct from AML in
other children. It is singularly responsive to conventional
chemotherapy and may warrant even less therapy. The increasing
proportion of DS patients with AML most likely reflects changes in
attitudes about entering DS patients on AML trials and possibly
increasing ability to distinguish megakaryoblastic leukemia from
lymphoid leukemia.
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INTRODUCTION |
BASED ON A mail survey in 1957, Krivit
and Good1 concluded that, in the United States, children
with Down syndrome (DS) had at least a threefold excess risk of
developing acute leukemia. Barber and Spiers2 estimated
that, in England and Wales, their excess risk was 10- to 100-fold.
Recent analyses place their risk at a 10- to 20-fold
increase.3-5
The decades between 1950 and 1980 brought considerable debate
about whether leukemia in DS was predominantly lymphoid or
myeloid.6 Ultimately, the consensus was that the ratio of
lymphoid to myeloid leukemia in DS approximated that of the general
pediatric population, ie, about four lymphoid to one
myeloid.3-5
Acute myeloid leukemia (AML) is the predominant form of leukemia in DS
children under age 4 and acute lymphoblastic leukemia (ALL) dominates
in older children.7,8 When megakaryoblastic leukemia
(French-American-British [FAB] M7) was formally defined, M7 was
recognized as the most common form of AML in children with DS.9,10 Children with DS have over a 400-fold excess risk of developing megakaryoblastic leukemia.10 Megakaryoblastic leukemia may present as a myelodysplastic syndrome (MDS) or it may
superficially resemble ALL.11-14 In retrospect, some cases of megakaryoblastic leukemia in children with DS were misdiagnosed as
ALL.11,13,14
In the 1960s and 1970s many children with DS and AML were not treated.
By 1983, inclusion of children with DS in large cooperative group
studies became standard practice. With few exceptions, these studies
showed that children with DS have an outcome significantly better than
other children with AML or MDS.15-18
This report describes AML/MDS in 118 children with DS registered on two
sequential Children's Cancer Group studies, CCG-2861 and CCG-2891. The
aims of these studies with respect to the DS subgroup were (1) to
provide unselected, unbiased protocol-based therapy to children with DS
and (2) to compare the demography, biology, and response to therapy of
AML and MDS in children with DS with those of the other children
registered on CCG-2861 and CCG-2891.
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PATIENTS AND METHODS |
Patients from birth though 20 years of age with previously untreated
AML or MDS were eligible for CCG-2861 or CCG-2891 after Institutional
Review Board approval and written, signed consent. Between March 16, 1988 and October 12, 1995, 143 children registered on CCG-2861 and
1,126 on CCG-2891.19,20 Seventeen patients were ineligible.
Forty-six patients were excluded from this analysis, 26 because they
had second malignant neoplasms, 11 because they presented with isolated
chloromas, and 9 because their DS status was unknown.
AML and MDS were classified according to the FAB
criteria.9,21-23 Morphology, histochemistry, and
institutional immunophenotype reports were reviewed centrally in 69%
of cases. When central review was not available, institutional results
were used. Methods and concordance have been described
previously.24 Together, central and institutional review
allowed FAB classification of 1,131 (94%) patients. Karyotypes
performed on stimulated and unstimulated cultures were centrally
reviewed in 53% of patients on CCG-2891 with 83% acceptance.
CCG-2861 was a pilot study testing the toxicity and efficacy of
intensively timed induction therapy followed by
4-hydroperoxycyclophosphamide (4-HC)-purged autologous bone marrow
transplant (BMT) or matched related allogeneic marrow transplant in
children with previously untreated AML or MDS.19 CCG-2891,
the successor Phase III randomized trial, compared intensively timed
induction therapy with conventionally timed induction therapy.
Postremission high-dose cytosine arabinoside (ara-C)-based
chemotherapy was compared with 4-HC-purged autologous BMT or
matched-related allogeneic BMT.20 The last cohort of 283 children on CCG-2891 received granulocyte colony-stimulating factor
after day 6 of intensively timed induction. This last cohort of
patients is grouped with intensive-timing induction for comparisons of
presenting features and outcome of induction therapy. When interim
analyses showed excessive toxicity in children with DS, CCG-2891
excluded them first from allogeneic BMT (August 29, 1988) then
autologous BMT and intensively timed induction (July 18, 1992).
