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1
acute myeloblastic leukemia childhood 2005:2010[pubdate] *count=100
271 results
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Items 1 to 100 of about 271
1.
Cogulu O, Kosova B, Gunduz C, Karaca E, Aksoylar S, Erbay A, Karapinar D, Vergin C, Vural F, Tombuloglu M, Cetingul N, Ozkinay F:
The evaluation of hTERT mRNA expression in acute leukemia children and 2 years follow-up of 40 cases.
Int J Hematol
; 2008 Apr;87(3):276-83
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[Title]
The evaluation of hTERT mRNA expression in
acute leukemia
children and 2 years follow-up of 40 cases.
The aim of this study is to evaluate (1) the human telomerase-specific reverse transcriptase (hTERT) mRNA expression in
childhood acute leukemia
, (2) the association between the hTERT mRNA expression with the patients' characteristics and the known prognostic factors and (3) the correlation of the patients' survival with the initial hTERT mRNA value at diagnosis.
A total of 40 newly diagnosed patients consist of children [31 cases with
acute
lymphoblastic
leukemia
(ALL) and 9 cases with
acute myeloblastic leukemia
(
AML
)] were prospectively included into the study.
The highest hTERT mRNA value was observed in Pre B-cell ALL patients followed by B-cell ALL, T-cell ALL and
AML
.
The hTERT mRNA relative ratio difference between the ALL and
AML
groups was significant.
Although DFS and OS was longer in
AML
patients with lower initial hTERT mRNA, the difference was not significant.
In conclusion, the hTERT mRNA expression values were not significantly associated with the known prognostic factors in children both with ALL and
AML
. hTERT mRNA value is a significant factor for
childhood
ALL at diagnosis in relation to the estimated survival.
[MeSH-major]
Biomarkers, Tumor / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. RNA, Messenger / metabolism. Telomerase / metabolism
[MeSH-minor]
Adolescent.
Child
.
Child
, Preschool. Disease-Free Survival. Female. Follow-Up Studies. Humans. Infant. Male. Prospective Studies
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
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[Cites]
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[
9815729.001
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[Cites]
Leuk Lymphoma. 2004 Dec;45(12):2477-80
[
15621763.001
]
(PMID = 18293058.001).
[ISSN]
0925-5710
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / RNA, Messenger; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
2.
Styczynski J, Toporski J, Wysocki M, Debski R, Chybicka A, Boruczkowski D, Wachowiak J, Wojcik B, Kowalczyk J, Gil L, Balwierz W, Matysiak M, Krawczuk-Rybak M, Balcerska A, Sonta-Jakimczyk D:
Fludarabine, treosulfan and etoposide sensitivity and the outcome of hematopoietic stem cell transplantation in childhood acute myeloid leukemia.
Anticancer Res
; 2007 May-Jun;27(3B):1547-51
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[Title]
Fludarabine, treosulfan and etoposide sensitivity and the outcome of hematopoietic stem cell transplantation in
childhood acute
myeloid
leukemia
.
BACKGROUND: The prognostic role of the ex vivo drug resistance profile has not yet been proved in
childhood acute
myeloid
leukemia
(
AML
).
The aim of the study was the analysis of the impact of the ex vivo drug resistance profile in a cohort of 44 children with
AML
undergoing hematopoietic stem cell transplantation (HSCT).
CONCLUSION: The combined drug resistance profile to fludarabine, treosulfan and etoposide may be useful for better stratification of children with
AML
undergoing stem cell transplantation or to indicate the necessity for additional post-transplant therapy.
[MeSH-major]
Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Granulocyte Precursor Cells / drug effects. Hematopoietic Stem Cell Transplantation.
Leukemia
,
Myeloid
/ surgery
[MeSH-minor]
Acute
Disease. Adolescent. Busulfan / analogs & derivatives. Busulfan / pharmacology.
Child
.
Child
, Preschool. Etoposide / pharmacology. Female. Humans. Infant. Male. Prognosis. Recurrence. Treatment Outcome. Vidarabine / analogs & derivatives. Vidarabine / pharmacology
Genetic Alliance.
consumer health - Acute Myeloid Leukemia, Childhood
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
Genetic Alliance.
consumer health - Transplantation
.
Hazardous Substances Data Bank.
FLUDARABINE
.
Hazardous Substances Data Bank.
TREOSULFAN
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
Hazardous Substances Data Bank.
BUSULFAN
.
Hazardous Substances Data Bank.
VIDARABINE
.
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(PMID = 17595774.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Antineoplastic Agents; 6PLQ3CP4P3 / Etoposide; CO61ER3EPI / treosulfan; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
3.
Perel Y, Auvrignon A, Leblanc T, Michel G, Reguerre Y, Vannier JP, Dalle JH, Gandemer V, Schmitt C, Méchinaud F, Lejars O, Piguet C, Couillaud G, Pautard B, Landman-Parker J, Thuret I, Aladjidi N, Baruchel A, Leverger G, French LAME (Leucémie Aiguë Myéloblastique Enfant) Cooperative Group:
Treatment of childhood acute myeloblastic leukemia: dose intensification improves outcome and maintenance therapy is of no benefit--multicenter studies of the French LAME (Leucémie Aiguë Myéloblastique Enfant) Cooperative Group.
Leukemia
; 2005 Dec;19(12):2082-9
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[Title]
Treatment of
childhood acute myeloblastic leukemia
: dose intensification improves outcome and maintenance therapy is of no benefit--multicenter studies of the French LAME (Leucémie Aiguë Myéloblastique Enfant) Cooperative Group.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antineoplastic Protocols / standards.
Leukemia
,
Myeloid
,
Acute
/ therapy
[MeSH-minor]
Adolescent. Bone Marrow Transplantation.
Child
.
Child
, Preschool. Dose-Response Relationship, Drug. Follow-Up Studies. France. Humans. Infant. Infant, Newborn. Remission Induction. Risk Assessment. Survival Analysis. Treatment Outcome
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 16121218.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Randomized Controlled Trial
[Publication-country]
England
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4.
Sayed HA, El-Mahallawy HA, Kaddah AM, Ismael HT, Talaat SM:
Profile of infections in newly diagnosed patients with acute leukemia during the induction phase of treatment.
J Egypt Natl Canc Inst
; 2009 Dec;21(4):315-22
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[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Profile of infections in newly diagnosed patients with
acute leukemia
during the induction phase of treatment.
BACKGROUND AND PURPOSE:
Acute leukemia
is the most common
pediatric
malignancy.
The aim of the present study is to assess the type, frequency, and severity of infectious complications in a cohort of
pediatric
cancer patients treated at a single medical institution.
We also aim to identify factors affecting bloodstream infections in newly diagnosed ALL and
AML pediatric
patients during the induction phase of treatment.
PATIENTS AND METHODS: This study was carried out at the Department of
Pediatric
Oncology, National Cancer Institute, Cairo University, during the time period from January 1st to June 30th 2007.
Inclusion criteria were
pediatric
age group (from 0-16 years), newly diagnosed
acute leukemia
, positive blood culture and documented site of infection.
RESULTS: This is a retrospective study including 100 newly diagnosed cases of
acute leukemia
.
Fifty-four patients had ALL, and 46 patients had
AML
.
KEY WORDS:
Acute leukemia
- Blood stream infection - Bacterial infection -
Pediatric
cancer patients.
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(PMID = 21415868.001).
[ISSN]
1110-0362
[Journal-full-title]
Journal of the Egyptian National Cancer Institute
[ISO-abbreviation]
J Egypt Natl Canc Inst
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Egypt
5.
Tosi S, Ballabio E, Teigler-Schlegel A, Boultwood J, Bruch J, Harbott J:
Characterization of 6q abnormalities in childhood acute myeloid leukemia and identification of a novel t(6;11)(q24.1;p15.5) resulting in a NUP98-C6orf80 fusion in a case of acute megakaryoblastic leukemia.
Genes Chromosomes Cancer
; 2005 Nov;44(3):225-32
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[Title]
Characterization of 6q abnormalities in
childhood acute
myeloid
leukemia
and identification of a novel t(6;11)(q24.1;p15.5) resulting in a NUP98-C6orf80 fusion in a case of
acute
megakaryoblastic
leukemia
.
Chromosome abnormalities of 6q are not frequently observed in
myeloid
disorders.
In this article, we report the incidence of these chromosome changes in
childhood
myeloid
leukemia
as 2%-4% based on the cytogenetic database of a single institution.
We applied fluorescence in situ hybridization (FISH) to characterize precisely the types of 6q abnormalities in seven patients (six with
acute
myeloid
leukemia
and one with myelodysplastic syndrome).
Among these, we identified a novel translocation, t(6;11)(q24.1;p15.5), in a patient with
acute
megakaryoblastic
leukemia
.
Further studies will aim to fully characterize C6orf80 and will elucidate the role of this new NUP98 fusion in
myeloid
leukemia
.
[MeSH-major]
Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 6 / genetics.
Leukemia
,
Myeloid
/ genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
[MeSH-minor]
Acute
Disease. Adolescent. Amino Acid Sequence. Base Sequence.
Child
.
Child
, Preschool. Chromosome Breakage. Chromosomes, Artificial, Bacterial. Cytogenetic Analysis. DNA, Neoplasm / analysis. Humans. In Situ Hybridization, Fluorescence. Infant. Molecular Sequence Data. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction
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[Copyright]
(c) 2005 Wiley-Liss, Inc.
(PMID = 16028218.001).
[ISSN]
1045-2257
[Journal-full-title]
Genes, chromosomes & cancer
[ISO-abbreviation]
Genes Chromosomes Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Neoplasm; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / nuclear pore complex protein 98
6.
Zwaan CM, den Boer ML, Kazemier KM, Hählen K, Loonen AH, Reinhardt D, Creutzig U, Kaspers GJ, Pieters R:
Does modulation of P-glycoprotein have clinical relevance in pediatric acute myeloid leukemia?
Blood
; 2006 Jun 15;107(12):4975-6; author reply 4976-7
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[Title]
Does modulation of P-glycoprotein have clinical relevance in
pediatric
acute
myeloid
leukemia
?
[MeSH-major]
Drug Resistance, Neoplasm. Gene Expression Regulation, Leukemic. Immunosuppressive Agents / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ metabolism. P-Glycoprotein / biosynthesis
[MeSH-minor]
Adult. Age Factors. Antibodies, Monoclonal / chemistry.
Child
.
Child
, Preschool. Cyclosporine / pharmacology. Female. Flow Cytometry. Humans. Male. Randomized Controlled Trials as Topic. Remission Induction
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.
Hazardous Substances Data Bank.
CYCLOSPORIN A
.
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[CommentOn]
Blood. 2006 Feb 15;107(4):1315-24
[
16254147.001
]
(PMID = 16754781.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Comment; Letter
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Immunosuppressive Agents; 0 / P-Glycoprotein; 83HN0GTJ6D / Cyclosporine
7.
Simmons HM, Ruis BL, Kapoor M, Hudacek AW, Conklin KF:
Identification of NOM1, a nucleolar, eIF4A binding protein encoded within the chromosome 7q36 breakpoint region targeted in cases of pediatric acute myeloid leukemia.
Gene
; 2005 Feb 28;347(1):137-45
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[Title]
Identification of NOM1, a nucleolar, eIF4A binding protein encoded within the chromosome 7q36 breakpoint region targeted in cases of
pediatric
acute
myeloid
leukemia
.
In this report, we describe the characterization of a novel MIF4G/MA3 family member called NOM1 (nucleolar protein with MIF4G domain 1) that was identified at the chromosome 7q36 breakpoint involved in 7;12 translocations associated with certain
acute
leukemias of
childhood
.
[MeSH-major]
Chromosomes, Human, Pair 7 / genetics. Eukaryotic Initiation Factor-4A / metabolism. Exons / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Nuclear Proteins / genetics. RNA-Binding Proteins / genetics
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.
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.
COS Scholar Universe.
author profiles
.
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
Saccharomyces Genome Database.
Saccharomyces Genome Database
.
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(PMID = 15715967.001).
[ISSN]
0378-1119
[Journal-full-title]
Gene
[ISO-abbreviation]
Gene
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Codon, Nonsense; 0 / Nom1 protein, human; 0 / Nuclear Proteins; 0 / RNA-Binding Proteins; EC 2.7.7.- / Eukaryotic Initiation Factor-4A
8.
Anak S, Saribeyoglu ET, Bilgen H, Unuvar A, Karakas Z, Devecioglu O, Agaoglu L, Gedikoglu G:
Allogeneic versus autologous versus peripheral stem cell transplantation in CR1 pediatric AML patients: a single center experience.
Pediatr Blood Cancer
; 2005 Jun 15;44(7):654-9
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[Title]
Allogeneic versus autologous versus peripheral stem cell transplantation in CR1
pediatric AML
patients: a single center experience.
BACKGROUND: Treatment of
childhood acute
myelocytic
leukemia
(
AML
) in first remission, is still evolving.
PROCEDURE: Out of 81
pediatric
patients with
AML
in first CR, 67 were biologically randomized for allogeneic (n = 31), autologous (n = 20), or peripheral stem cell transplant (n = 16) after completing consolidation treatment, with the remaining (n = 11) dropping out or receiving chemotherapy.
CONCLUSION: In
pediatric AML
patients without a donor, autologous BMT or autologous PBSCT appears to be an effective treatment option with low transplant related mortality especially in less privileged countries where the chemotherapy only results are still low.
[MeSH-major]
Bone Marrow Transplantation.
Leukemia
,
Myeloid
/ therapy. Peripheral Blood Stem Cell Transplantation
[MeSH-minor]
Acute
Disease. Adolescent.
Child
.
Child
, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Transplantation, Autologous. Transplantation, Homologous
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[Copyright]
Copyright 2005 Wiley-Liss, Inc.
(PMID = 15700262.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
9.
Radhi M, Meshinchi S, Gamis A:
Prognostic factors in pediatric acute myeloid leukemia.
Curr Hematol Malig Rep
; 2010 Oct;5(4):200-6
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[Title]
Prognostic factors in
pediatric
acute
myeloid
leukemia
.
Acute
myeloid
leukemia
(
AML
), a heterogeneous group of diseases with variable responses to the same therapy, comprises nearly a quarter of
childhood acute
leukemias.
Although historically very few prognostic markers have been incorporated into therapeutic decision making in
AML
, recent advances in technology have enabled identification of numerous factors associated with disease outcome.
This review provides a detailed analysis of most clinically relevant factors associated with disease outcome in
childhood
AML
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ diagnosis
[MeSH-minor]
Age Factors. Biomarkers, Tumor. Body Mass Index.
Child
. Cytogenetics. Humans. Polymorphism, Genetic. Prognosis. Risk Factors. Sex Factors
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J Clin Oncol. 2004 Apr 15;22(8):1404-12
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15084614.001
]
(PMID = 20652454.001).
[ISSN]
1558-822X
[Journal-full-title]
Current hematologic malignancy reports
[ISO-abbreviation]
Curr Hematol Malig Rep
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor
10.
Children's Oncology Group, Aplenc R, Alonzo TA, Gerbing RB, Smith FO, Meshinchi S, Ross JA, Perentesis J, Woods WG, Lange BJ, Davies SM:
Ethnicity and survival in childhood acute myeloid leukemia: a report from the Children's Oncology Group.
Blood
; 2006 Jul 1;108(1):74-80
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[Title]
Ethnicity and survival in
childhood acute
myeloid
leukemia
: a report from the Children's Oncology Group.
We evaluated differences in outcome by ethnicity among children with
acute
myeloid
leukemia
(
AML
).
In conclusion, Hispanic and black children with
AML
have worse survival than white children.
Access to chemotherapy, differences in supportive care or
leukemia
phenotype, and reduced compliance are unlikely explanations for this difference because therapy was given intravenously according to CCG protocols.
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[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / 1 U10 CA98413-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ PMC1895824
11.
Karabacak BH, Erbey F, Bayram I, Yilmaz S, Acipayam C, Kilinç Y, Tanyeli A:
Fms-like tyrosine kinase 3 mutations in childhood acute leukemias and their association with prognosis.
Asian Pac J Cancer Prev
; 2010;11(4):923-7
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[Title]
Fms-like tyrosine kinase 3 mutations in
childhood acute
leukemias and their association with prognosis.
OBJECTIVE: In this study, the presence of FLT3 mutations in
childhood acute
leukemias patients and their association with prognosis were investigated.
MATERIALS AND METHODS: A total of 120 patients, 80 with
acute
lymphoblastic
leukemia
(ALL) and 40 with
acute myeloblastic leukemia
(
AML
), were included.
RESULTS: FLT3/ITD (internal tandem duplication) mutations were found in 6 (7.5%) of the patients with ALL and in 9 (22.5%) of those with
AML
, whereas no FLT3/TKD (trans kinase domain) mutation was evident in any case.
However, in FLT3/ITD positive and negative
AML
patients, there was a statistically significant difference in OS (p=0.0041), but not EFS and DFS (p=0.09, p=0.095, respectively).
CONCLUSION: We found that FLT3/ITD positivity increased with age and that it was associated with decrease in OS in
AML
patients, providing further evidence that it is an independent factor negatively influencing prognosis.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ mortality. Mutation. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / mortality. fms-Like Tyrosine Kinase 3 / genetics
[MeSH-minor]
Adolescent. Age Factors.
Child
.
Child
, Preschool. Disease-Free Survival. Humans. Infant. Kaplan-Meier Estimate. Male. Prognosis. Recurrence
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(PMID = 21133602.001).
[ISSN]
2476-762X
[Journal-full-title]
Asian Pacific journal of cancer prevention : APJCP
[ISO-abbreviation]
Asian Pac. J. Cancer Prev.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Thailand
[Chemical-registry-number]
EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
12.
Latino-Martel P, Chan DS, Druesne-Pecollo N, Barrandon E, Hercberg S, Norat T:
Maternal alcohol consumption during pregnancy and risk of childhood leukemia: systematic review and meta-analysis.
Cancer Epidemiol Biomarkers Prev
; 2010 May;19(5):1238-60
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[Title]
Maternal alcohol consumption during pregnancy and risk of
childhood leukemia
: systematic review and meta-analysis.
BACKGROUND:
Leukemia
is the most frequently occurring cancer in children.
Although its etiology is largely unknown,
leukemia
is believed to result from an interaction between genetic and environmental factors.
METHODS: To assess the association between maternal alcohol consumption during pregnancy and
childhood leukemia
, a systematic review and meta-analysis of published studies was done.
Analyses were conducted by type of
leukemia
, children's age at diagnosis, and type of alcoholic beverage and trimester of pregnancy at alcohol use.
Alcohol intake during pregnancy (yes versus no) was statistically significantly associated with
childhood acute
myeloid
leukemia
(
AML
) [odds ratio (OR), 1.56; 95% confidence interval (CI), 1.13-2.15] but not with
acute
lymphoblastic
leukemia
(OR, 1.10; 95% CI, 0.93-1.29).
The OR of
AML
for an increase of a drink per week was 1.24 (95% CI, 0.94-1.64).
The association of alcohol intake during pregnancy with
AML
was observed for cancers diagnosed at age 0 to 4 years (OR, 2.68; 95% CI, 1.85-3.89) in five studies without heterogeneity (I2<or=0.1%).
CONCLUSIONS: The results of case-control studies indicate that maternal alcohol consumption during pregnancy is associated with a significantly increased risk of
AML
in young children.
IMPACT: Avoidance of maternal alcohol drinking during pregnancy might contribute to a decrease in the risk of
childhood
AML
.
[MeSH-major]
Alcohol Drinking / adverse effects.
Leukemia
/ chemically induced. Prenatal Exposure Delayed Effects
[MeSH-minor]
Adolescent. Adult.
Child
.
Child
, Preschool. Female. Humans. Infant. Infant, Newborn. Mothers. Pregnancy. Risk Factors. Young Adult
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[Copyright]
Copyright (c) 2010 AACR
(PMID = 20447918.001).
[ISSN]
1538-7755
[Journal-full-title]
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
[ISO-abbreviation]
Cancer Epidemiol. Biomarkers Prev.
[Language]
eng
[Publication-type]
Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
[Publication-country]
United States
13.
Morerio C, Acquila M, Rapella A, Tassano E, Rosanda C, Panarello C:
Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia.
Cancer Genet Cytogenet
; 2006 Dec;171(2):122-5
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[Title]
Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in
pediatric
acute
myeloid
leukemia
.
The inv(11)(p15q22), a rare but recurrent chromosome abnormality that creates a NUP98-DDX10 fusion gene, is associated with de novo or secondary
myeloid
malignancies.
We report a case of
acute
monocytic
leukemia
presenting this rearrangement, studied using fluorescence in situ hybridization (FISH) and reverse transcriptase-PCR (RT-PCR).
[MeSH-major]
Chromosome Inversion. Chromosomes, Human, Pair 11 / genetics. DEAD-box RNA Helicases / genetics. Gene Fusion.
Leukemia
,
Myeloid
,
Acute
/ genetics. Nuclear Pore Complex Proteins / genetics
[MeSH-minor]
Child
. Humans. Male. Molecular Sequence Data
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(PMID = 17116492.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Databank-accession-numbers]
GENBANK/ AB040537/ AB040538
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; EC 3.6.1.- / DDX10 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases
[Number-of-references]
12
14.
Dorantes-Acosta E, Chávez-González A, Santos JI, Medina-Sanson A, Mayani H:
Defective in vitro growth of primitive hematopoietic cells from pediatric patients with acute myeloid leukemia.
Pediatr Blood Cancer
; 2008 Dec;51(6):741-6
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[Title]
Defective in vitro growth of primitive hematopoietic cells from
pediatric
patients with
acute
myeloid
leukemia
.
BACKGROUND:
Acute
myeloid
leukemia
(
AML
) is a neoplastic hematologic disorder that arises at the level of a primitive stem/progenitor cell.
Most studies on the biology of the hematopoietic system in
AML
have focused on cells from adult patients; much less is known about hematopoietic cells from
childhood
AML
.
PROCEDURE: By using a negative immunoselection system, we have obtained a primitive cell population (enriched for CD34(+) Lin(-) cells) from the bone marrow (BM) of 17
pediatric AML
patients and characterized its proliferation, expansion, and differentiation potentials in liquid cultures supplemented with a mixture of 8 different recombinant stimulatory cytokines.
RESULTS: The proportion of CD34(+) cells in
AML
patients was extremely heterogeneous, ranging from 0% to 74%.
Regardless of their CD34(+) cell content, and in contrast to normal cells,
AML
cells showed a deficient capacity to proliferate even in the presence of the stimulatory cytokines.
AML
progenitors were unable to generate new progenitor cells, indicating their inability to expand.
Interestingly,
AML
cells were able to differentiate in culture, giving rise to morphologically recognizable precursors.
A major difference, however, as compared to hematopoietic progenitors from normal subjects, was the fact that whereas in cultures of normal cells both
myeloid
and erythroid precursors were produced, in
AML
cultures the vast majority of the cells generated corresponded to
myeloid
cells, mostly mature macrophages.
CONCLUSION: As compared to their normal counterparts, primitive hematopoietic cells from
pediatric
patients with
AML
possess impaired proliferation, expansion, and differentiation potentials in vitro.
[MeSH-major]
Bone Marrow Cells / pathology. Hematopoietic Stem Cells / pathology.
Leukemia
,
Myeloid
,
Acute
/ blood
[MeSH-minor]
Adolescent. Antigens, CD34 / blood. Cell Differentiation. Cell Proliferation. Cells, Cultured.
Child
.
Child
, Preschool. Cytokines / metabolism. Female. Humans. In Vitro Techniques. Male
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(PMID = 18680148.001).
[ISSN]
1545-5017
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD34; 0 / Cytokines
15.
Rubnitz JE, Inaba H, Dahl G, Ribeiro RC, Bowman WP, Taub J, Pounds S, Razzouk BI, Lacayo NJ, Cao X, Meshinchi S, Degar B, Airewele G, Raimondi SC, Onciu M, Coustan-Smith E, Downing JR, Leung W, Pui CH, Campana D:
Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial.
Lancet Oncol
; 2010 Jun;11(6):543-52
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[Title]
Minimal residual disease-directed therapy for
childhood acute
myeloid
leukaemia: results of the AML02 multicentre trial.
BACKGROUND: We sought to improve outcome in patients with
childhood acute
myeloid
leukaemia (
AML
) by applying risk-directed therapy that was based on genetic abnormalities of the leukaemic cells and measurements of minimal residual disease (MRD) done by flow cytometry during treatment.
METHODS: From Oct 13, 2002, to June 19, 2008, 232 patients with de-novo
AML
(n=206), therapy-related or myelodysplasia-related
AML
(n=12), or mixed-lineage leukaemia (n=14) were enrolled at eight centres.
Other analyses were limited to the 216 patients with
AML
, excluding those with mixed-lineage leukaemia.
INTERPRETATION: Our findings suggest that the use of targeted chemotherapy and HSCT, in the context of a comprehensive risk-stratification strategy based on genetic features and MRD findings, can improve outcome in patients with
childhood
AML
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ pathology
[MeSH-minor]
Adolescent. Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Child
.
Child
, Preschool. Cytarabine / administration & dosage. Cytogenetic Analysis. Daunorubicin / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Flow Cytometry. Humans. Infant. Infant, Newborn. Male. Neoplasm, Residual. Remission Induction. Survival Rate. Young Adult
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DAUNORUBICIN
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ETOPOSIDE
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[Copyright]
Copyright 2010 Elsevier Ltd. All rights reserved.
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[CommentIn]
Lancet Oncol. 2010 Jun;11(6):502-3
[
20522371.001
]
(PMID = 20451454.001).
[ISSN]
1474-5488
[Journal-full-title]
The Lancet. Oncology
[ISO-abbreviation]
Lancet Oncol.
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00136084
[Grant]
United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA115422; United States / NCI NIH HHS / CA / R01 CA115422-02
[Publication-type]
Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 93NS566KF7 / gemtuzumab; ZS7284E0ZP / Daunorubicin; DAV regimen
[Other-IDs]
NLM/ NIHMS319127; NLM/ PMC3171799
16.
Choi HW, Shin MG, Sawyer JR, Cho D, Kee SJ, Baek HJ, Kook H, Kim HJ, Shin JH, Suh SP, Hwang TJ, Ryang DW:
Unusual type of TLS/FUS-ERG chimeric transcript in a pediatric acute myelocytic leukemia with 47,XX,+10,t(16;21)(p11;q22).
Cancer Genet Cytogenet
; 2006 Jun;167(2):172-6
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[Title]
Unusual type of TLS/FUS-ERG chimeric transcript in a
pediatric
acute
myelocytic
leukemia
with 47,XX,+10,t(16;21)(p11;q22).
We report on a case of
pediatric
acute
myelocytic
leukemia
showing 47,XX,+10,t(16;21)(p11;q22) that resulted in an unusual TLS/FUS-ERG chimeric transcript.
The leukemic cells showed erythrophagocytosis, positive reactions for myeloperoxidase and Sudan black B stains, and negative reactions for periodic acid-Schiff and alpha-naphtyl butyrate esterase stains as well as expression of
myeloid
antigens.
[MeSH-major]
Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21.
Leukemia
,
Myeloid
,
Acute
/ genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic
[MeSH-minor]
Bone Marrow Cells / cytology.
Child
, Preschool. Chromosomes, Human, Pair 10. Female. Humans. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA. Trisomy
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(PMID = 16737920.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
17.
Bellezza I, Tucci A, Minelli A:
2-Chloroadenosine and human prostate cancer cells.
Anticancer Agents Med Chem
; 2008 Oct;8(7):783-9
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Cladribine, i.e.2-deoxy-Chloroadenosine is currently in use as chemotherapeutic agent in chronic lymphoid malignancies and
pediatric
acute
myelogenous
leukemia
whereas the structurally related counterpart, 2-Chloroadenosine, has been less studied.
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(PMID = 18855579.001).
[ISSN]
1871-5206
[Journal-full-title]
Anti-cancer agents in medicinal chemistry
[ISO-abbreviation]
Anticancer Agents Med Chem
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Interleukin-23; 0 / Receptor, PAR-1; 146-77-0 / 2-Chloroadenosine
[Number-of-references]
137
18.
Shimada A, Taki T, Kubota C, Tawa A, Horibe K, Tsuchida M, Hanada R, Tsukimoto I, Hayashi Y:
No nucleophosmin mutations in pediatric acute myeloid leukemia with normal karyotype: a study of the Japanese Childhood AML Cooperative Study Group.
Leukemia
; 2007 Jun;21(6):1307
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[Title]
No nucleophosmin mutations in
pediatric
acute
myeloid
leukemia
with normal karyotype: a study of the Japanese
Childhood
AML
Cooperative Study Group.
[MeSH-major]
Leukemia
,
Myeloid
/ genetics. Nuclear Proteins / genetics
[MeSH-minor]
Acute
Disease. Adolescent.
Child
.
Child
, Preschool. DNA Mutational Analysis. Humans. Infant. Infant, Newborn. Japan. Karyotyping. Mutation
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(PMID = 17315018.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Letter; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
19.
Harrison CJ, Hills RK, Moorman AV, Grimwade DJ, Hann I, Webb DK, Wheatley K, de Graaf SS, van den Berg E, Burnett AK, Gibson BE:
Cytogenetics of childhood acute myeloid leukemia: United Kingdom Medical Research Council Treatment trials AML 10 and 12.
J Clin Oncol
; 2010 Jun 01;28(16):2674-81
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[Title]
Cytogenetics of
childhood acute
myeloid
leukemia
: United Kingdom Medical Research Council Treatment trials
AML
10 and 12.
PURPOSE: Karyotype is an independent indicator of prognosis in
acute
myeloid
leukemia
(
AML
) that is widely applied to risk-adapted therapy.
Because
AML
is rare in children, the true prognostic significance of individual chromosomal abnormalities in this age group remains unclear.
PATIENTS AND METHODS: This cytogenetic study of 729
childhood
patients classified them into 22 subgroups and evaluated their incidence and risk.
Abnormalities of 3q and complex karyotypes, in the absence of favorable-risk features, have been associated with an adverse outcome in adults, but the results were not significant in this
childhood
series.
CONCLUSION: Because the spectrum of chromosomal changes and their risk association seem to differ between children and adults with
AML
, biologic differences are emerging, which will contribute to the redefinition of risk stratification for different age groups in the future.
[MeSH-major]
Chromosome Aberrations. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 12.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ mortality
[MeSH-minor]
Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation.
Child
.
Child
, Preschool. Confidence Intervals. Cytogenetic Analysis. Disease-Free Survival. Female. Fluorescence. Genetic Predisposition to Disease / epidemiology. Humans. In Situ Hybridization. Infant. Kaplan-Meier Estimate. Karyotyping. Logistic Models. Male. Multivariate Analysis. Odds Ratio. Probability. Prognosis. Proportional Hazards Models. Registries. Retrospective Studies. Risk Assessment. Survival Analysis. Treatment Outcome. United Kingdom
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(PMID = 20439644.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0300133
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
20.
Shimada A, Ichikawa H, Taki T, Kubota C, Hongo T, Sako M, Morimoto A, Tawa A, Tsukimoto I, Hayashi Y:
Low frequency of KIT gene mutation in pediatric acute myeloid leukemia with inv(16)(p13q22): a study of the Japanese Childhood AML Cooperative Study Group.
Int J Hematol
; 2007 Oct;86(3):289-90
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[Title]
Low frequency of KIT gene mutation in
pediatric
acute
myeloid
leukemia
with inv(16)(p13q22): a study of the Japanese
Childhood
AML
Cooperative Study Group.
[MeSH-major]
Chromosome Inversion.
Leukemia
,
Myeloid
,
Acute
/ genetics. Proto-Oncogene Proteins c-kit / genetics
[MeSH-minor]
Adolescent. Adult.
Child
.
Child
, Preschool. Disease-Free Survival. Female. Follow-Up Studies. Humans. Infant. Male. Survival Rate
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J Clin Oncol. 2006 Aug 20;24(24):3904-11
[
16921041.001
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Leukemia. 2006 Jun;20(6):965-70
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(PMID = 17989000.001).
[ISSN]
0925-5710
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Letter; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
21.
Styczynski J, Wysocki M, Dluzniewska A, Juraszewska E, Balwierz W, Czyzewski K, Wieczorek M, Olejnik I, Krawczuk-Rybak M, Kuzmicz M, Kowalczyk J, Stefaniak J, Badowska W, Sonta-Jakimczyk D, Szczepanski T, Matysiak M, Stanczak E, Malinowska I, Wachowiak J, Konatkowska B, Gil L, Balcerska A, Kapuscinska L, Szczepanek J, Kolodziej B, Rafinska B, Kubicka M:
Prognostic impact of combined fludarabine, treosulfan and mitoxantrone resistance profile in childhood acute myeloid leukemia.
Anticancer Res
; 2008 May-Jun;28(3B):1927-31
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[Title]
Prognostic impact of combined fludarabine, treosulfan and mitoxantrone resistance profile in
childhood acute
myeloid
leukemia
.
BACKGROUND: The role of cellular drug resistance in
childhood acute
myeloid
leukemia
(
AML
) has not yet been established.
The aim of the study was the analysis of the clinical value of ex vivo drug resistance in
pediatric AML
.
PATIENTS AND METHODS: A cohort of 90 children with de novo
AML
were assayed for drug resistance profile by the 3-4,5-dimethylthiazol-2-yl-2,5-difenyl tetrazolium bromide (MTT) assay and prognostic model of in vitro drug sensitivity was analyzed.
A combined in vitro drug resistance profile to fludarabine, treosulfan and mitoxantrone (FTM score) was defined and it had an independent prognostic significance for disease free survival in
pediatric AML
.
CONCLUSION: The combined fludarabine, treosulfan and mitoxantrone resistance profile to possibly may be used for better stratification of children with
AML
or indicate the necessity for additional therapy.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy
[MeSH-minor]
Busulfan / administration & dosage. Busulfan / analogs & derivatives.
Child
.
Child
, Preschool. Cohort Studies. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Female. Humans. Infant. Male. Mitoxantrone / administration & dosage. Prognosis. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives
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.
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.
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.
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.
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.
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(PMID = 18630483.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
BZ114NVM5P / Mitoxantrone; CO61ER3EPI / treosulfan; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
22.
Roman E, Cooney E, Harrison L, Militano O, Wolownik K, Hawks R, Foley S, Satwani P, Unal E, Bhatia M, Bradley B, Del Toro G, George D, Garvin J, van de Ven C, Cairo MS:
Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+ acute myeloid leukemia.
Clin Cancer Res
; 2005 Oct 1;11(19 Pt 2):7164s-7170s
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[Title]
Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+
acute
myeloid
leukemia
.
PURPOSE: Myeloablative allogeneic stem cell transplantation (SCT) has been successful in the treatment of
childhood acute
myeloid
leukemia
(
AML
), but may be associated with significant toxicity and recurrent disease.
Reduced-intensity allogeneic SCT may offer a less toxic approach to patients with
AML
.
Targeted immunotherapy with gemtuzumab ozogamicin has been shown to be safe, well tolerated in children, and, as a single agent, gemtuzumab ozogamicin has induced responses in 30% of patients with recurrent CD33+
AML
.
Therefore, we explored the feasibility and toxicity of targeted immunotherapy following reduced-intensity allogeneic SCT in children with CD33+
AML
.
EXPERIMENTAL DESIGN: Eight patients with CD33+
AML
received a reduced-intensity allogeneic SCT following fludarabine 30 mg/m2 for 6 days and busulfan 3.2 mg/kg (<4 years, 4 mg/kg/d) for 2 days.
CONCLUSIONS: The administration of gemtuzumab ozogamicin post reduced-intensity allogeneic SCT in children with average risk
AML
is feasible and well tolerated with minimal toxicity.
The maximal tolerated dose has yet to be determined for gemtuzumab ozogamicin post reduced-intensity allogeneic SCT in children with CD33+
AML
.
[MeSH-major]
Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Immunotherapy / methods.
Leukemia
,
Myeloid
,
Acute
/ therapy. Stem Cell Transplantation / methods
[MeSH-minor]
Adolescent. Antibodies, Monoclonal, Humanized. Busulfan / administration & dosage.
Child
.
Child
, Preschool. Combined Modality Therapy. Female. Graft vs Host Disease / prevention & control. Histocompatibility Testing. Humans. Infant. Male. Pilot Projects. Recurrence. Sialic Acid Binding Ig-like Lectin 3. Time Factors. Transplantation Conditioning. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives
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(PMID = 16203817.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Grant]
United States / NHLBI NIH HHS / HL / T32 HL07968
[Publication-type]
Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
23.