Thereafter, children with DS were assigned to standard-timing induction
followed by chemotherapy (Fig 1). Because
three fourths of the children with DS had treatment assigned,
"as-treated" analyses rather than "intent-to-treat"
analyses are presented. In the patients without DS, the intent-to-treat
and as-treated analyses are essentially identical.20
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| Fig 1.
The five-drug DCTER regimen consists of dexamethasone, 6 mg/m2/d by mouth (PO); ara-C, 200 mg/m2/d
continuous infusion (CI); 6-TG, 50 mg/m2 PO twice daily;
etoposide, 100 mg/m2/d CI; and rubidomycin, 20 mg/m2/d CI.20 Ara-C, etoposide, and rubidomycin
are mixed in a single bag. Children under 3 years receive per kilogram
dosing. One course of intensively-timed DCTER is given on days 0 to 3 and 10 to 13; standard-timing DCTER is given on days 0 to 3 and after
marrow recovery if the day-14 marrow has <5% blasts or on days 14 to 17 if there are 5% blasts. Patients receive two courses of induction therapy. Transplant cytoreduction consists of busulfan 1 mg/kg every 6 hours for 16 doses. Graft-versus-host prophylaxis is with methotrexate.
Chemotherapy consists of Capizzi II high-dose ara-C, 3 g/m2
or 100 mg/kg 3-hour intravenous infusion every 12 hours four times on
days 0 and 1 and days 7 and 8; and L-asparaginase, 6,000 U/m2 or 200 U/kg intramuscular at 42 hours. After marrow
recovery patients receive daily 6-TG with ara-C, 75 mg/m2
and 5-azacytidine at 100 mg/m2 four times, and
cyclophosphamide, 75 mg/m2 four times for 2 months.
Treatment ends with a modified DCTER regimen. Central nervous system
prophylaxis is with 7 doses of intrathecal ara-C. Boxed in regimens are
those used for DS patients after July 18, 1996.
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Comparisons between the patients with DS and the others are made using
a log rank statistic.25 Comparisons of prognostic factors
among subsets of patients are made using Yates adjusted  2 tables.26 P values are two sided.
Actuarial estimates of survival, event-free survival (EFS), and
disease-free survival (DFS) are calculated using the Kaplan-Meier
method; 95% confidence intervals (CI95), by the method of
Simon and Lee.27,28 EFS is the time from on study to
induction failure, marrow relapse, or death. DFS is the time from the
end of induction to marrow relapse or death. Relapse-free survival
(RFS) is the time from the end of induction to marrow relapse or death
caused by progressive disease (PD); censored are deaths from other
causes, presumably treatment related. Not all patients had data for all
comparisons. Hence, numbers vary in some analyses. Data sets were
frozen in January 1996.
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RESULTS |
One hundred eighteen eligible patients (9.8%) with DS and 1,088 children without DS entered the two trials.
Table 1 compares their presenting
characteristics. Those with DS were significantly younger, with a
median age of 1.8 years compared with 7.5 years. Figure
2 shows that, whereas over 95% of those with DS were under 5 years,
40% of the others presented under age 5. Two patients with DS were
under 2 months of age.
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| Fig 2.
Age-related incidence of AML and MDS in children with and
without DS treated on CCG-2861 and CCG-2891.
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Table 1 shows that the presenting white blood cell (WBC) count and
platelet count were significantly lower in those with DS and that a
significantly greater percentage with DS had a history of antecedent
myelodysplastic presentation (P < .001). Of those with AML,
62% of the children with DS had FAB M7, acute megakaryoblastic leukemia and 10% had undifferentiated AML (FAB M0), whereas the FAB M1
and M2 granulocytic and M4 and M5 monocytic subtypes each comprised about 40% of the AML/MDS among those without DS (P < .001).
Table 2 shows that, in the leukemic
marrows, normal or abnormal karyotypes were equally distributed among
those with and without DS. As a group, t(8;21), t(15;17), and
rearrangements of chromosomal band 16q22 were significantly
under-represented among those with DS (P < .001), whereas an
additional nonconstitutional chromosome 21 occurred more frequently in
the children with DS (P = .05), as do numerical abnormalities
in the aggregate (P = .04, not shown).