Ashfaq K, Yahaya I, Hyde C, Andronis L, Barton P, Bayliss S, Chen YF:
Clinical effectiveness and cost-effectiveness of stem cell transplantation in the management of acute leukaemia: a systematic review.
Health Technol Assess
; 2010 Dec;14(54):iii-iv, ix-xi, 1-141
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[Title]
Clinical effectiveness and cost-effectiveness of stem cell transplantation in the management of
acute
leukaemia: a systematic review.
BACKGROUND:
Acute
leukaemia is a group of rapidly progressing cancers of bone marrow and blood classified as either
acute
myeloid
leukaemia (
AML
) or
acute
lymphoblastic leukaemia (ALL).
OBJECTIVES: A systematic overview of the best available evidence on the clinical effectiveness and cost-effectiveness of SCT in the treatment of
acute
leukaemia.
Included randomised controlled trials (RCTs) and donor versus no donor (DvND) studies were mapped to the evidence covered in existing systematic reviews and meta-analyses according to a framework of 12 decision problems (DPs): DP1 related to SCT in adults with
AML
in first complete remission (CR1); DP2 to adults with
AML
in second or subsequent remission or with refractory disease (CR2+); DP3 to children with
AML
in CR1; DP4 to children with
AML
in CR2+; DP5 to adults with ALL in CR1; DP6 to adults with ALL in CR2+; DP7 to children with ALL in CR1; DP8 to children with ALL in CR2+; DP9 to comparison of different sources of stem cells in transplantation; DP10 to different conditioning regimens; DP11 to the use of purging in autologous SCT; and DP12 to the use of T-cell depletion in allogeneic SCT.
Although there is a wealth of information on costs and some information on cost-effectiveness of allogeneic SCT in adults with
AML
(DPs 1 and 2), there is very limited evidence on relative costs and cost-effectiveness for other DPs.
CONCLUSIONS: Bearing in mind the limitations, existing evidence suggests that sibling donor allogeneic SCT may be more effective than chemotherapy in adult
AML
(except in good-risk patients) in CR1,
childhood
AML
in CR1 and adult ALL in CR1, and that autologous SCT is equal to or less effective than chemotherapy.
[MeSH-major]
Hematopoietic Stem Cell Transplantation / methods.
Leukemia
,
Myeloid
,
Acute
/ surgery. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / surgery
[MeSH-minor]
Adult.
Child
. Cost-Benefit Analysis. Humans
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(PMID = 21138675.001).
[ISSN]
2046-4924
[Journal-full-title]
Health technology assessment (Winchester, England)
[ISO-abbreviation]
Health Technol Assess
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
24.
Sung L, Gamis A, Alonzo TA, Buxton A, Britton K, Deswarte-Wallace J, Woods WG:
Infections and association with different intensity of chemotherapy in children with acute myeloid leukemia.
Cancer
; 2009 Mar 1;115(5):1100-8
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[Title]
Infections and association with different intensity of chemotherapy in children with
acute
myeloid
leukemia
.
BACKGROUND: The objectives were to compare infections during different intensities of therapy in children with
acute
myeloid
leukemia
(
AML
).
METHODS: Subjects were children enrolled in Children's Cancer Group 2891 with
AML
.
This information sheds insight into the mechanisms behind susceptibility and outcome of infections in
pediatric AML
.
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[Copyright]
(c) 2009 American Cancer Society.
[Cites]
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10784625.001
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[ErratumIn]
Cancer. 2009 Jun 15;115(12):2807
(PMID = 19156894.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U10 CA098543-06; United States / NCI NIH HHS / CA / U10 CA098413-06; United States / NCI NIH HHS / CA / U10 CA095861-08; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA095861; United States / NCI NIH HHS / CA / U10 CA098543; None / None / / U10 CA098413-06; United States / NCI NIH HHS / CA / U10 CA095861-06; United States / NCI NIH HHS / CA / CA095861-06; None / None / / U10 CA098543-06
[Publication-type]
Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS107661; NLM/ PMC2677372
25.
Klingebiel T, Reinhardt D, Bader P, EBMT Paediatric Diseases Working Party:
Place of HSCT in treatment of childhood AML.
Bone Marrow Transplant
; 2008 Oct;42 Suppl 2:S7-9
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[Title]
Place of HSCT in treatment of
childhood
AML
.
This short review focuses on the role of hematopoietic SCT (HSCT) in
childhood
AML
.
Data on haploidentical HSCT and on cord blood HSCT are still lacking in the case of
AML
.
[MeSH-major]
Hematopoietic Stem Cell Transplantation.
Leukemia
,
Myeloid
,
Acute
/ therapy. Living Donors
[MeSH-minor]
Adolescent.
Child
.
Child
, Preschool. Clinical Trials as Topic. Disease-Free Survival. Humans. Infant. Remission Induction. Siblings. Survival Rate. Transplantation, Autologous. Transplantation, Homologous
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(PMID = 18978749.001).
[ISSN]
1476-5365
[Journal-full-title]
Bone marrow transplantation
[ISO-abbreviation]
Bone Marrow Transplant.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Number-of-references]
15
26.
Shah M, Agarwal B:
Recent advances in management of acute myeloid leukemia (AML).
Indian J Pediatr
; 2008 Aug;75(8):831-7
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[Title]
Recent advances in management of
acute
myeloid
leukemia
(
AML
).
Acute
myeloid
leukemia
(
AML
) is the most common
childhood
malignancy.
AML
has therapeutically been difficult to treat.
In 2001, the World Health Organization (WHO), in conjunction with the Society for Hematopathology and the European Association of Hematopathology, published a new classification for
myeloid
neoplasms.
A number of chromosomal abnormalities are used to predict outcome and stratify therapeutic risk groups in children with
AML
.
Recently, alterations in receptor tyrosine kinases, tyrosine phosphatases and in oncogenes such as RAS have been implicated in the pathogenesis of
AML
.
This article aims to review the recent development in diagnosis, treatment and monitoring of
AML
.
Better understanding of the molecular pathogenesis of
AML
has led to the development of target-specific therapies.
The role of allogenic SCT, particularly whether it should be done during first CR or reserved for second remission, remains the most controversial issue in
pediatric AML
.
There is a need of collaboration with international
pediatric
cooperative oncology groups and definitive clinical trials in order to establish use of these newer molecules in
pediatric
populations.
[MeSH-major]
Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Immunologic Factors / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ therapy. Neoplasm, Residual / drug therapy
[MeSH-minor]
Antigens, CD / blood. Antigens, Differentiation, Myelomonocytic / blood.
Child
.
Child
, Preschool. Humans. Prognosis. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors. fms-Like Tyrosine Kinase 3 / genetics
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[ISSN]
0973-7693
[Journal-full-title]
Indian journal of pediatrics
[ISO-abbreviation]
Indian J Pediatr
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
India
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Immunologic Factors; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
[Number-of-references]
43
27.
Marques-Salles Tde J, Mkrtchyan H, Leite EP, Soares-Ventura EM, Muniz MT, Silva EF, Liehr T, Silva ML, Santos N:
Complex karyotype defined by molecular cytogenetic FISH and M-FISH in an infant with acute megakaryoblastic leukemia and neurofibromatosis.
Cancer Genet Cytogenet
; 2010 Jul 15;200(2):167-9
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[Title]
Complex karyotype defined by molecular cytogenetic FISH and M-FISH in an infant with
acute
megakaryoblastic
leukemia
and neurofibromatosis.
Acute
myeloid
leukemia
in
childhood
is a heterogeneous group of diseases, and different epidemiologic factors are involved in the etiopathogenesis.
Genetic syndromes are one of the predisposing factors of
acute
myeloid
leukemia
(
AML
), including Down syndrome, Bloom syndrome, and neurofibromatosis.
Acute
megakaryoblastic
leukemia
(AMKL) is the main subtype in Down syndrome infants, and acquired chromosomal anomalies are closely related to the physiopathology of the illness.
[MeSH-major]
In Situ Hybridization, Fluorescence / methods.
Leukemia
, Megakaryoblastic,
Acute
/ genetics. Neurofibromatoses / genetics
[MeSH-minor]
Female. Genes, p53. Histone-Lysine N-Methyltransferase. Humans. Infant. Karyotyping.
Myeloid
-Lymphoid
Leukemia
Protein / genetics
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[Copyright]
Copyright (c) 2010 Elsevier Inc. All rights reserved.
(PMID = 20620601.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
28.
Oliansky DM, Rizzo JD, Aplan PD, Arceci RJ, Leone L, Ravindranath Y, Sanders JE, Smith FO 3rd, Wilmot F, McCarthy PL Jr, Hahn T:
The role of cytotoxic therapy with hematopoietic stem cell transplantation in the therapy of acute myeloid leukemia in children: an evidence-based review.
Biol Blood Marrow Transplant
; 2007 Jan;13(1):1-25
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[Title]
The role of cytotoxic therapy with hematopoietic stem cell transplantation in the therapy of
acute
myeloid
leukemia
in children: an evidence-based review.
Clinical research examining the role of hematopoietic stem cell transplantation (SCT) in the therapy of
acute
myeloid
leukemia
(
AML
) in children is presented and critically evaluated in this systematic evidence-based review.
Treatment recommendations based on the evidence are presented in the table entitled "Summary of Treatment Recommendations Made by the Expert Panel for
Pediatric
Acute
Myeloid
Leukemia
" and were reached unanimously by a panel of experts in
AML
.
The identified priority areas of needed future research in
pediatric AML
include: What is the role of risk group stratification, including the role of cytogenetics, in selection of patients for allogeneic SCT, especially those in first CR?
and What is the role of biologically targeted agents (ie, tyrosine kinase inhibitors, farnesyl transferase inhibitors, Flt-3 inhibitors, etc) in the treatment of
AML
, including induction, consolidation, conditioning regimens, and after SCT?
[MeSH-major]
Hematopoietic Stem Cell Transplantation / methods.
Leukemia
,
Myeloid
/ therapy.
Leukemia
,
Myeloid
,
Acute
/ therapy
[MeSH-minor]
Acute
Disease. Adolescent. Bone Marrow Transplantation.
Child
.
Child
, Preschool. Evidence-Based Medicine. Humans. Remission Induction / methods. Transplantation Conditioning / methods. Transplantation, Autologous. Transplantation, Homologous
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(PMID = 17222748.001).
[ISSN]
1083-8791
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
69
29.
Mehta PA, Gerbing RB, Alonzo TA, Elliott JS, Zamzow TA, Combs M, Stover E, Ross JA, Perentesis JP, Meschinchi S, Lange BJ, Davies SM:
FAS promoter polymorphism: outcome of childhood acute myeloid leukemia. A children's oncology group report.
Clin Cancer Res
; 2008 Dec 1;14(23):7896-9
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[Title]
FAS promoter polymorphism: outcome of
childhood acute
myeloid
leukemia
. A children's oncology group report.
Previous work has shown increased risk of developing
acute
myeloid
leukemia
(
AML
) in adult patients with a variant allele at this site.
The same authors have shown that the presence of an adenine residue rather than a guanine residue at -1,377 bp significantly attenuates transcription factor stimulatory protein 1 binding and may contribute to a reduction in FAS expression and ultimately to the enrichment of apoptosis-resistant clones in
AML
.
We hypothesized that FAS genotype by altering susceptibility to apoptosis might affect outcome of
childhood
AML
therapy.
EXPERIMENTAL DESIGN: Four hundred forty-four children treated for de novo
AML
on a uniform protocol were genotyped for FAS 1377.
CONCLUSIONS: FAS 1377 genotype does not alter outcome of de novo
AML
in children.
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]
(PMID = 19047119.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U10 CA098543-06; United States / NCI NIH HHS / CA / R01 CA093552-01; United States / NCI NIH HHS / CA / R01 CA093552; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R01 CA 76326-01; None / None / / U10 CA098543-06; United States / NCI NIH HHS / CA / CA093552-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD95
[Other-IDs]
NLM/ NIHMS103099; NLM/ PMC2787450
30.
Menegaux F, Ripert M, Hémon D, Clavel J:
Maternal alcohol and coffee drinking, parental smoking and childhood leukaemia: a French population-based case-control study.
Paediatr Perinat Epidemiol
; 2007 Jul;21(4):293-9
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[Title]
Maternal alcohol and coffee drinking, parental smoking and
childhood
leukaemia: a French population-based case-control study.
We investigated the role of maternal alcohol and coffee drinking during pregnancy and that of parental smoking in the aetiology of
childhood
leukaemia.
A French, population-based, case-control study was conducted, comparing 472 [407
acute
lymphoblastic leukaemia (ALL) and 62
acute myeloblastic
leukaemia] cases of
childhood acute
leukaemia (AL) and 567 population controls, frequency-matched with cases on age, gender and region of residence.
The present results suggest a possible role of the highest consumption of alcohol by the mother during pregnancy in the aetiology of
childhood
AL.
[MeSH-major]
Alcohol Drinking / adverse effects. Caffeine / adverse effects. Central Nervous System Stimulants / adverse effects.
Leukemia
,
Myeloid
,
Acute
/ etiology. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / etiology. Smoking / adverse effects
[MeSH-minor]
Adolescent. Case-Control Studies.
Child
.
Child
, Preschool. Female. France / epidemiology. Humans. Infant. Male. Mothers. Pregnancy. Risk Factors
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CAFFEINE
.
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(PMID = 17564585.001).
[ISSN]
0269-5022
[Journal-full-title]
Paediatric and perinatal epidemiology
[ISO-abbreviation]
Paediatr Perinat Epidemiol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Central Nervous System Stimulants; 3G6A5W338E / Caffeine
31.
Castellino SM, Alonzo TA, Buxton A, Gold S, Lange BJ, Woods WG:
Outcomes in childhood AML in the absence of transplantation in first remission--Children's Cancer Group (CCG) studies 2891 and CCG 213.
Pediatr Blood Cancer
; 2008 Jan;50(1):9-16
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[Title]
Outcomes in
childhood
AML
in the absence of transplantation in first remission--Children's Cancer Group (CCG) studies 2891 and CCG 213.
BACKGROUND: The majority of
childhood acute
myeloid
leukemia
(
AML
) patients lack a matched-related bone marrow transplant (BMT) donor in first remission.
PROCEDURE: Disease-free survival (DFS), overall survival (OS), relapse-free survival (RFS), and post-relapse outcome were evaluated for children with de novo
AML
on CCG 213 and the standard timing (ST) and intensive timing (IT) induction arms of CCG 2891 who were randomized to (intent-to-treat, ITT) or who received (as-treated, AT) only chemotherapy intensification.
Overall survival for
childhood
AML
in the absence of BMT in CR1 is influenced by duration of CR1 and by race.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy
[MeSH-minor]
Child
. Disease-Free Survival. Female. Humans. Male. Remission Induction. Survival Analysis. Survival Rate
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[Copyright]
(c) 2007 Wiley-Liss, Inc.
(PMID = 17252564.001).
[ISSN]
1545-5017
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA 13539; United States / NCI NIH HHS / CA / CA 98543
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
[Publication-country]
United States
32.
Kardos G, Zwaan CM, Kaspers GJ, de-Graaf SS, de Bont ES, Postma A, Bökkerink JP, Weening RS, van der Does-van den Berg A, van Wering ER, Korbijn C, Hählen K:
Treatment strategy and results in children treated on three Dutch Childhood Oncology Group acute myeloid leukemia trials.
Leukemia
; 2005 Dec;19(12):2063-71
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[Title]
Treatment strategy and results in children treated on three Dutch
Childhood
Oncology Group
acute
myeloid
leukemia
trials.
This report describes the long-term follow-up data of three consecutive Dutch
Childhood
Oncology Group
acute
myeloid
leukemia
(
AML
) protocols.
A total of 303 children were diagnosed with
AML
, of whom 209 were eligible for this report.
The first study was the
AML
-82 protocol.
Study
AML
-87 was based on the BFM-87 protocol, with prophylactic cranial irradiation in high-risk patients only, and without maintenance therapy.
The subsequent study
AML
-92/94 consisted of a modified BFM-93 protocol, that is, without maintenance therapy and prophylactic cranial irradiation.
Our results demonstrate that outcome in
childhood
AML
is still unsatisfactory, and that further intensification of therapy carries the risk of enhanced toxicity.
Our patients are currently included in the MRC
AML
studies, based on the results of their
AML
10 trial.
[MeSH-major]
Antineoplastic Protocols / standards.
Leukemia
,
Myeloid
/ therapy
[MeSH-minor]
Acute
Disease. Adolescent.
Child
.
Child
, Preschool. Cranial Irradiation. Female. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Infant. Infant, Newborn. Male. Recurrence. Risk Assessment. Survival Analysis. Treatment Outcome
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(PMID = 16107896.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial
[Publication-country]
England
33.
Velardi A, Ruggeri L, Mancusi A, Aversa F, Christiansen FT:
Natural killer cell allorecognition of missing self in allogeneic hematopoietic transplantation: a tool for immunotherapy of leukemia.
Curr Opin Immunol
; 2009 Oct;21(5):525-30
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[Title]
Natural killer cell allorecognition of missing self in allogeneic hematopoietic transplantation: a tool for immunotherapy of
leukemia
.
Donor-versus-recipient natural killer (NK) cell alloreactivity has been established as a key therapeutic element in HLA haplotype mismatched hematopoietic transplants in adult
AML
and
pediatric
ALL and as a possible beneficial effector in cord blood transplant for
AML
.
At present NK cell allotherapy for
leukemia
is deployed through stem cell transplantation (and ensuing NK cell reconstitution) across KIR ligand mismatches.
[MeSH-major]
Hematopoietic Stem Cell Transplantation. Killer Cells, Natural / immunology.
Leukemia
,
Myeloid
/ immunology. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / immunology
[MeSH-minor]
Acute
Disease. Adult.
Child
. Humans. Immunotherapy / methods. Transplantation, Homologous
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(PMID = 19717293.001).
[ISSN]
1879-0372
[Journal-full-title]
Current opinion in immunology
[ISO-abbreviation]
Curr. Opin. Immunol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / 1 PO1 CA100265
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Number-of-references]
46
34.
Willasch AM, Gruhn B, Coliva T, Kalinova M, Schneider G, Kreyenberg H, Steinbach D, Weber G, Hollink IH, Zwaan CM, Biondi A, van der Velden VH, Reinhardt D, Cazzaniga G, Bader P, Trka J, European Study Group on WT1 Expression in Childhood AML:
Standardization of WT1 mRNA quantitation for minimal residual disease monitoring in childhood AML and implications of WT1 gene mutations: a European multicenter study.
Leukemia
; 2009 Aug;23(8):1472-9
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[Title]
Standardization of WT1 mRNA quantitation for minimal residual disease monitoring in
childhood
AML
and implications of WT1 gene mutations: a European multicenter study.
A standardized, sensitive and universal method for minimal residual disease (MRD) detection in
acute
myeloid
leukemia
(
AML
) is still pending.
Although hyperexpression of Wilms' tumor (WT1) gene transcript has been frequently proposed as an MRD marker in
AML
, wide comparability of the various methods used for evaluating WT1 expression has not been given.
In a series of quality-control rounds, we analyzed 69
childhood
AML
samples and 47 normal bone marrow (BM) samples from 4 participating centers.
In
AML
samples, the median WT1/1E+04 Abelson (ABL) expression was 3.5E+03 compared with that of 2.3E+01 in healthy BM samples.
As 11.5% of
childhood
AML
samples in this cohort harbored WT1 mutations in exon 7, the effect of mutations on WT1 expression has been investigated, showing that mutated cases expressed significantly higher WT1 levels than wild-type cases.
[MeSH-major]
Bone Marrow Examination / standards. Genes, Wilms Tumor.
Leukemia
,
Myeloid
/ pathology. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction / standards
[MeSH-minor]
Acute
Disease. Adolescent. Adult.
Child
.
Child
, Preschool. Cohort Studies. DNA Primers. Exons / genetics. Female. Gene Expression Regulation, Leukemic. Humans. Infant. Male. Middle Aged. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Neoplasm, Residual. Sensitivity and Specificity. WT1 Proteins / biosynthesis. Young Adult
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(PMID = 19322206.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA Primers; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / WT1 Proteins
35.
Fazlina N, Maha A, Jamal R, Zarina AL, Cheong SK, Hamidah H, Ainoon O, Zulkifli SZ, Hamidah NH:
Expression of multidrug resistance (MDR) proteins and in vitro drug resistance in acute leukemias.
Hematology
; 2007 Feb;12(1):33-7
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[Title]
Expression of multidrug resistance (MDR) proteins and in vitro drug resistance in
acute
leukemias.
The expression of the multidrug resistance (MDR) proteins may influence the outcome of treatment in patients with
acute leukemia
.
A total of 82 newly diagnosed
acute leukemia
cases (43 adult
myeloid
leukaemia,
AML
cases and 39
acute
lymphoblastic leukaemia, ALL cases) and 16 relapsed cases (8
AML
cases and 8 ALL cases) were studied.
In newly diagnosed cases, we found that
childhood
ALL samples showed higher IC50 values of dnr (0.040 +/- 2.320) compared to adult
AML
samples (0.021 +/- 0.158).
In contrast, newly diagnosed adult
AML
samples showed higher IC50 values of ara-C (0.157 +/- 0.529) compared to
childhood
ALL samples (0.100 +/- 2.350).
In relapsed cases, two samples of
childhood
ALL showed IC50 values of dnr (0.910 +/- 1.760) and ara-C (1.310 +/- 2.390), which was higher compared to
childhood
AML
samples (0.129 +/- 0.214 and 0.210 +/- 0.003, respectively).
In conclusion, we found that MTS assay is an easy, rapid and non laborious method to study in vitro drug resistance in
acute
leukaemia cases.
[MeSH-major]
Antineoplastic Agents / pharmacology. Drug Resistance, Multiple. Drug Resistance, Neoplasm.
Leukemia
/ metabolism. Neoplasm Proteins / metabolism. P-Glycoproteins / metabolism
[MeSH-minor]
Acute
Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Cell Survival.
Child
.
Child
, Preschool. Coloring Agents / analysis. Cytarabine / pharmacology. Daunorubicin / pharmacology. Female. Humans. Infant. Inhibitory Concentration 50.
Leukemia
,
Myeloid
/ drug therapy.
Leukemia
,
Myeloid
/ metabolism. Male. Methylphenazonium Methosulfate / pharmacology. Middle Aged. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / metabolism. Recurrence. Staining and Labeling / methods. Tetrazolium Salts / analysis. Thiazoles / analysis. Treatment Outcome. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / ultrastructure
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.
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DAUNORUBICIN
.
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(PMID = 17364990.001).
[ISSN]
1607-8454
[Journal-full-title]
Hematology (Amsterdam, Netherlands)
[ISO-abbreviation]
Hematology
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Coloring Agents; 0 / Neoplasm Proteins; 0 / P-Glycoproteins; 0 / Tetrazolium Salts; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 138169-43-4 / 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium; 299-11-6 / Methylphenazonium Methosulfate; ZS7284E0ZP / Daunorubicin
36.
Gra OA, Glotov AS, Kozhekbaeva Zhm, Makarova OV, Nasedkina TV:
[Genetic polymorphism in GST, NAT2, and MTRR and susceptibility to childhood acute leukemia].
Mol Biol (Mosk)
; 2008 Mar-Apr;42(2):214-25
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[Title]
[Genetic polymorphism in GST, NAT2, and MTRR and susceptibility to
childhood acute leukemia
].
In the present work the frequencies of xenobiotic-metabolizing gene polymorphisms in 332 children with the diagnosis
acute
lymphoblastic
leukemia
(ALL), 71 children with the diagnosis
acute myeloblastic leukemia
(
AML
) and 490 healthy donors have been determined using allele-specific hybridization on the biochip.
Statistically significant increase in the frequency of GSTT1 "null" genotype (OR = 1.9, p = 4.7E-5) and GSTT1/GSTM1 double "null" genotype (OR = 3.1, p = 2.5E-8) in children with
acute leukemia
relative to healthy donors group has been revealed.
Also 1.8-fold increase in the frequency of NAT2 genotype 341T/T, 481C/C, 590G/G in children with
acute leukemia
relative to healthy donors group (p = 0.026) has been recognized.
Analysis of gene-gene interactions has showed that in patients with
acute leukemia
genotype NAT2 341T/T, 481C/C, 590G/G in combination with GSTT1 "null" and/or GSTM1 "null" genotype is significantly more frequent than in population control.
Besides the reduction of MTRR genotype 66G/G frequency in girls with
acute leukemia
relative to female healthy donors has been found (OR = 0.50, p = 0.0015).
Analysis of gene-gene interactions has shown that the presence of GSTT1 "null" and/or GSTM1 "null" genotype in combination with MTRR genotype 66A/- may consider as risk factor of
acute leukemia
in girls.
Thus, the studied polymorphic variants of genes GSTT1, GSTM1, NAT2 and MTRR can modulate the risk of
childhood acute leukemia
, residents of European part of Russia.
[MeSH-major]
Arylamine N-Acetyltransferase / genetics. Ferredoxin-NADP Reductase / genetics. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / genetics
[MeSH-minor]
Adolescent. Alleles.
Child
.
Child
, Preschool. Female. Gene Frequency / genetics. Humans. Infant. Male. Risk Factors. Russia. Sex Factors
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(PMID = 18610829.001).
[ISSN]
0026-8984
[Journal-full-title]
Molekuliarnaia biologiia
[ISO-abbreviation]
Mol. Biol. (Mosk.)
[Language]
rus
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Russia (Federation)
[Chemical-registry-number]
EC 1.18.1.- / methionine synthase reductase; EC 1.18.1.2 / Ferredoxin-NADP Reductase; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / NAT2 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
37.
Lehrnbecher T, Bernig T, Hanisch M, Koehl U, Behl M, Reinhardt D, Creutzig U, Klingebiel T, Chanock SJ, Schwabe D:
Common genetic variants in the interleukin-6 and chitotriosidase genes are associated with the risk for serious infection in children undergoing therapy for acute myeloid leukemia.
Leukemia
; 2005 Oct;19(10):1745-50
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[Title]
Common genetic variants in the interleukin-6 and chitotriosidase genes are associated with the risk for serious infection in children undergoing therapy for
acute
myeloid
leukemia
.
Infectious complications represent a substantial cause of morbidity and mortality in children undergoing therapy for
acute
myeloid
leukemia
(
AML
).
Since it has been shown that alterations in innate immune pathways contribute to the risk for serious infections, we analyzed well-characterized variants in innate immune genes (TNF, IL6, IL8, MPO, CHIT, FCGR2A, TLR2, and TLR4) to determine their possible contribution to infectious complications during therapy for
pediatric AML
.
The study population consisted of 168 North European Caucasian children enrolled on the clinical trial
AML
-BFM 93.
Our data suggest that variant alleles of both IL6 and CHIT could influence susceptibility to infection with Gram-negative bacteria in children undergoing therapy for
AML
.
[MeSH-major]
Gram-Negative Bacterial Infections / etiology. Hexosaminidases / genetics. Interleukin-6 / genetics.
Leukemia
,
Myeloid
/ genetics. Polymorphism, Genetic. Promoter Regions, Genetic / genetics
[MeSH-minor]
Acute
Disease. Adolescent. Alleles. Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Child
.
Child
, Preschool. Clinical Trials as Topic. Female. Genetic Variation. Genotype. Gram-Negative Bacteria / isolation & purification. Humans. Infant. Infant, Newborn. Male
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(PMID = 16107886.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Interleukin-6; EC 3.2.1.- / Hexosaminidases; EC 3.2.1.- / chitotriosidase
38.
Brown P, Smith FO:
Molecularly targeted therapies for pediatric acute myeloid leukemia: progress to date.
Paediatr Drugs
; 2008;10(2):85-92
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[Title]
Molecularly targeted therapies for
pediatric
acute
myeloid
leukemia
: progress to date.
While
acute
myeloid
leukemia
(
AML
) is significantly less common than
acute
lymphoblastic
leukemia
(ALL) in
childhood
, it is significantly more deadly with only half as many children likely to be cured with standard therapy.
In addition, the typical treatment for
AML
is among the most toxic of treatments for
pediatric
cancer; it includes intensive multiagent chemotherapy and, often, hematopoietic stem cell transplantation.
Given the poor prognosis of
pediatric AML
and the significant toxicity of standard
AML
therapy, novel therapies are needed.
Improved understanding of the molecular and cellular biology of
leukemia
has facilitated the development of molecularly targeted therapies.
In this article, we review progress to date with agents that are showing promise in the treatment of
pediatric AML
including targeted immunoconjugates, inhibitors of signaling molecules (e.g.
For the specific agents in each of these classes, we summarize the published preclinical data and the clinical trials that have been completed, are in progress, or are being planned for children with
AML
.
Finally, we discuss potential challenges to the success of molecularly targeted therapy including demonstrating adequate targeting of
leukemia
stem cells, developing synergistic and tolerable combinations of agents, and designing adequately powered clinical trials to test efficacy in molecularly defined subsets of patients.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
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[ISSN]
1174-5878
[Journal-full-title]
Paediatric drugs
[ISO-abbreviation]
Paediatr Drugs
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / K23 CA111728
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Histone Deacetylase Inhibitors; 0 / Proteasome Inhibitors; 0 / Protein Kinase Inhibitors; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
[Number-of-references]
92
39.
Bachas C, Schuurhuis GJ, Hollink IH, Kwidama ZJ, Goemans BF, Zwaan CM, van den Heuvel-Eibrink MM, de Bont ES, Reinhardt D, Creutzig U, de Haas V, Assaraf YG, Kaspers GJ, Cloos J:
High-frequency type I/II mutational shifts between diagnosis and relapse are associated with outcome in pediatric AML: implications for personalized medicine.
Blood
; 2010 Oct 14;116(15):2752-8
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[Title]
High-frequency type I/II mutational shifts between diagnosis and relapse are associated with outcome in
pediatric AML
: implications for personalized medicine.
Although virtually all
pediatric
patients with
acute
myeloid
leukemia
(
AML
) achieve a complete remission after initial induction therapy, 30%-40% of patients will encounter a relapse and have a dismal prognosis.
To determine relevance of established
AML
type I/II mutations that may serve as therapeutic targets, we assessed frequencies of these mutations and their persistence during disease progression in a large group (n = 69) of paired diagnosis and relapse
pediatric AML
specimens.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation. Precision Medicine
[MeSH-minor]
Adolescent. Base Sequence. Biomarkers, Tumor / genetics.
Child
.
Child
, Preschool. Cohort Studies. DNA Mutational Analysis. DNA Primers / genetics. DNA, Neoplasm / genetics. Female. Follow-Up Studies. Genes, Wilms Tumor. Genes, ras. Humans. Infant. Male. Prognosis. Recurrence. Time Factors. Treatment Outcome. fms-Like Tyrosine Kinase 3 / genetics
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[CommentIn]
Blood. 2010 Oct 14;116(15):2622-3
[
20947687.001
]
(PMID = 20592250.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / DNA Primers; 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
40.
Lee DH, Kwon YJ, Lim J, Kim Y, Han K, Chung NG, Jeong DC, Cho B, Kim HK:
Comparable outcomes of HLA-matched unrelated and HLA-identical sibling donor bone marrow transplantation for childhood acute myeloid leukemia in first remission.
Pediatr Transplant
; 2009 Mar;13(2):210-6
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[Title]
Comparable outcomes of HLA-matched unrelated and HLA-identical sibling donor bone marrow transplantation for
childhood acute
myeloid
leukemia
in first remission.
We retrospectively investigated the outcomes of HLA-matched unrelated BMT (MU-BMT, n = 13) and HLA-identical sibling donor BMT (MS-BMT, n = 17) for
childhood
AML
in CR1 between June 2002 and August 2005.
The cumulative incidence of grade II-IV
acute
GVHD and any chronic GVHD at three yr was not different between MS-BMT and MU-BMT.
The outcome of HLA-matched unrelated BMT is comparable to that of HLA-identical sibling BMT for
childhood
AML
in CR1.
HLA-matched unrelated BMT may be recommended for patients who have
AML
in CR1 without an HLA-matched sibling donor.
[MeSH-major]
Bone Marrow Transplantation / methods. HLA Antigens / metabolism.
Leukemia
,
Myeloid
,
Acute
/ therapy
[MeSH-minor]
Adolescent. Adult. Blood Platelets / metabolism.
Child
.
Child
, Preschool. Female. Humans. Living Donors. Male. Neutrophils / metabolism. Remission Induction. Retrospective Studies. Siblings. Treatment Outcome
Genetic Alliance.
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.
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.
Genetic Alliance.
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(PMID = 18627512.001).
[ISSN]
1399-3046
[Journal-full-title]
Pediatric transplantation
[ISO-abbreviation]
Pediatr Transplant
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Denmark
[Chemical-registry-number]
0 / HLA Antigens
41.
Mizushima Y, Taki T, Shimada A, Yui Y, Hiraumi Y, Matsubara H, Watanabe M, Watanabe K, Kamitsuji Y, Hayashi Y, Tsukimoto I, Kobayashi R, Horibe K, Tawa A, Nakahata T, Adachi S:
Prognostic significance of the BAALC isoform pattern and CEBPA mutations in pediatric acute myeloid leukemia with normal karyotype: a study by the Japanese Childhood AML Cooperative Study Group.
Int J Hematol
; 2010 Jun;91(5):831-7
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[Title]
Prognostic significance of the BAALC isoform pattern and CEBPA mutations in
pediatric
acute
myeloid
leukemia
with normal karyotype: a study by the Japanese
Childhood
AML
Cooperative Study Group.
High BAALC (brain and
acute leukemia
, cytoplasmic) gene expression may indicate an adverse prognosis for adults who have
acute
myeloid
leukemia
(
AML
) and a normal karyotype, but its prognostic significance for
pediatric AML
cases is unclear.
Newly diagnosed
AML
patients with normal karyotype who were treated by the Japanese
Childhood
AML
Cooperative Treatment Protocol
AML
99 were analyzed in terms of their BAALC expression levels (n = 29), BAALC isoforms (n = 29), and CEBPA mutations (n = 49).
Thus, 1-5-6-8 isoform expression may be associated with an adverse prognosis in
pediatric AML
with normal karyotype.
[MeSH-major]
Asian Continental Ancestry Group / genetics. CCAAT-Enhancer-Binding Proteins. Gene Expression Regulation, Leukemic.
Leukemia
,
Myeloid
,
Acute
/ diagnosis. Mutation. Neoplasm Proteins
[MeSH-minor]
Adolescent.
Child
.
Child
, Preschool. Female. Humans. Infant. Infant, Newborn. Karyotyping. Male. Prognosis. Protein Isoforms / genetics
Genetic Alliance.
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.
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.
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20376583.001
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[Cites]
Leukemia. 2005 Mar;19(3):329-34
[
15674366.001
]
(PMID = 20495894.001).
[ISSN]
1865-3774
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / BAALC protein, human; 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Neoplasm Proteins; 0 / Protein Isoforms
42.
Mehta PA, Alonzo TA, Gerbing RB, Elliott JS, Wilke TA, Kennedy RJ, Ross JA, Perentesis JP, Lange BJ, Davies SM, Children's Oncology Group:
XPD Lys751Gln polymorphism in the etiology and outcome of childhood acute myeloid leukemia: a Children's Oncology Group report.
Blood
; 2006 Jan 1;107(1):39-45
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[Title]
XPD Lys751Gln polymorphism in the etiology and outcome of
childhood acute
myeloid
leukemia
: a Children's Oncology Group report.
Polymorphisms in XPD, a member of the nucleotide excision repair pathway, have been associated with development of treatment-related
acute
myeloid
leukemia
(
AML
) and with poor outcome of
AML
in elderly patients.
We hypothesized that XPD Lys751Gln polymorphism may play a role in causation of
AML
in children and, as shown in adults, may affect the outcome of
childhood
AML
therapy.
Genotyping of 456 children treated for de novo
AML
was performed at XPD exon 23.
Gene frequencies in
AML
patients and healthy controls were similar.
There were no significant differences in overall survival (P = .82), event-free survival (P = .78), treatment-related mortality (P = .43), or relapse rate (RR) (P = .92) between patients with XPD751AA versus 751AC versus 751CC genotypes, in contrast to reports in adult
AML
.
These data, representing the only data in
pediatric AML
, suggest that XPD genotype does not affect the etiology or outcome of
childhood
AML
.
[MeSH-major]
Leukemia
,
Myeloid
/ genetics. Polymorphism, Single Nucleotide. Xeroderma Pigmentosum Group D Protein / genetics
[MeSH-minor]
Acute
Disease. Adolescent. Adult. Case-Control Studies.
Child
.