Figure 3 shows a 68% 4-year EFS in DS
(CI95, 47%-84%) compared with 35% (CI95,
30%-41%) in those without (P < .0001). Survivals at 4 years are 67% in DS (CI95, 46%-83%) and 43% in others
(CI95, 38%-49%). Table 3 lists events
among the two groups according to induction therapy. Among DS patients
with a determinate outcome (n = 110), intensive timing of induction was
associated with a 32% mortality in the children with DS and 11%
mortality in the others (P = .003). Standard timing achieved a
95% remission induction rate in those with DS, with 2.4% dying and
2.4% not entering remission. Only 64% of DS patients achieved
remission with intensive timing. Among those without DS, intensive
timing affected a significantly higher survival, EFS, and DFS than
standard timing of induction (not shown).20 In contrast,
intensive timing significantly reduced EFS (74% v 52%,
P = .008) and survival in those with DS and had no effect on
DFS (not shown). Conventional induction followed by chemotherapy
achieved an 88%, 4-year DFS in DS patients versus 42% in others
(P < .001).
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| Fig 3.
Kaplan-Meier plot of actuarial EFS in children with and
without DS on CCG-2861 and CCG-2891; numbers in parentheses indicate number at risk. EFS in DS is 68%; (CI95, 47%-84%); in
non-DS, 35%; (CI95, 30%-41%).
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Table 4 shows postremission outcomes
independent of induction therapy. DS patients had an overall RFS of
86% (CI95, 58%-97%) at 4 years compared with 57%
(CI95, 49%-65%) in non-DS patients (P = .0002).
Among those with DS, postremission treatment-related mortality is 6%;
progressive disease, 8%. Among those without DS, treatment-related
mortality is 15% and progressive disease, 15%. Table 4 shows that
chemotherapy was the best postremission regimen among those with DS,
and allogeneic BMT was best for those without DS. As with the intensive
induction, the transplant regimens in DS were associated with
unacceptably high mortality and no significant reduction in failure
rate. Among those with DS, chemotherapy achieved a 91% RFS
(CI95=38%-99%) compared with 52% among the others
(P = .0001).
Whereas WBC at diagnosis is a significant predictor of outcome in
non-DS patients, it is not predictive in DS patients, nor is antecedent
MDS. Three DS patients were over age 5; two died of disease and one of
toxicity. To determine whether the disparate proportions of M7 AML
could account for the disparate results among those with and without
DS, we compared outcomes among those with and without FAB M7 in DS and
non-DS patients. Figure 4 shows that EFS
for FAB M7 was significantly better among those with DS (73% v
21% EFS, P < .001, for DS v non-DS patients). Among children with DS, M7 was not a significant variable (EFS 73% v 64% for those with and without FAB M7). Among non-DS patients, FAB M7
was significantly unfavorable (EFS 21% v 37%, P = .001). FAB M0 was also over-represented among the DS, but was
prognostically neutral in both DS and non-DS patients. Outcome for
those with MDS was not significantly different from AML in either group
(not shown).
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| Fig 4.
Kaplan-Meier plot of actuarial EFS in children with and
without DS with megakaryoblastic leukemia on CCG-2861 and CCG-2891; numbers in parentheses indicate number at risk. EFS in DS M7 is 73%
(CI95, 41%-91%); DS non-M7, 64% (CI95,
31%-87%); non-DS M7, 21% (CI95, 6%-53%); non-DS
non-M7, 37% (CI95, 32%-43%).
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We compared EFS, DFS, and survival among those DS patients with
tetrasomy 21 in the leukemic clone to the DS patients with trisomy 21;
among the non-DS patients, we compared trisomy 21 with disomy 21. Figure 5 shows that an extra chromosome 21 in the leukemic cells was not favorable among those without DS. Figure 5 suggests that an additional nonconstitutional chromosome 21 in the
leukemic clone may even be unfavorable; however, the log-rank statistic
is compromised by early crossing of the curves (EFS, 36% disomy 21 v 22% in trisomy 21). In the four DS patients with tetrasomy
21 there were no deaths, no failures, and no relapses.
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| Fig 5.
Kaplan-Meier plot of actuarial EFS for DS and non-DS
patients with and without trisomy 21 in the leukemic clone. EFS in DS, tetrasomy 21 is 100%; DS, trisomy 21, 69% (CI95,
45%-85%); non-DS trisomy 21, 22% (4%-66%); non-DS disomy 21 (CI95, 32%-46%).
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To examine the effects of ara-C as a relatively isolated variable in
CCG-2891, we compared the duration of therapy, morbidity, and mortality
of the Capizzi II high-dose ara-C/L-asparaginase in patients with and
without DS. Table 5 shows that the median duration of course, gastrointestinal and hepatic toxicity, and mortality were similar in DS and non-DS patients.