Child
, Preschool. Female. Gene Frequency. Genetic Testing. Genotype. Humans. Infant. Infant, Newborn. Male. Mutation, Missense. Survival Analysis. Treatment Outcome
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(PMID = 16150943.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human
43.
Petridou E, Mantzoros CS, Dessypris N, Dikalioti SK, Trichopoulos D:
Adiponectin in relation to childhood myeloblastic leukaemia.
Br J Cancer
; 2006 Jan 16;94(1):156-60
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[Title]
Adiponectin in relation to
childhood myeloblastic
leukaemia.
Adiponectin, an adipocyte-specific secretory protein known to induce apoptosis, has been reported to be inversely related to breast and endometrial cancers and recently found to inhibit proliferation of
myeloid
but not lymphoid cell lines.
We hypothesised that adiponectin may be inversely associated with
acute myeloblastic
leukaemia (
AML
), but not with
acute
lymphoblastic leukaemia of B (ALL-B) or T (ALL-T) cell origin in children.
Blood samples and clinical information were collected over the period 1996-2000 from 201 children (0-14 years old) with leukaemia (22
AML
, 161 ALL-B and 18 ALL-T cases) through a national network of
childhood
Hematology-Oncology units in Greece and from 201 controls hospitalised for minor
pediatric
ailments.
Adiponectin was inversely associated with
AML
(OR=0.56; 95% CI, 0.34-0.94), whereas it was not significantly associated with either ALL-B (OR=0.88; 95% CI, 0.71-1.10) or ALL-T (OR=1.08; 95% CI, 0.67-1.72).
Biological plausibility and empirical evidence point to the importance of this hormone in the pathogenesis of
childhood
AML
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ physiopathology. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / physiopathology
[MeSH-minor]
Adiponectin / analysis. Adiponectin / biosynthesis. Adolescent. Apoptosis. Body Height. Body Weight. Case-Control Studies. Cell Proliferation.
Child
.
Child
, Preschool. Female. Gene Expression Profiling. Greece. Humans. Infant. Infant, Newborn.
Leukemia
, B-Cell.
Leukemia
, T-Cell. Male. Odds Ratio
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[ISSN]
0007-0920
[Journal-full-title]
British journal of cancer
[ISO-abbreviation]
Br. J. Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / ADIPOQ protein, human; 0 / Adiponectin
[Other-IDs]
NLM/ PMC2361080
44.
Kaspers GJ, Creutzig U:
Pediatric acute myeloid leukemia: international progress and future directions.
Leukemia
; 2005 Dec;19(12):2025-9
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[Title]
Pediatric
acute
myeloid
leukemia
: international progress and future directions.
[MeSH-major]
Leukemia
,
Myeloid
/ therapy
[MeSH-minor]
Acute
Disease.
Child
. Forecasting. Humans. Prognosis. Treatment Outcome
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(PMID = 16304569.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Editorial; Review
[Publication-country]
England
[Number-of-references]
30
45.
Walter RB, Alonzo TA, Gerbing RB, Ho PA, Smith FO, Raimondi SC, Hirsch BA, Gamis AS, Franklin JL, Hurwitz CA, Loken MR, Meshinchi S:
High expression of the very late antigen-4 integrin independently predicts reduced risk of relapse and improved outcome in pediatric acute myeloid leukemia: a report from the children's oncology group.
J Clin Oncol
; 2010 Jun 10;28(17):2831-8
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[Title]
High expression of the very late antigen-4 integrin independently predicts reduced risk of relapse and improved outcome in
pediatric
acute
myeloid
leukemia
: a report from the children's oncology group.
PURPOSE: To evaluate the prognostic significance of the integrin cell adhesion molecule very late antigen-4 (VLA-4) in
acute
myeloid
leukemia
(
AML
).
Subgroup analyses indicated that the prognostic role of VLA-4 expression was most prominent in patients with standard-risk
AML
, in whom low VLA-4 expression was associated with inferior DFS (34% +/- 16% v 69% +/- 14% for high expression; P = .011) and higher RR (61% +/- 16% v 26% +/- 14% for high expression; P = .009).
CONCLUSION: High VLA-4 expression is associated with better clinical outcome in
pediatric AML
and is an independent predictor of relapse that may refine our abilities to stratify patients without identifiable cytogenetic or molecular risk factors.
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Cell. 2002 Sep 20;110(6):673-87
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Genome Biol. 2007;8(5):215
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17543136.001
]
(PMID = 20421533.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U24 CA114766; United States / NCI NIH HHS / CA / K23 CA137161; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Integrin alpha4beta1
[Other-IDs]
NLM/ PMC2903318
46.
Ho PA, Zeng R, Alonzo TA, Gerbing RB, Miller KL, Pollard JA, Stirewalt DL, Heerema NA, Raimondi SC, Hirsch B, Franklin JL, Lange B, Meshinchi S:
Prevalence and prognostic implications of WT1 mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group.
Blood
; 2010 Aug 05;116(5):702-10
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[Title]
Prevalence and prognostic implications of WT1 mutations in
pediatric
acute
myeloid
leukemia
(
AML
): a report from the Children's Oncology Group.
Recent studies of WT1 mutations in
acute
myeloid
leukemia
(
AML
) mostly report an association with unfavorable clinical outcome.
We screened 842 patients treated on 3 consecutive
pediatric AML
trials for WT1 zinc-finger mutations.
In current risk stratification schemes incorporating cytogenetics and FLT3/ITD status, the presence of WT1 mutations has no independent prognostic significance in predicting outcome in
pediatric AML
.
[MeSH-major]
Genes, Wilms Tumor.
Leukemia
,
Myeloid
/ genetics. Mutation
[MeSH-minor]
Acute
Disease. Adolescent.
Child
.
Child
, Preschool. Cohort Studies. DNA Mutational Analysis. DNA, Neoplasm / genetics. Exons / genetics. Female. Humans. Infant. Infant, Newborn. Kaplan-Meier Estimate. Karyotyping. Male. Prevalence. Prognosis. Proportional Hazards Models. Retrospective Studies. Tandem Repeat Sequences / genetics. Treatment Outcome. Young Adult. fms-Like Tyrosine Kinase 3 / genetics
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Gene. 2001 Aug 8;273(2):141-61
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(PMID = 20413658.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00002798/ NCT00070174
[Grant]
United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R21CA10262-01; United States / NCI NIH HHS / CA / U10 CA98543
[Publication-type]
Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
[Other-IDs]
NLM/ PMC2918327
47.
Mulrooney DA, Dover DC, Li S, Yasui Y, Ness KK, Mertens AC, Neglia JP, Sklar CA, Robison LL, Davies SM, Childhood Cancer Survivor Study:
Twenty years of follow-up among survivors of childhood and young adult acute myeloid leukemia: a report from the Childhood Cancer Survivor Study.
Cancer
; 2008 May 1;112(9):2071-9
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[Title]
Twenty years of follow-up among survivors of
childhood
and young adult
acute
myeloid
leukemia
: a report from the
Childhood
Cancer Survivor Study.
BACKGROUND: Limited data exist on the comprehensive assessment of late medical and social effects experienced by survivors of
childhood
and young adult
acute
myeloid
leukemia
(
AML
).
METHODS: This analysis included 272 5-year
AML
survivors who participated in the
Childhood
Cancer Survivor Study (CCSS).
The cumulative incidence of recurrent
AML
was 6.6% at 10 years (95% CI, 3.7%-9.6%) and 8.6% at 20 years (95% CI, 5.1%-12.1%).
CONCLUSIONS: Long-term survival from
childhood
AML
> or =5-years after diagnosis was favorable.
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(PMID = 18327823.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
ENG
[Grant]
United States / NCRR NIH HHS / RR / K12 RR023247; United States / NCI NIH HHS / CA / U24 CA055727; United States / NCRR NIH HHS / RR / 1 K12 RR 023247; United States / NCI NIH HHS / CA / U24 CA 55727
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Investigator]
Robison LL; Hudson M; Armstrong G; Perkins J; O'Leary M; Friedman D; Pendergrass T; Greffe B; Odom L; Ruccione K; Mulvihill J; Ginsberg J; Meadows A; Tersak J; Ritchey A; Blatt J; Reaman G; Packer R; Davies S; Bhatia S; Qualman S; Hammond S; Termuhlen A; Ruymann F; Diller L; Grier H; Li F; Meacham L; Mertens A; Leisenring W; Potter J; Greenberg M; Nathan PC; Boice J; Rodriguez V; Smithson WA; Gilchrist G; Sklar C; Oeffinger K; Finklestein J; Anderson B; Inskip P; Vik TA; Weetman R; Green DM; Hayashi R; Vietti T; Marina N; Donaldson SS; Link MP; Dreyer Z; Whelan K; Sande J; Berkow R; Yasui Y; Casallis J; Zeltzer L; Goldsby R; Ablin A; Hutchinson R; Neglia J; Deapen D; Breslow N; Bowers D; Tomlinson G; Buchanan GR; Strong L; Stovall M
48.
Schultz KA, Chen L, Chen Z, Zeltzer LK, Nicholson HS, Neglia JP:
Health and risk behaviors in survivors of childhood acute myeloid leukemia: a report from the Children's Oncology Group.
Pediatr Blood Cancer
; 2010 Jul 15;55(1):157-64
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[Title]
Health and risk behaviors in survivors of
childhood acute
myeloid
leukemia
: a report from the Children's Oncology Group.
BACKGROUND: Survivors of
childhood acute
myeloid
leukemia
(
AML
) face increased risks of chronic disease and secondary malignancies.
PROCEDURES: Participants were diagnosed with
AML
at <21 years of age and survived > or =5 years following diagnosis.
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]
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J Natl Cancer Inst. 2001 Apr 18;93(8):618-29
[
11309438.001
]
(PMID = 20232426.001).
[ISSN]
1545-5017
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U24 CA055727; United States / NCI NIH HHS / CA / U10 CA98413; United States / NCI NIH HHS / CA / 5U10CA78960; United States / NCI NIH HHS / CA / U24 CA55727; United States / NCI NIH HHS / CA / U10 CA007306-39; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA098543-08; None / None / / U10 CA098543-08; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA078960-04; United States / NCI NIH HHS / CA / CA007306-39; United States / NCI NIH HHS / CA / U10 CA098413-08; None / None / / U10 CA098413-08; United States / NCI NIH HHS / CA / U10 CA98543; United States / NCI NIH HHS / CA / 5U10 CA07306; United States / NCI NIH HHS / CA / R01 CA078960-04
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS166508; NLM/ PMC3152207
49.
Belson M, Kingsley B, Holmes A:
Risk factors for acute leukemia in children: a review.
Environ Health Perspect
; 2007 Jan;115(1):138-45
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[Title]
Risk factors for
acute leukemia
in children: a review.
Although overall incidence is rare,
leukemia
is the most common type of
childhood
cancer.
Within this population,
acute
lymphocytic
leukemia
(ALL) occurs approximately five times more frequently than
acute
myelogenous
leukemia
(
AML
) and accounts for approximately 78% of all
childhood leukemia
diagnoses.
Epidemiologic studies of
acute
leukemias in children have examined possible risk factors, including genetic, infectious, and environmental, in an attempt to determine etiology.
Only one environmental risk factor (ionizing radiation) has been significantly linked to ALL or
AML
.
Most environmental risk factors have been found to be weakly and inconsistently associated with either form of
acute childhood leukemia
.
Our review focuses on the demographics of
childhood leukemia
and the risk factors that have been associated with the development of
childhood
ALL or
AML
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ etiology. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / etiology
[MeSH-minor]
Child
. Communicable Diseases / complications. Environmental Exposure. Genetic Predisposition to Disease. Humans. Risk Factors
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
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(PMID = 17366834.001).
[ISSN]
0091-6765
[Journal-full-title]
Environmental health perspectives
[ISO-abbreviation]
Environ. Health Perspect.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
145
[Other-IDs]
NLM/ PMC1817663
50.
Yeh TC, Liu HC, Wang LY, Chen SH, Lin WY, Liang DC:
The development of a novel protocol for the treatment of de novo childhood acute myeloid leukemia in a single institution in Taiwan.
J Pediatr Hematol Oncol
; 2007 Dec;29(12):826-31
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[Title]
The development of a novel protocol for the treatment of de novo
childhood acute
myeloid
leukemia
in a single institution in Taiwan.
From November 1, 1995 to July 31, 2004, 49 children with de novo
acute
myeloid
leukemia
(
AML
) were treated at our institution.
In total, 48 patients with de novo
AML
were enrolled in this study.
Forty-two patients with
AML
other than
acute
promyelocytic
leukemia
(non-APL) were treated consecutively with 2 novel protocols: Mackay Memorial Hospital (MMH)-
AML
-96, designed as a pilot phase, and Taiwan
Pediatric
Oncology Group (TPOG)-
AML
-97A, on the basis of MMH-
AML
-96 with minor modifications.
The 5-year overall survival was 64%+/-6.9% (SE), and the 5-year event-free survival was 60%+/-7.1%; for non-APL
AML
, the rates were 62%+/-7.5% and 59%+/-7.6%; for APL, 83+/-15.2 and 67+/-19.3%.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Tretinoin / therapeutic use
[MeSH-minor]
Child
.
Child
, Preschool. Drug Administration Schedule. Female. Humans. Infant. Male. Survival Rate. Survivors. Taiwan
Genetic Alliance.
consumer health - Acute Myeloid Leukemia, Childhood
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
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.
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.
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(PMID = 18090930.001).
[ISSN]
1077-4114
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
51.
Bierings M, Nachman JB, Zwaan CM:
Stem cell transplantation in pediatric leukemia and myelodysplasia: state of the art and current challenges.
Curr Stem Cell Res Ther
; 2007 Jan;2(1):53-63
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[Title]
Stem cell transplantation in
pediatric
leukemia
and myelodysplasia: state of the art and current challenges.
The role of stem cell transplantation in the treatment of
leukemia
and myelodysplasia (MDS) in children has changed over the past decade.
In
pediatric
acute
lymphoblastic
leukemia
(ALL), the overall cure-rate is high with conventional chemotherapy.
In
pediatric
acute
myeloid
leukemia
(
AML
) the role of allo-HSCT in CR1 is declining, due to better outcome with modern multi-agent chemotherapy.
In relapsed
AML
patients, allo-HSCT still seems indispensable.
Targeted therapy may change the role of HSCT, in particular in chronic
myeloid
leukemia
, where the role of allografting is changing in the imatinib era.
[MeSH-major]
Leukemia
/ therapy. Myelodysplastic Syndromes / therapy. Stem Cell Transplantation / trends
[MeSH-minor]
Child
. Humans.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / therapy.
Leukemia
,
Myeloid
,
Acute
/ therapy
Genetic Alliance.
consumer health - Transplantation
.
MedlinePlus Health Information.
consumer health - Leukemia
.
MedlinePlus Health Information.
consumer health - Myelodysplastic Syndromes
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 18240454.001).
[ISSN]
1574-888X
[Journal-full-title]
Current stem cell research & therapy
[ISO-abbreviation]
Curr Stem Cell Res Ther
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United Arab Emirates
[Number-of-references]
88
52.
Mantadakis E, Samonis G, Kalmanti M:
A comprehensive review of acute promyelocytic leukemia in children.
Acta Haematol
; 2008;119(2):73-82
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[Source]
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[Title]
A comprehensive review of
acute
promyelocytic
leukemia
in children.
The outcome of patients with
acute
promyelocytic
leukemia
(APL) has substantially improved since the successful introduction of tretinoin, and nowadays combining tretinoin with chemotherapy is potentially curative for at least 70-75% of patients with newly diagnosed APL.
In most
pediatric
series, APL represents < or = 10% of
childhood acute
myelogenous
leukemia
.
[MeSH-major]
Leukemia
, Promyelocytic,
Acute
/ diagnosis.
Leukemia
, Promyelocytic,
Acute
/ therapy
[MeSH-minor]
Antineoplastic Agents / therapeutic use.
Child
. Humans. Prognosis. Risk Factors. Treatment Outcome
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[Copyright]
2008 S. Karger AG, Basel
(PMID = 18285695.001).
[ISSN]
1421-9662
[Journal-full-title]
Acta haematologica
[ISO-abbreviation]
Acta Haematol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antineoplastic Agents
[Number-of-references]
70
53.
Liu CF, Liu GL, Zhang LP, Cheng YF, Lu AD, Tian KG, Liu YR, Qin YZ:
[Clinical significance of detection of AML1/ETO fusion transcripts in childhood AML using real-time quantitative reverse transcription polymerase chain reaction].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2005 Feb;13(1):76-82
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[Title]
[Clinical significance of detection of AML1/ETO fusion transcripts in
childhood
AML
using real-time quantitative reverse transcription polymerase chain reaction].
Fourteen AML1/ETO positive children out of 52
AML
children were selected.
It is concluded that real-time RT-PCR is a suitable approach for quantifying AML1/ETO transcripts in monitoring of
AML
patients with t(8;21) during/after chemotherapy and provides data of diagnostic relevance.
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(PMID = 15748440.001).
[ISSN]
1009-2137
[Journal-full-title]
Zhongguo shi yan xue ye xue za zhi
[ISO-abbreviation]
Zhongguo Shi Yan Xue Ye Xue Za Zhi
[Language]
CHI
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
54.
Ghosh I, Thulkar S, Arora R, Bakhshi S:
Multifocal osteomyelitis as a presenting manifestation of childhood acute myeloid leukemia.
J Pediatr Hematol Oncol
; 2009 Jan;31(1):75-6
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[Title]
Multifocal osteomyelitis as a presenting manifestation of
childhood acute
myeloid
leukemia
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ diagnosis. Osteomyelitis / diagnosis
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(PMID = 19125096.001).
[ISSN]
1536-3678
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
55.
Wang J, Ouyang J, Zhou R, Chen B, Yang Y:
Autologous hematopoietic stem cell transplantation for acute myeloid leukemia in first complete remission: a meta-analysis of randomized trials.
Acta Haematol
; 2010;124(2):61-71
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[Title]
Autologous hematopoietic stem cell transplantation for
acute
myeloid
leukemia
in first complete remission: a meta-analysis of randomized trials.
METHODS: A meta-analysis evaluating autologous SCT versus further chemotherapy or no treatment for
acute
myeloid
leukemia
(
AML
) in first complete remission (CR1) was completed.
Four studies were in
pediatric
patients and 9 were in adults.
For adults,
AML
in CR1 compared with non-SCT, lower relapse and higher transplantation-related mortality were associated with autologous SCT, a significant disease-free survival benefit of autologous SCT was documented, and there was no difference in overall survival when studies were pooled.
For
pediatric AML
in CR1, there were no differences in relapse, transplantation-related mortality, disease-free survival and overall survival.
CONCLUSION: Our results support the conclusion that autologous SCT should not be considered as the first-line post-remission therapy for
AML
patients in CR1.
[MeSH-major]
Hematopoietic Stem Cell Transplantation / mortality. Hematopoietic Stem Cell Transplantation / statistics & numerical data.
Leukemia
,
Myeloid
,
Acute
/ mortality.
Leukemia
,
Myeloid
,
Acute
/ therapy
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[Copyright]
Copyright © 2010 S. Karger AG, Basel.
(PMID = 20616541.001).
[ISSN]
1421-9662
[Journal-full-title]
Acta haematologica
[ISO-abbreviation]
Acta Haematol.
[Language]
eng
[Publication-type]
Journal Article; Meta-Analysis
[Publication-country]
Switzerland
56.
Cazzaniga G, Dell'Oro MG, Mecucci C, Giarin E, Masetti R, Rossi V, Locatelli F, Martelli MF, Basso G, Pession A, Biondi A, Falini B:
Nucleophosmin mutations in childhood acute myelogenous leukemia with normal karyotype.
Blood
; 2005 Aug 15;106(4):1419-22
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[Title]
Nucleophosmin mutations in
childhood acute
myelogenous
leukemia
with normal karyotype.
Nucleophosmin (NPM) is a nucleocytoplasmic shuttling protein involved in
leukemia
-associated chromosomal translocations, and it regulates the alternate reading frame (ARF)-p53 tumor-suppressor pathway.
Cytoplasmic NPM was detected in 35% of adult patients with primary non-French-American-British (FAB) classification M3
acute
myeloid
leukemia
(
AML
), associated mainly with normal karyotype.
We evaluated the prevalence of the NPM1 gene mutation in non-M3
childhood
AML
patients enrolled in the ongoing Associazione Italiana di Ematologia e Oncologia Pediatrica (AIEOP-AML02) protocol in Italy.
Thus, the NPM1 mutation is a frequent abnormality in
AML
patients without known genetic marker; the mutation may represent a new target to monitor minimal residual disease in
AML
and a potential candidate for alternative and targeted treatments.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation. Nuclear Proteins / genetics
[MeSH-minor]
Adolescent. Age Factors. Base Sequence.
Child
.
Child
, Preschool. Cytoplasm / chemistry. DNA Mutational Analysis. Exons. Female. Humans. Karyotyping. Male. Molecular Sequence Data
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(PMID = 15870172.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
57.
Xie C, Edwards H, Xu X, Zhou H, Buck SA, Stout ML, Yu Q, Rubnitz JE, Matherly LH, Taub JW, Ge Y:
Mechanisms of synergistic antileukemic interactions between valproic acid and cytarabine in pediatric acute myeloid leukemia.
Clin Cancer Res
; 2010 Nov 15;16(22):5499-510
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[Title]
Mechanisms of synergistic antileukemic interactions between valproic acid and cytarabine in
pediatric
acute
myeloid
leukemia
.
PURPOSE: To determine the possibility of synergistic antileukemic activity and the underlying molecular mechanisms associated with cytarabine combined with valproic acid (VPA; a histone deacetylase inhibitor and a Food and Drug Administration-licensed drug for treating both children and adults with epilepsy) in
pediatric
acute
myeloid
leukemia
(
AML
).
EXPERIMENTAL DESIGN: The type and extent of antileukemic interactions between cytarabine and VPA in clinically relevant
pediatric AML
cell lines and diagnostic blasts from children with
AML
were determined by MTT assays and standard isobologram analyses.
RESULTS: We showed synergistic antileukemic activities between cytarabine and VPA in four
pediatric AML
cell lines and nine diagnostic
AML
blast samples. t(8;21)
AML
blasts were significantly more sensitive to VPA and showed far greater sensitivities to combined cytarabine and VPA than non-t(8;21)
AML
cases.
CONCLUSIONS: Our results establish global synergistic antileukemic activity of combined VPA and cytarabine in
pediatric AML
and provide compelling evidence to support the use of VPA in the treatment of children with this deadly disease.
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.
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.
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[Copyright]
©2010 AACR.
[Cites]
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(PMID = 20889917.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA120772-01A2; United States / NCI NIH HHS / CA / R01 CA120772; United States / NCI NIH HHS / CA / CA120772; United States / NCI NIH HHS / CA / R01 CA120772-01A2
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
04079A1RDZ / Cytarabine; 614OI1Z5WI / Valproic Acid; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9
[Other-IDs]
NLM/ NIHMS238223; NLM/ PMC3018695
58.
Forestier E, Schmiegelow K, Nordic Society of Paediatric Haematology and Oncology NOPHO:
The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations.
J Pediatr Hematol Oncol
; 2006 Aug;28(8):486-95
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[Title]
The incidence peaks of the
childhood acute
leukemias reflect specific cytogenetic aberrations.
The correlation between age and karyotype was studied in 1425, 0 to 14.9 years old children who were diagnosed with
acute
lymphoblastic
leukemia
(ALL) or
acute myeloblastic leukemia
.
Among
acute myeloblastic leukemia
patients, frequency peaks were found for those with MLL/11q23 rearrangements (peak: first year), Down syndrome (peak: second to third year), or cytogenetic abnormalities other than translocations t(8;21), t(15;17), and inv(16)/t(16;16) (peak: first to third year).
The epidemiology of the cytogenetic subsets of
acute
leukemias questions whether age as a disease-related prognostic parameter has any relevance in
childhood leukemia
clinical research beyond being a surrogate marker for more important, truly biologic features such as cytogenetic aberrations and white cell count at diagnosis.
Further research is needed to explore whether the 2 to 7 years age incidence peak in
childhood
ALL harbor yet unidentified cytogenetic subsets with the same natural history as the high-hyperdiploid and t(12;21)-positive leukemias.
[MeSH-major]
Chromosome Aberrations.
Leukemia
,
Myeloid
,
Acute
/ genetics. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / genetics
[MeSH-minor]
Adolescent. Age Distribution.
Child
.
Child
, Preschool. Cohort Studies. Comorbidity. Cytogenetic Analysis / methods. Down Syndrome / diagnosis. Down Syndrome / epidemiology. Down Syndrome / genetics. Female. Humans. Incidence. Infant. Infant, Newborn. Karyotyping. Male. Ploidies. Recurrence. Registries / statistics & numerical data. Risk Factors. Scandinavian and Nordic Countries / epidemiology
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(PMID = 16912588.001).
[ISSN]
1077-4114
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
59.
Styczynski J:
Drug resistance in childhood acute myeloid leukemia.
Curr Pharm Biotechnol
; 2007 Apr;8(2):59-75
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[Title]
Drug resistance in
childhood acute
myeloid
leukemia
.
Therapy results in
childhood
AML
differ from those of ALL.
The development of drug resistance is the limiting factor in the therapy of
AML
.
Different problems of drug resistance in
childhood
AML
, with emphasis to age and in comparison to adult
AML
are presented.
Taking into account both children and adults, it seems that age is adversely related to therapy outcome in
AML
, and the percentage of patients with favorable cytogenetics decreases with age; however, age is positively correlated with multi-drug resistance and the proportion of patients with unfavorable cytogenetics.
AML
is considered a stem cell disease.
Cellular drug resistance in
AML
cells seems to be similar throughout all other age groups, however the higher the age, the worse the outcome.
In
childhood
AML
, no drug is more effective in comparison to ALL, and cellular drug resistance is partially related to chromosomal abnormalities.
Pediatric AML
is equally resistant as adult
AML
.
Pediatric
and adult
AML
, respectively, are possibly equally drug resistant on initial diagnosis and at relapse.
In contrast to ALL, the prognostic value of in vitro drug resistance in
childhood
AML
has not been well documented yet.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm.
Leukemia
,
Myeloid
/ drug therapy.
Leukemia
,
Myeloid
/ epidemiology. Neoplasm Recurrence, Local / epidemiology. Neoplasm Recurrence, Local / prevention & control
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(PMID = 17430154.001).
[ISSN]
1873-4316
[Journal-full-title]
Current pharmaceutical biotechnology
[ISO-abbreviation]
Curr Pharm Biotechnol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antineoplastic Agents
[Number-of-references]
165
60.
Nebral K, König M, Schmidt HH, Lutz D, Sperr WR, Kalwak K, Brugger S, Dworzak MN, Haas OA, Strehl S:
Screening for NUP98 rearrangements in hematopoietic malignancies by fluorescence in situ hybridization.
Haematologica
; 2005 Jun;90(6):746-52
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BACKGROUND AND OBJECTIVES: The aim of this study was to determine the incidence of rearrangements of NUP98 (the gene coding for nucleoporin 98kDa protein) in
childhood acute
myeloid
leukemia
(
AML
) and selected patients with 11p13-15 rearrangements.
DESIGN AND METHODS: Screening of 59 consecutive patients enrolled in the Austrian
AML
-BFM93 clinical trial was performed by dual-color FISH.
RESULTS: Among the 59
AML
patients, one NUP98-NSD1 positive case (1.7%) was detected.
INTERPRETATION AND CONCLUSIONS: The observed frequency of 1.7% confirmed the low incidence of NUP98 rearrangements in
childhood
AML
.
[MeSH-major]
Chromosome Aberrations. Hematologic Neoplasms / diagnosis. Hematologic Neoplasms / genetics.
Leukemia
,
Myeloid
,
Acute
/ diagnosis.
Leukemia
,
Myeloid
,
Acute
/ genetics. Nuclear Pore Complex Proteins / biosynthesis
[MeSH-minor]
Adolescent. Adult. Aged. Amino Acid Sequence. Base Sequence.
Child
.
Child
, Preschool. Chromosome Inversion. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Molecular Sequence Data. Translocation, Genetic
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(PMID = 15951287.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / Nuclear Pore Complex Proteins; 0 / nuclear pore complex protein 98
61.
Castagnola E, Rossi MR, Cesaro S, Livadiotti S, Giacchino M, Zanazzo G, Fioredda F, Beretta C, Ciocchello F, Carli M, Putti MC, Pansini V, Berger M, Licciardello M, Farina S, Caviglia I, Haupt R:
Incidence of bacteremias and invasive mycoses in children with acute non-lymphoblastic leukemia: results from a multi-center Italian study.
Pediatr Blood Cancer
; 2010 Dec 1;55(6):1103-7
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[Title]
Incidence of bacteremias and invasive mycoses in children with
acute
non-lymphoblastic
leukemia
: results from a multi-center Italian study.
BACKGROUND: Data on the epidemiology of bacteremias and invasive fungal diseases (IFD) in children with
acute
myeloid
leukemia
(
AML
) are scarce.
DESIGN AND METHODS: In a multi-center, retrospective study, we analyzed proportion, rate per 1,000 person-days at risk, and cumulative risk of bacteremias and IFD in children with
AML
.
RESULTS: Between January 1998 and December 2005, 240 children were treated for
AML
at 8 Italian Centers, for a total of 521 treatment courses and 63,232 person-days at risk.
The epidemiology of bacteremias and IFD was different during front-line therapy for M3 as compared to other types of
AML
, but the differences were not statistically significant.
CONCLUSIONS: Severe infectious complications are frequent during the treatment of
pediatric AML
, especially during relapse treatment, and bacteremias are more frequent than IFD.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bacteremia / etiology.
Leukemia
,
Myeloid
,
Acute
/ microbiology. Mycoses / etiology
[MeSH-minor]
Child
. Female. Follow-Up Studies. Humans. Incidence. Italy. Male. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / microbiology. Retrospective Studies
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(PMID = 20680968.001).
[ISSN]
1545-5017
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
62.
Cloos J, Goemans BF, Hess CJ, van Oostveen JW, Waisfisz Q, Corthals S, de Lange D, Boeckx N, Hählen K, Reinhardt D, Creutzig U, Schuurhuis GJ, Zwaan ChM, Kaspers GJ:
Stability and prognostic influence of FLT3 mutations in paired initial and relapsed AML samples.
Leukemia
; 2006 Jul;20(7):1217-20
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[Title]
Stability and prognostic influence of FLT3 mutations in paired initial and relapsed
AML
samples.
In
acute
myeloid
leukemia
(
AML
), activating mutations in the fms-like tyrosine kinase 3 (FLT3) gene predict poor prognosis.
We determined FLT3 internal tandem duplications (FLT3/ITD) and D835 point mutations in paired initial and relapse samples from 80
pediatric
and adult
AML
patients.
One D835 point mutation was found in an initial
pediatric AML
sample.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ epidemiology.
Leukemia
,
Myeloid
,
Acute
/ genetics. Point Mutation. fms-Like Tyrosine Kinase 3 / genetics
[MeSH-minor]
Adolescent. Adult. Female. Genetic Markers. Genetic Predisposition to Disease / epidemiology. Humans.
Leukemia
, Erythroblastic,
Acute
/ genetics.
Leukemia
, Megakaryoblastic,
Acute
/ genetics.
Leukemia
, Monocytic,
Acute
/ genetics.
Leukemia
, Myelomonocytic,
Acute
/ genetics.
Leukemia
, Promyelocytic,
Acute
/ genetics. Male. Neoplasm, Residual / epidemiology. Neoplasm, Residual / genetics. Prognosis. Recurrence. Risk Factors. Tandem Repeat Sequences
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(PMID = 16642044.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Genetic Markers; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
63.
Burjanivova T, Madzo J, Muzikova K, Meyer C, Schneider B, Votava F, Marschalek R, Stary J, Trka J, Zuna J:
Prenatal origin of childhood AML occurs less frequently than in childhood ALL.
BMC Cancer
; 2006;6:100
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[Title]
Prenatal origin of
childhood
AML
occurs less frequently than in
childhood
ALL.
BACKGROUND: While there is enough convincing evidence in
childhood acute
lymphoblastic
leukemia
(ALL), the data on the pre-natal origin in
childhood acute
myeloid
leukemia
(
AML
) are less comprehensive.
Our study aimed to screen Guthrie cards (neonatal blood spots) of non-infant
childhood
AML
and ALL patients for the presence of their respective leukemic markers.
In
AML
patients (n = 13, age 1-14 years) PML/RARalpha (n = 4), CBFbeta/MYH11 (n = 3), AML1/ETO (n = 2), MLL/AF6 (n = 1), MLL/AF9 (n = 1) and MLL/AF10 (n = 1) fusion genes and/or internal tandem duplication of FLT3 gene (FLT3/ITD) (n = 2) were used as clonotypic markers.
We did not find patient-specific molecular markers in any patient with
AML
.
CONCLUSION: In the largest cohort examined so far we used identical approach for the backtracking of non-infant
childhood
ALL and
AML
.
Our data suggest that either the prenatal origin of
AML
is less frequent or the load of pre-leukemic cells is significantly lower at birth in
AML
compared to ALL cases.
[MeSH-major]
Biomarkers, Tumor / blood. DNA, Neoplasm / blood. Fetal Blood / chemistry. Gene Rearrangement, B-Lymphocyte. Gene Rearrangement, T-Lymphocyte.
Leukemia
,
Myeloid
/ embryology. Oncogene Proteins, Fusion / blood. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / embryology
[MeSH-minor]
Bone Marrow Cells / chemistry.
Child
.
Child
, Preschool. Clone Cells / chemistry. Cohort Studies. Core Binding Factor Alpha 2 Subunit / blood. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Duplication. Humans. Infant. Infant, Newborn. Male.
Myeloid
-Lymphoid
Leukemia
Protein / blood.
Myeloid
-Lymphoid
Leukemia
Protein / genetics. Neonatal Screening. Neoplasm Proteins / blood. Neoplasm Proteins / genetics. Polymerase Chain Reaction. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3 / blood. fms-Like Tyrosine Kinase 3 / genetics
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]
(PMID = 16630339.001).
[ISSN]
1471-2407
[Journal-full-title]
BMC cancer
[ISO-abbreviation]
BMC Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Neoplasm; 0 / MLL-AF10 fusion protein, human; 0 / MLL-AF6 fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
[Other-IDs]
NLM/ PMC1463004
64.
Manola KN:
Cytogenetics of pediatric acute myeloid leukemia.
Eur J Haematol
; 2009 Nov;83(5):391-405
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[Title]
Cytogenetics of
pediatric
acute
myeloid
leukemia
.
Acute
myeloid
leukemia
(
AML
) is a clinically and genetically heterogeneous disease accounting for 15-20% of all
childhood acute
leukemias, while it is responsible for more than half of the leukemic deaths in these patients.
This article focuses on the significance of cytogenetic analysis in
pediatric AML
supporting the importance of cytogenetic analysis in the pathogenesis, diagnosis, prognosis, follow-up and treatment selection in
childhood
AML
.
Furthermore, it discusses the association of specific chromosome rearrangements with prenatal exposure to carcinogenic agents or therapeutic agents and highlights the ongoing and future research on
pediatric AML
in the evolving field of Cytogenetics.
[MeSH-major]
Cytogenetics / methods.
Leukemia
,
Myeloid
,
Acute
/ diagnosis.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ pathology
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(PMID = 19563518.001).
[ISSN]
1600-0609
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Carcinogens, Environmental
[Number-of-references]
123
65.
Zhang H, Luo XQ, Zhang P, Huang LB, Zheng YS, Wu J, Zhou H, Qu LH, Xu L, Chen YQ:
MicroRNA patterns associated with clinical prognostic parameters and CNS relapse prediction in pediatric acute leukemia.
PLoS One
; 2009;4(11):e7826
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[Title]
MicroRNA patterns associated with clinical prognostic parameters and CNS relapse prediction in
pediatric
acute leukemia
.
BACKGROUND: Recent reports have indicated that microRNAs (miRNAs) play a critical role in malignancies, and regulations in the progress of adult
leukemia
.
The role of miRNAs in
pediatric
leukemia
still needs to be established.
The purpose of this study was to investigate the aberrantly expressed miRNAs in
pediatric
acute leukemia
and demonstrate miRNA patterns that are
pediatric
-specific and prognostic parameter-associated.
METHODOLOGY/PRINCIPAL FINDINGS: A total of 111
pediatric
bone marrow samples, including 99 patients and 12 normal donors, were enrolled in this study.
Of those samples, 36 patients and 7 normal samples were used as a test cohort for the evaluation of miRNA profiling; 63
pediatric
patients and 5 normal donors were used as a validation cohort to confirm the miRNA differential expression.