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DISCUSSION |
These two CCG studies showed that 9.8% of children with AML/MDS have
DS, nearly twice that recently reported by the Pediatric Oncology Group
(POG) and more than four times that previously reported by the
CCG.4,15 This increase makes the ratio of AML to ALL in DS
about one to one. The large proportion of DS patients in CCG-2861 and
CCG-2891 probably results from greater recognition of megakaryoblastic
leukemia, inclusion of MDS, and more registrations of children with DS
on cooperative group trials. The high number may also reflect parental
and medical responses to Baby Doe legislation in the United States and
general recognition that AML in DS is treatable.29-31 A
similar increase has been noted in the population-based Nordic AML
study in which 13% of the pediatric AML patients had DS.32
A big increase in incidence of AML among children with DS over the last
two decades is unlikely.
The superior response of children with DS to AML therapy in CCG-2861
and CCG-2891 confirms earlier results.8,15,32-35
Explanations for this outcome are that either the disease is different
or the host is different or both. Compared with AML/MDS in children
without DS, AML in those with DS presents at a younger age with lower WBC and platelet counts. In this study, all three patients over age 3 years died. Possibly they have a biologically different disease from
younger patients. Morphology is most often megakaryoblastic or
undifferentiated, and there is a high frequency of numerical karyotypic
abnormalities and a paucity of translocations.14,16,36-40 Among the infants without DS, 60% to 70% have monocytic, high tumor
burden variants of AML with 11q23 abnormalities, a rare constellation
of findings among the infants with DS.41 These findings
suggest that the disease is different in the two populations.
Both the excessive toxicity of dose-intensive induction therapy and BMT
postremission therapy in DS patients in these studies argue for
host-related differences as well. Taub et al18 have proposed that the superior outcome in DS patients is a result of
altered metabolism of ara-C. Dose-dependent alterations of folate pools
and abnormally high levels of the active metabolite of ara-C in DS
myeloblasts and Epstein Barr virus-transformed DS cell lines in the
presence of ara-C occur in vitro.18 Altered ara-C
metabolism may explain the responsiveness of AML to conventional therapy, but it should also contribute to excessive ara-C-mediated toxicity. However, our failure to find excessive toxicity in the high-dose ara-C postremission therapy among the children with DS does
not support this hypothesis. It is possible that the dose of ara-C in
the Capizzi II regimen is too high to discriminate between the DS and
non-DS patients.
Other host factors may also contribute to the toxicity of intensive
regimens. For example, children with DS experience excess toxicity with
ALL induction therapy that does not involve the folate
pathways,4,42,43 and children with DS have excess early
mortality even when they do not have leukemia.44-48
Additional host factors may involve metabolism of other drugs. DS
patients have increased risk of steroid-induced and
L-asparaginase-induced diabetes; they experience a vast spectrum of
endogenous hematologic and immunologic disorders, congenital heart
disease, and other factors as yet to be defined that render them
vulnerable to disease-related and treatment-related morbidity and
mortality.8,44-49
At one point, only 25% of transplant-eligible children with DS and
leukemia actually underwent BMT.31,32 Demonstration that
BMT could be successfully accomplished without obvious psychological devastation and the goal of providing unbiased care led us to enroll
these children in the BMT regimens on these studies.31,50 Now, despite the small numbers of DS patients undergoing BMT, the
results of CCG-2861 and CCG-2891 suggest that BMT adds toxicity without
any apparent therapeutic gain in children with DS in AML in first
remission. The results of CCG with standard timing induction therapy
followed by chemotherapy, the results of POG 8498, and the
use of low-dose ara-C alone in some children indicate that the majority
of these children can be cured with regimens of moderate intensity.15,32,33,35
To explore the disease itself, we examined the obvious features that
distinguish AML in the DS patients from AML in others: FAB M7 and an
extra chromosome 21. Whereas megakaryoblastic morphology is
prognostically neutral in the DS patients, it is significantly unfavorable in the others. FAB M7 encompasses heterogeneous diseases, some of which are responsive and others unresponsive. FAB M0 is also
over-represented in the DS patients. Although generally regarded as an
unfavorable form of AML because of its association with monosomy 7 and
7q-, FAB M0 is not unfavorable in those with
DS.51 Interestingly, even monosomy 7 may not be
unfavorable in those with DS.12 Morphology,
immunophenotype, and karyotype in children with and without DS warrant
further scrutiny.