Pediatric
ALL- and
AML
-specific microRNA expression patterns were identified in this study.
The most highly expressed miRNAs in
pediatric
ALL were miR-34a, miR-128a, miR-128b, and miR-146a, while the highly expressed miRNAs in
pediatric AML
were miR-100, miR-125b, miR-335, miR-146a, and miR-99a, which are significantly different from those reported for adult CLL and
AML
. miR-125b and miR-126 may serve as favorable prognosticators for M3 and M2 patients, respectively.
CONCLUSIONS/SIGNIFICANCE: There are existing
pediatric
-associated and prognostic parameter-associated miRNAs that are independent of cell lineage and could provide therapeutic direction for individual risk-adapted therapy for
pediatric
leukemia
patients.
[MeSH-major]
Central Nervous System Neoplasms / diagnosis.
Leukemia
/ diagnosis.
Leukemia
/ pathology. MicroRNAs
[MeSH-minor]
Child
.
Child
, Preschool. Cohort Studies. Female. Gene Expression Profiling. Gene Expression Regulation. Humans. Infant. Male. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk
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.
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[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MicroRNAs
[Other-IDs]
NLM/ PMC2773830
66.
Evrard AS, Hémon D, Billon S, Laurier D, Jougla E, Tirmarche M, Clavel J:
Childhood leukemia incidence and exposure to indoor radon, terrestrial and cosmic gamma radiation.
Health Phys
; 2006 Jun;90(6):569-79
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[Title]
Childhood leukemia
incidence and exposure to indoor radon, terrestrial and cosmic gamma radiation.
This study was undertaken to evaluate the ecological association between terrestrial and cosmic gamma radiation, indoor radon, and
acute leukemia
incidence among children under 15 y of age.
From 1990 to 2001, 5,330 cases of
acute leukemia
were registered by the French National Registry of
Childhood Leukemia
and Lymphoma.
There was no evidence of an ecological association between terrestrial gamma dose (range: 0.22-0.90 mSv y) or total gamma dose (range: 0.49-1.28 mSv y) and
childhood acute leukemia
incidence, for
acute
myeloid
leukemia
(
AML
) or for
acute
lymphoblastic
leukemia
(ALL), in univariate or multivariate regression analyses including indoor radon.
A significant positive association between indoor radon (range: 22-262 Bq m) and
AML
incidence among children was observed and remained significant in multivariate regression analyses including either terrestrial gamma dose [SIR per 100 Bq m = 1.29 (1.09-1.53)] or total gamma dose [SIR per 100 Bq m = 1.29 (1.09-1.53)].
The study showed no ecological association between terrestrial gamma radiation and
childhood leukemia
for the range of variation in gamma dose rates observed in France.
The moderate ecological association between
childhood
AML
incidence and indoor radon does not appear to be confounded by terrestrial gamma dose.
[MeSH-major]
Air Pollution, Indoor / analysis. Cosmic Radiation. Environmental Exposure / statistics & numerical data. Gamma Rays.
Leukemia
, Radiation-Induced / epidemiology. Radon / analysis. Risk Assessment / methods
[MeSH-minor]
Body Burden.
Child
.
Child
, Preschool. Confounding Factors (Epidemiology). Female. France / epidemiology. Humans. Incidence. Male. Radiation Dosage. Registries. Relative Biological Effectiveness. Risk Factors
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RADON, RADIOACTIVE
.
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(PMID = 16691105.001).
[ISSN]
0017-9078
[Journal-full-title]
Health physics
[ISO-abbreviation]
Health Phys
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
Q74S4N8N1G / Radon
67.
Rubnitz JE, Razzouk BI, Lensing S, Pounds S, Pui CH, Ribeiro RC:
Prognostic factors and outcome of recurrence in childhood acute myeloid leukemia.
Cancer
; 2007 Jan 1;109(1):157-63
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[Title]
Prognostic factors and outcome of recurrence in
childhood acute
myeloid
leukemia
.
BACKGROUND: Outcome after recurrence of
childhood acute
myeloid
leukemia
(
AML
) is poor.
We performed this study to identify prognostic factors for recurrence and for survival after recurrence of
AML
.
METHODS: The clinical characteristics, biological features, treatment modalities, and outcomes of children with de novo
AML
who were enrolled on 3 consecutive clinical protocols from 1987 to 2002 at St. Jude Children's Research Hospital were studied.
CONCLUSIONS: Survival after recurrence was poor in children with
AML
.
Novel therapies are urgently needed to prevent or to treat recurring
AML
.
[MeSH-major]
Leukemia
,
Myeloid
/ mortality
[MeSH-minor]
Acute
Disease.
Child
.
Child
, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Multivariate Analysis. Prognosis. Recurrence. Sex Factors. Stem Cell Transplantation. Survival Rate. Time Factors. Transplantation, Autologous
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[Copyright]
(c) 2006 American Cancer Society.
(PMID = 17133407.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA-21765
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
68.
van der Velden VH, van der Sluijs-Geling A, Gibson BE, te Marvelde JG, Hoogeveen PG, Hop WC, Wheatley K, Bierings MB, Schuurhuis GJ, de Graaf SS, van Wering ER, van Dongen JJ:
Clinical significance of flowcytometric minimal residual disease detection in pediatric acute myeloid leukemia patients treated according to the DCOG ANLL97/MRC AML12 protocol.
Leukemia
; 2010 Sep;24(9):1599-606
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[Title]
Clinical significance of flowcytometric minimal residual disease detection in
pediatric
acute
myeloid
leukemia
patients treated according to the DCOG ANLL97/MRC AML12 protocol.
Analysis of minimal residual disease (MRD) in
childhood acute
myeloid
leukemia
(
AML
) may predict for clinical outcome.
MRD levels were assessed by flowcytometric immunophenotyping in 94 children with
AML
enrolled into a single trial (United Kingdom Medical Research Council AML12 and similar Dutch
Childhood
Oncology Group ANLL97).
In conclusion, flowcytometric MRD detection is possible in children with
AML
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ diagnosis. Neoplasm, Residual / diagnosis
[MeSH-minor]
Child
. Clinical Protocols. Flow Cytometry. Humans. Immunophenotyping. Probability. Prognosis. RNA, Messenger / genetics. Recurrence
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(PMID = 20668473.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0300133
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / RNA, Messenger
69.
Anuchapreeda S, Thanarattanakorn P, Sittipreechacharn S, Tima S, Chanarat P, Limtrakul P:
Inhibitory effect of curcumin on MDR1 gene expression in patient leukemic cells.
Arch Pharm Res
; 2006 Oct;29(10):866-73
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The leukemic cells were collected from 78
childhood leukemia
patients admitted at Maharaj Nakorn Chiang Mai Hospital, Chiang Mai, Thailand, in the period from July 2003 to February 2005.
There were 61 cases of
acute
lymphoblastic
leukemia
(ALL), 14 cases of
acute myeloblastic leukemia
(
AML
), and 3 cases of chronic
myelocytic
leukemia
(CML).
Thus, curcumin treatment may provide a lead for clinical treatment of
leukemia
patients in the future.
[MeSH-minor]
Acute
Disease. Adolescent. Age Factors. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Bone Marrow / drug effects. Bone Marrow / metabolism. Bone Marrow / pathology. Cell Survival / drug effects.
Child
, Preschool. Female. Humans. Infant.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / blood.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / genetics.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / pathology.
Leukemia
,
Myeloid
/ blood.
Leukemia
,
Myeloid
/ genetics.
Leukemia
,
Myeloid
/ pathology. Male. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / blood. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / pathology. RNA, Messenger / genetics. RNA, Messenger / isolation & purification. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Cells, Cultured
Hazardous Substances Data Bank.
CURCUMIN
.
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(PMID = 17121181.001).
[ISSN]
0253-6269
[Journal-full-title]
Archives of pharmacal research
[ISO-abbreviation]
Arch. Pharm. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / RNA, Messenger; IT942ZTH98 / Curcumin
70.
Urbanová D, Bubanská E, Hrebík M, Mladosievicová B:
[Severe heart failure in consequence of late anthracycline-induced cardiotoxicity--case report].
Klin Onkol
; 2009;22(1):34-7
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The patient was treated for
childhood acute
myeloid
leukemia
by chemotherapy containing anthracyclines.
[MeSH-minor]
Adolescent. Heart Transplantation. Humans.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Male
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(PMID = 19534438.001).
[ISSN]
0862-495X
[Journal-full-title]
Klinická onkologie : casopis Ceské a Slovenské onkologické spolecnosti
[ISO-abbreviation]
Klin Onkol
[Language]
slo
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Czech Republic
[Chemical-registry-number]
0 / Anthracyclines; 0 / Antibiotics, Antineoplastic
71.
Meyer C, Kowarz E, Hofmann J, Renneville A, Zuna J, Trka J, Ben Abdelali R, Macintyre E, De Braekeleer E, De Braekeleer M, Delabesse E, de Oliveira MP, Cavé H, Clappier E, van Dongen JJ, Balgobind BV, van den Heuvel-Eibrink MM, Beverloo HB, Panzer-Grümayer R, Teigler-Schlegel A, Harbott J, Kjeldsen E, Schnittger S, Koehl U, Gruhn B, Heidenreich O, Chan LC, Yip SF, Krzywinski M, Eckert C, Möricke A, Schrappe M, Alonso CN, Schäfer BW, Krauter J, Lee DA, Zur Stadt U, Te Kronnie G, Sutton R, Izraeli S, Trakhtenbrot L, Lo Nigro L, Tsaur G, Fechina L, Szczepanski T, Strehl S, Ilencikova D, Molkentin M, Burmeister T, Dingermann T, Klingebiel T, Marschalek R:
New insights to the MLL recombinome of acute leukemias.
Leukemia
; 2009 Aug;23(8):1490-9
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[Title]
New insights to the MLL recombinome of
acute
leukemias.
Chromosomal rearrangements of the human MLL gene are associated with high-risk
pediatric
, adult and therapy-associated
acute
leukemias.
Genomic DNA was isolated from individual
acute leukemia
patients to identify and characterize chromosomal rearrangements involving the human MLL gene.
A total of 760 MLL-rearranged biopsy samples obtained from 384
pediatric
and 376 adult
leukemia
patients were characterized at the molecular level.
The distribution of MLL breakpoints for clinical subtypes (
acute
lymphoblastic
leukemia
,
acute
myeloid
leukemia
,
pediatric
and adult) and fused translocation partner genes (TPGs) will be presented, including novel MLL fusion genes.
[MeSH-major]
Leukemia
/ genetics.
Myeloid
-Lymphoid
Leukemia
Protein / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Recombination, Genetic. Translocation, Genetic
[MeSH-minor]
Acute
Disease. Adult. Biopsy. Bone Marrow / chemistry. Bone Marrow / pathology.
Child
. Chromosome Breakage. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 11 / ultrastructure. Computational Biology. DNA, Neoplasm / blood. DNA, Neoplasm / genetics. Gene Duplication. Histone-Lysine N-Methyltransferase. Humans. Polymerase Chain Reaction
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(PMID = 19262598.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA, Neoplasm; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
72.
Larson RA:
Micro-RNAs and copy number changes: new levels of gene regulation in acute myeloid leukemia.
Chem Biol Interact
; 2010 Mar 19;184(1-2):21-5
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[Title]
Micro-RNAs and copy number changes: new levels of gene regulation in
acute
myeloid
leukemia
.
Together with epigenetic alterations, these result in dysplasia, clonal expansion, and ultimately
myeloid
leukemia
.
Combinations of lesions are required to induce overt
leukemia
.
Recent studies have shown that cytogenetically normal (CN-)
AML
is quite heterogeneous at the molecular level.
Patients with CN-
AML
harboring mutations in NPM1, FLT3, CEBPA, WT1 or expressing high levels of BAALC, ERG, or MN1 have distinctly different clinical outcomes.
NPM1 mutations are independently associated with higher remission rates and longer disease-free and overall survival in
AML
.
Fewer CNAs have been detected in
AML
than in
pediatric
ALL.
Distinctive genome-wide miR expression profiles have been associated with different subsets of
AML
.
A miR signature that is associated with clinical outcome in patients with high-risk molecular features of
AML
(those who have FLT3-ITD or wild-type NPM1) has been reported.
This subgroup constitutes approximately 65% of patients with CN-
AML
and one-third of all patients with
AML
<60 years old.
Down-regulation of the miR-181 family contributes to an aggressive
leukemia
phenotype through mechanisms associated with the activation of pathways of innate immunity mediated by toll-like receptors and interleukin-1beta.
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[Copyright]
Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
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[Cites]
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Blood. 2002 Aug 15;100(4):1224-32
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(PMID = 19822134.001).
[ISSN]
1872-7786
[Journal-full-title]
Chemico-biological interactions
[ISO-abbreviation]
Chem. Biol. Interact.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA014599-34; United States / NCI NIH HHS / CA / P30 CA014599; United States / NCI NIH HHS / CA / U10 CA031946; United States / NCI NIH HHS / CA / U10 CA031946-28; United States / NCI NIH HHS / CA / P30 CA014599-34; United States / NCI NIH HHS / CA / P01 CA040046-22; United States / NCI NIH HHS / CA / CA031946-28; United States / NCI NIH HHS / CA / CA040046-22; United States / NCI NIH HHS / CA / CA14599; United States / NCI NIH HHS / CA / CA31946
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
Ireland
[Chemical-registry-number]
0 / MicroRNAs; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
[Other-IDs]
NLM/ NIHMS156571; NLM/ PMC2846194
73.
Stasevich I, Utskevich R, Kustanovich A, Litvinko N, Savitskaya T, Chernyavskaya S, Saharova O, Aleinikova O:
Translocation (10;11)(p12;q23) in childhood acute myeloid leukemia: incidence and complex mechanism.
Cancer Genet Cytogenet
; 2006 Sep;169(2):114-20
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[Title]
Translocation (10;11)(p12;q23) in
childhood acute
myeloid
leukemia
: incidence and complex mechanism.
This translocation represented 28% of all cases of
childhood
AML
treated at our center in 2004, and 63% of
AML
with rearrangements of 11q23.
The median event-free survival of patients was 8.1 months, and we conclude that the t(10;11)(p12;q23) is associated with unfavorable prognosis in
childhood acute
myeloid
leukemia
.
[MeSH-major]
Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11.
Leukemia
,
Myeloid
/ genetics. Translocation, Genetic
[MeSH-minor]
Acute
Disease. Adolescent.
Child
.
Child
, Preschool. Chromosome Banding. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Karyotyping. Male. Reverse Transcriptase Polymerase Chain Reaction
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.
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(PMID = 16938568.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
74.
Lin CH, Hung GY, Chang CY, Chien JC:
Subdural hemorrhage in a child with acute promyelocytic leukemia presenting as subtle headache.
J Chin Med Assoc
; 2005 Sep;68(9):437-40
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[Title]
Subdural hemorrhage in a
child
with
acute
promyelocytic
leukemia
presenting as subtle headache.
Acute
promyelocytic
leukemia
(APL) is a distinct subtype of
acute
myeloid
leukemia
(
AML
) and is rare in children (< 10% of
childhood
AML
).
We report a 12-year-old
child
with APL who suffered a subdural hemorrhage and initially presented with a subtle headache mistaken as the side effect of all-trans-retinoic acid (ATRA).
Blood component therapy and a
pediatric
dosage of ATRA (25 mg/m2/day) combined with idarubicin as induction chemotherapy were administered in the first week, but the bleeding diathesis persisted and DIC profiles showed no improvement.
This case suggests that the ATRA dosage for
pediatric
APL patients must be modified according to clinical condition.
[MeSH-major]
Headache / etiology. Hematoma, Subdural / etiology.
Leukemia
, Promyelocytic,
Acute
/ complications
[MeSH-minor]
Child
. Disseminated Intravascular Coagulation / complications. Humans. Male. Partial Thromboplastin Time. Prothrombin Time. Tretinoin / adverse effects
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.
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.
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ALL-TRANS-RETINOIC ACID
.
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(PMID = 16187602.001).
[ISSN]
1726-4901
[Journal-full-title]
Journal of the Chinese Medical Association : JCMA
[ISO-abbreviation]
J Chin Med Assoc
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
China (Republic : 1949- )
[Chemical-registry-number]
5688UTC01R / Tretinoin
75.
Liang DC, Shih LY, Huang CF, Hung IJ, Yang CP, Liu HC, Jaing TH, Wang LY, Chang WH:
CEBPalpha mutations in childhood acute myeloid leukemia.
Leukemia
; 2005 Mar;19(3):410-4
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[Title]
CEBPalpha mutations in
childhood acute
myeloid
leukemia
.
CEBPalpha: mutations have been described in adult
acute
myeloid
leukemia
(
AML
) and conferred a favorable prognosis.
We investigated 117 children with de novo
AML
using DNA PCR assay followed by sequencing for each PCR product.
Our results showed that CEBPalpha mutations occurred in 6% of
childhood
AML
and most exhibited combined mutations in both N-terminal part and bZIP domain.
[MeSH-major]
CCAAT-Enhancer-Binding Protein-alpha / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation
[MeSH-minor]
Adolescent.
Child
.
Child
, Preschool. Clone Cells. DNA Mutational Analysis / methods. Gene Frequency. Humans. Infant. Infant, Newborn. Polymerase Chain Reaction / methods
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.
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.
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(PMID = 15618961.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / CCAAT-Enhancer-Binding Protein-alpha
76.
Abdel Rahman H, Farrag SA, El-Attar IA:
AML1/ETO Fusion Gene in de novo Pediatric Acute Myeloid Leukemia: Clinical Significance and Prognostic Implications.
J Egypt Natl Canc Inst
; 2007 Mar;19(1):39-47
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[Title]
AML1/ETO Fusion Gene in de novo
Pediatric
Acute
Myeloid
Leukemia
: Clinical Significance and Prognostic Implications.
The characterization of
leukemia
-associated chromosome translocations has contributed relevant insights into our understanding of
leukemia
pathogenesis and has provided new specific tumor markers essential in prognostic assessment and minimal residual disease studies.
The aim of this work is to study the frequency of AML1/ETO fusion gene in a series of Egyptian
childhood
AML
cases.
The clinical significance and prognostic implications of this aberration, including CR rate, duration of first CR, extramedullary
leukemia
(EML), and survival are investigated as well.
Peripheral blood and/or bone marrow mononuclear cells were available for analysis from 78 children, all newly diagnosed with
AML
.