An extra constitutional chromosome 21 clearly increases the risk of
developing acute leukemia and, in the case of AML, clearly increases
the chance of cure.15,18,30,35 Molecular mapping localizes
DS to chromosome 21, band q22.1-22.2, the region of AML1 gene involved in t(8;21), t(3;21), and
t(16;21) AML, the familial platelet/AML disorder, the interferon
 / receptor, the cytokine receptor family, and other genes that
regulate hematopoiesis, especially megakaryopoiesis.51-54
We examined the effect of an extra chromosome 21 in the leukemic
marrows of children with and without DS. An additional
nonconstitutional chromosome 21 conferred no benefit in non-DS
patients. In fact, in non-DS patients, there is a trend for the extra
chromosome 21 in the leukemic population to confer a poorer outcome,
whereas an extra nonconstitutional 21 in the DS patients appears to
have no prognostic value.
The results of CCG-2861 and CCG-2891 show that AML and MDS in DS
patients are characterized by demography, biology, and outcome that
differ from that of other patients with AML. Current investigations are
using less intensive therapy for AML in DS, defining the relationship between DS and the genes on chromosome 21, measuring differences in
metabolism of chemotherapy, and examining apoptosis in the leukemia
blasts of DS patients.
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FOOTNOTES |
Submitted April 2, 1997;
accepted September 8, 1997.
Supported by Grants from the Division of Cancer Treatment, National
Cancer Institute, National Institutes of Health, Department of Health
and Human Services, Bethesda, MD.
Contributing Children's Cancer Group Investigators, institutions, and
grant numbers are given in the Appendix.
Address reprint requests to Beverly J. Lange, MD, Children's Cancer
Group, PO Box 60012, Arcadia, CA 91066-6012.
The publication costs of this article were defrayed in part by page
charge payment. This article must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. section 1734 solely
to indicate this fact.
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ACKNOWLEDGMENT |
The authors gratefully acknowledge the following cytogeneticists who
contributed karyotypes to this study: T.W. Glover and S. Sheldon,
University of Michigan; C. Sandin, Integrated Genetics; T.K. Mohandas,
Harbor/UCLA Medical Center; C.W. Yu and L.L. Immken, Valley Children's
Hospital; W.D. Loughman, Oakland Children's Hospital; R.S. Sparkes,
UCLA Health Sciences Center; S.R. Patil, University of Iowa; L. McGavran, University of Colorado; V.M. Park, R. Stallard, and S. Schwartz, Case Western Reserve University; G.W. Dewald, Mayo Clinic; R. Gasparini, Baystate Medical Center; W.S. Stanley and S.A. Schonberg,
Children's National Medical Center; K.W. Rao, University of North
Carolina; K.-L. Ying, Children's Hospital Los Angeles; L.E. McMorrow
and L.J. Sciorra, University of Medicine & Dentistry New Jersey; K.S.
Theil, Ohio State University; L.M. Pasztor, Children's Mercy Hospital
Kansas City; D. Warburton, Babies Hospital Columbia University; W.G.
Sanger, University of Nebraska; S.L. Wenger, Children's Hospital
Pittsburgh; S.M. Gollin, University of Pittsburgh; R.G. Best,
University of South Carolina; M.G. Butler, Vanderbilt University; K.L.
Satya-Prakash, Medical College of Georgia; M.M. LeBeau and D. Roulston,
University of Chicago; R.E. Magenis, Oregon Health Sciences University;
P.B. Jacky, Kaiser Permanente NW Regional Laboratory; D.C. Arthur, University of Minnesota; G. Williams and A.J. Dawson, Health Sciences Center of Winnipeg; P. Nowell, University of Pennsylvania; P.A. Farber,
Geisinger Medical Center; S.C. Jhanwar, Memorial Sloan-Kettering Cancer
Center; P.R.K. Koduru, North Shore University Hospital; P. Benn,
University of Connecticut; N.A. Heerema, Indiana University; A.R.
Brothman, University of Utah; D.K. Kalousek, British Columbia Children's Hospital; C. Phillips, Emory University; J.R. Waterson, Children's Hospital Medical Center Akron; D.E. Powell and A.L. Pettigrew, University of Kentucky.
| |
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Abstract
Introduction
Abstract