Patients with de novo
AML
were treated by 2 courses of induction chemotherapy, followed by 4 courses of consolidation treatment if the patient achieved complete remission (CR).
Lymph nodes were enlarged in 8/15 cases (53.34%), hepatomegly was observed in 4/15 cases (26.67%), splenomegaly in 8/15 cases (53.34%), purpura in 6/15 cases (40%), while pallor was observed in all fifteen cases.Extramedullary
leukemia
occurred in 4/15 cases (26.67%).
In conclusion, we report a frequency of 19.2% of AML1/ETO fusion gene in our newly diagnosed
pediatric AML
cases.
Key Words:
Pediatric
acute
myeloid
leukemia
, AML1/ETO fusion gene , RT-PCR , Clinical outcome , Prognostic significance.
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(PMID = 18839034.001).
[ISSN]
1110-0362
[Journal-full-title]
Journal of the Egyptian National Cancer Institute
[ISO-abbreviation]
J Egypt Natl Canc Inst
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Egypt
77.
Meyer S, Barber LM, White DJ, Will AM, Birch JM, Kohler JA, Ersfeld K, Blom E, Joenje H, Eden TO, Malcolm Taylor G:
Spectrum and significance of variants and mutations in the Fanconi anaemia group G gene in children with sporadic acute myeloid leukaemia.
Br J Haematol
; 2006 May;133(3):284-92
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[Title]
Spectrum and significance of variants and mutations in the Fanconi anaemia group G gene in children with sporadic
acute
myeloid
leukaemia.
Childhood acute
myeloid
leukaemia (
AML
) is uncommon.
Children with Fanconi anaemia (FA), however, have a very high risk of developing
AML
.
To address to what extent FANCG variants contribute to sporadic
childhood
AML
, we determined the spectrum of FANCG sequence variants in 107 children diagnosed with sporadic
AML
, using polymerase chain reaction (PCR), fluorescent single-strand conformational polymorphism (SSCP) and sequencing methodologies.
R513Q, which affects a semi-conserved amino acid, was carried in two additional children with
AML
.
Although not significant, the frequency of R513Q was higher in children with
AML
than unselected cord bloods.
While FANCG mutation carrier status does not predispose to sporadic
AML
, the identification of unrecognised FA patients implies that FA presenting with primary
AML
in
childhood
is more common than suspected.
[MeSH-major]
Fanconi Anemia / complications. Fanconi Anemia Complementation Group G Protein / genetics.
Leukemia
,
Myeloid
/ genetics. Mutation
[MeSH-minor]
Acute
Disease. Adolescent. Amino Acid Sequence. Animals.
Child
.
Child
, Preschool. DNA, Neoplasm / genetics. Female. Humans. Infant. Male. Molecular Sequence Data. Polymerase Chain Reaction / methods. Polymorphism, Single-Stranded Conformational. Sequence Alignment
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(PMID = 16643430.001).
[ISSN]
0007-1048
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA, Neoplasm; 0 / Fanconi Anemia Complementation Group G Protein
78.
Meyer S, Fergusson WD, Whetton AD, Moreira-Leite F, Pepper SD, Miller C, Saunders EK, White DJ, Will AM, Eden T, Ikeda H, Ullmann R, Tuerkmen S, Gerlach A, Klopocki E, Tönnies H:
Amplification and translocation of 3q26 with overexpression of EVI1 in Fanconi anemia-derived childhood acute myeloid leukemia with biallelic FANCD1/BRCA2 disruption.
Genes Chromosomes Cancer
; 2007 Apr;46(4):359-72
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[Title]
Amplification and translocation of 3q26 with overexpression of EVI1 in Fanconi anemia-derived
childhood acute
myeloid
leukemia
with biallelic FANCD1/BRCA2 disruption.
Fanconi anemia (FA) is an inherited disease with congenital abnormalities and an extreme risk of
acute
myeloid
leukemia
(
AML
).
Genetic events occurring during malignant transformation in FA and the biology of FA-associated
AML
are poorly understood, but are often preceded by the development of chromosomal aberrations involving 3q26-29 in bone marrow of FA patients.
We report here the molecular cytogenetic characterization of FA-derived
AML
cell lines SB1685CB and SB1690CB by conventional and array comparative genomic hybridization, fluorescence in situ hybridization, and SKY.
We identified gains of a 3.7 MB chromosomal region on 3q26.2-26.31, which preceded transformation to overt
leukemia
.
Rearrangements of 3q, which are rare in
childhood
AML
, commonly result in overexpression of EVI1, which determines specific gene expression patterns and confers poor prognosis.
We detected overexpression of EVI1 in all three FA-derived
AML
.
We hypothesize that constitutional or acquired FA defects might be a common factor for the development of 3q abnormalities in
AML
.
In addition, cryptic imbalances as detected here might account for overexpression of EVI1 in
AML
without overt 3q26 rearrangements.
[MeSH-major]
BRCA2 Protein / genetics. Chromosomes, Human, Pair 3 / genetics. DNA-Binding Proteins / genetics. Fanconi Anemia / genetics. Gene Amplification.
Leukemia
,
Myeloid
/ genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
[MeSH-minor]
Acute
Disease. Cell Line.
Child
. Humans
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[Copyright]
(c) 2007 Wiley-Liss, Inc.
(PMID = 17243162.001).
[ISSN]
1045-2257
[Journal-full-title]
Genes, chromosomes & cancer
[ISO-abbreviation]
Genes Chromosomes Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / BRCA2 Protein; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Transcription Factors
79.
Yuan J, McDonough C, Kulharya A, Ramalingam P, Manaloor E:
Isolated trisomy 10 in an infant with acute myeloid leukemia: a case report and review of literature.
Int J Clin Exp Pathol
; 2010;3(7):718-22
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[Title]
Isolated trisomy 10 in an infant with
acute
myeloid
leukemia
: a case report and review of literature.
Trisomy 10 as the sole cytogenetic abnormality in
AML
is rare, with an incidence rate of < 0.5%.
It tends to affect the elderly and is extremely rare in
pediatric
patients.
Compared to the two other reported
pediatric
cases, our patient has some unique features such as much younger age and additional findings such as bilineage dysplasia and bone marrow fibrosis.
Both reported cases and our case were classified as
AML
-M2 indicating that this may be a common subtype in
pediatric
patients.
These findings suggest that isolated trisomy 10 may be associated with distinct clinicopathologic features in
pediatric AML
.
[MeSH-major]
Chromosomes, Human, Pair 10 / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ pathology. Trisomy / genetics. Trisomy / pathology
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[Cites]
Cancer Genet Cytogenet. 1999 Nov;115(1):47-51
[
10565299.001
]
[Cites]
Cancer Genet Cytogenet. 1996 Jul 15;89(2):114-7
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8697414.001
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Cancer Genet Cytogenet. 1996 Jul 15;89(2):173-4
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8697428.001
]
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Cancer Genet Cytogenet. 1998 Jan 1;100(1):84-7
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9406587.001
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Cancer Genet Cytogenet. 1998 Jun;103(2):130-2
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Cancer Genet Cytogenet. 1999 Jan 15;108(2):175
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Cancer Genet Cytogenet. 1999 Feb;109(1):88-9
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9973969.001
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Ann Genet. 1999;42(1):5-10
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10214501.001
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Int J Hematol. 2008 Jul;88(1):123-4
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18566741.001
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Clin Pediatr (Phila). 2009 May;48(4):444-8
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19224868.001
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Cancer Genet Cytogenet. 2000 Jul 15;120(2):141-3
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10942805.001
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Cancer Genet Cytogenet. 2002 Apr 1;134(1):81-3
[
11996802.001
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Leuk Res. 1990;14(6):515-23
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1695699.001
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Leuk Res. 1992 Aug;16(8):789-96
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1528067.001
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Leukemia. 1995 Jul;9(7):1167-72
[
7630192.001
]
[Cites]
Cancer Genet Cytogenet. 2000 Apr 15;118(2):148-50
[
10748296.001
]
(PMID = 20830243.001).
[ISSN]
1936-2625
[Journal-full-title]
International journal of clinical and experimental pathology
[ISO-abbreviation]
Int J Clin Exp Pathol
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2933392
[Keywords]
NOTNLM ; CD13 / CD33 / CD34 / CD7 / Trisomy 10 / acute myeloid leukemia / infant / review
80.
Zou Y, Wang H, Chen XJ, Wang SC, Zhang L, Chen YM, Zhu XF:
[Study of clinical outcome and analysis of prognosis related factor in children with acute myeloid leukemia].
Zhonghua Xue Ye Xue Za Zhi
; 2006 Sep;27(9):621-5
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[Title]
[Study of clinical outcome and analysis of prognosis related factor in children with
acute
myeloid
leukemia
].
OBJECTIVE: To analyse the clinical outcome and the prognostic factor of
childhood acute
myeloid
leukemia
(
AML
).
METHODS: Disease-free survival (DFS), event-free survival (EFS) and overall survival (OS) rates were estimated by Kaplan-Meier method and prognostic factors were evaluated by Cox regression with SPSS in 141
childhood
AML
in our hospital from August 1995 to July 2004.
The patients were divided into 2 groups:
acute
promyelocytic
leukemia
(APL) as group A and
AML
other than APL as group B.
The cumulative 5 year DFS and OS rate for group B patients were (28.4 +/- 9.0)% and (35.5 +/- 6.3)%, the 51 group A patients were (94.3 +/- 4.0)% and (81.4 +/- 5.7)%, and for total 141
AML
patients were (56.9 +/- 6.3)% and (53.3 +/- 4.8)% respectively.
Multivariate analysis demonstrated that higher bone marrow blast cell percentage at diagnosis, CR after more than one course of chemotherapy and less than six courses of consolidation chemotherapy were risk prognostic factors in
childhood
AML
other than APL (P < 0.05).
CONCLUSION: The prognosis of
childhood
APL is better, while of
childhood
t(8;21)
AML
is no better than other FAB subtypes.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ therapy
[MeSH-minor]
Adolescent. Bone Marrow Cells / cytology.
Child
.
Child
, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Prognosis. Regression Analysis. Retrospective Studies. Treatment Outcome
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(PMID = 17278430.001).
[ISSN]
0253-2727
[Journal-full-title]
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
[ISO-abbreviation]
Zhonghua Xue Ye Xue Za Zhi
[Language]
chi
[Publication-type]
Controlled Clinical Trial; English Abstract; Journal Article
[Publication-country]
China
81.
Kar B, Nandhini B, Revathi R:
Ring chromosome 8 and trisomy 8 in a patient with acute myeloid leukemia.
Indian J Hematol Blood Transfus
; 2009 Mar;25(1):30-2
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[Title]
Ring chromosome 8 and trisomy 8 in a patient with
acute
myeloid
leukemia
.
We describe a
child
with
Acute
Myeloid
Leukemia
(
AML
M7) with trisomy 8 and ring chromosome 8.
Ring chromosome 8 associated with
AML
is uncommon and is reported to have a poor outcome.
Bone marrow aspirate confirmed the presence of
myeloid
blasts positive only for CD 41 and CD 61 on flow cytometry.
The
child
was treated as per UK MRC
AML
protocol (ADE 10+3+5).
Cytogenetic sub grouping in
AML
patients provides guidelines for the choice of optimal treatment strategy.
She developed
acute
myelofibrosis soon after the second cycle of chemotherapy with swinging fever and rapidly enlarging spleen.
This case illustrates the poor outcome in paediatric
AML
with trisomy and ring chromosome 8.
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[Cites]
Hematol Pathol. 1992;6(3):161-7
[
1429344.001
]
[Cites]
Cancer Genet Cytogenet. 1992 May;60(1):53-9
[
1591707.001
]
[Cites]
Cancer Genet Cytogenet. 1991 Nov;57(1):79-85
[
1756488.001
]
[Cites]
Am J Hematol. 1997 Dec;56(4):224-9
[
9395183.001
]
[Cites]
Leukemia. 1996 Dec;10(12):1883-90
[
8946926.001
]
[Cites]
Cancer Genet Cytogenet. 1994 Dec;78(2):181-8
[
7828151.001
]
[Cites]
Eur J Haematol. 1988 Oct;41(4):341-6
[
3197821.001
]
(PMID = 23100969.001).
[ISSN]
0971-4502
[Journal-full-title]
Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
[ISO-abbreviation]
Indian J Hematol Blood Transfus
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Other-IDs]
NLM/ PMC3453485
[Keywords]
NOTNLM ; Acute myeloid leukemia / Ring chromosome 8 / Trisomy 8
82.
Tan RM, Quah TC, Aung L, Liang S, Kirk RC, Yeoh AE:
Improved outcome in childhood acute myeloid leukemia in Singapore with the MRC AML 10 protocol.
Pediatr Blood Cancer
; 2007 Mar;48(3):262-7
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[Title]
Improved outcome in
childhood acute
myeloid
leukemia
in Singapore with the MRC
AML
10 protocol.
BACKGROUND: The introduction of the United Kingdom Medical Research Council's 10th
AML
trial (MRC
AML
10) protocol incorporating high-dose anthracycline therapy has improved outcome of children with
acute
myeloid
leukemia
(
AML
).
In this study, we review the results of
childhood
AML
therapy in a Singapore university hospital over the last 17 years emphasizing toxicity and outcome.
PROCEDURE: Retrospective analysis revealed 34 children with
AML
between 1988 and 2003.
From September 1996, all but one of 15 children received MRC
AML
10 treatment.
MRC
AML
10-treated patients (n = 14) had significantly better 3-year overall, event-free, and disease-free survival (74% vs. 35%, 77% vs. 20%, 83% vs. 31%; P = 0.019, P = 0.002, and P = 0.010, respectively) and were likelier to achieve complete remission (CR) than non-MRC
AML
10 patients (P = 0.102).
Among patients who achieved CR, MRC
AML
10-treated patients were significantly more likely to achieve CR after only one cycle of chemotherapy (P = 0.016).
CONCLUSIONS: These findings suggest that MRC
AML
10 treatment results in significantly superior survival, without excess toxicity.
Future studies should attempt to elucidate the relative importance of individual MRC
AML
10 components and reduce the high cumulative anthracycline dose without compromising outcome.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Myeloid
/ drug therapy
[MeSH-minor]
6-Mercaptopurine / administration & dosage. 6-Mercaptopurine / adverse effects.
Acute
Disease. Amsacrine / administration & dosage. Amsacrine / adverse effects. Azacitidine / administration & dosage. Azacitidine / adverse effects.
Child
.
Child
, Preschool. Cytarabine / administration & dosage. Cytarabine / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Developing Countries. Disease-Free Survival. Drug Evaluation. Drug-Induced Liver Injury / etiology. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Gastrointestinal Diseases / chemically induced. Heart Diseases / chemically induced. Hematologic Diseases / chemically induced. Humans. Infant. Infection / etiology. Kaplan-Meier Estimate. Male. Methotrexate / administration & dosage. Methotrexate / adverse effects. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Prednisone / administration & dosage. Prednisone / adverse effects. Remission Induction. Retrospective Studies. Singapore / epidemiology. Survival Analysis. Thioguanine / administration & dosage. Thioguanine / adverse effects. Treatment Outcome. Vincristine / administration & dosage. Vincristine / adverse effects
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CYTARABINE
.
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THIOGUANINE
.
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DAUNORUBICIN
.
Hazardous Substances Data Bank.
AZACITIDINE
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
Hazardous Substances Data Bank.
MERCAPTOPURINE
.
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.
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.
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.
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METHOTREXATE
.
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.
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[Copyright]
(c) 2006 Wiley-Liss, Inc.
(PMID = 16602120.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
00DPD30SOY / Amsacrine; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; E7WED276I5 / 6-Mercaptopurine; FTK8U1GZNX / Thioguanine; M801H13NRU / Azacitidine; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; MRC AML 10 protocol; POG-8498 protocol
83.
La Spina M, Russo G:
Presentation of childhood acute myeloid leukemia with erythema nodosum.
J Clin Oncol
; 2007 Sep 1;25(25):4011-2
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[Title]
Presentation of
childhood acute
myeloid
leukemia
with erythema nodosum.
[MeSH-major]
Erythema Nodosum / etiology. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / complications. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / diagnosis
[MeSH-minor]
Bone Marrow / pathology.
Child
, Preschool. Female. Humans. Physical Examination
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(PMID = 17761986.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
84.
Rogers PC, Meacham LR, Oeffinger KC, Henry DW, Lange BJ:
Obesity in pediatric oncology.
Pediatr Blood Cancer
; 2005 Dec;45(7):881-91
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[Title]
Obesity in
pediatric
oncology.
Its influences on outcomes of
childhood
cancer are unknown.
A recent Children's Oncology Group symposium considered epidemiology of obesity, pharmacology of chemotherapy and outcomes in obese adults with cancer, excess mortality in obese
pediatric
patients with
acute
myeloid
leukemia
(
AML
), and complications in obese survivors.
In the US, obesity prevalence (BMI > 95th centile) is increasing in all
pediatric
age groups and accelerating fastest among black and Hispanic adolescents.
In
pediatric
acute myeloblastic leukemia
, obese patients have greater treatment-related mortality (TRM), similar toxicity and relapse rates, and inferior survival compared with patients who are not obese.
An excess of female survivors of
childhood leukemia
who received cranial irradiation are obese.
Ongoing treatment effects of
childhood
cancer may predispose to a sedentary lifestyle.
These findings call for measures to prevent obesity, retrospective and prospective studies of chemotherapy pharmacology of analyzed according to BMI and outcomes, additional studies of the obesity impact on outcomes in
pediatric
cancer, and promotion of a healthy lifestyle among survivors.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
. Obesity. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma
[MeSH-minor]
Adolescent. Adult. Age Factors. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Body Mass Index. Bone Marrow Transplantation.
Child
.
Child
, Preschool. Female. Humans. Life Style. Male. Recurrence. Treatment Outcome
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.
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.
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[Copyright]
2005 Wiley-Liss, Inc.
(PMID = 16035086.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA 100474-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
81
85.
Haltrich I, Kost-Alimova M, Kovács G, Klein G, Fekete G, Imreh S:
Multipoint interphase FISH analysis of chromosome 3 abnormalities in 28 childhood AML patients.
Eur J Haematol
; 2006 Feb;76(2):124-33
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[Title]
Multipoint interphase FISH analysis of chromosome 3 abnormalities in 28
childhood
AML
patients.
To examine chromosome 3 abnormalities, in 28
childhood acute
myeloid
leukemia
bone marrow samples, we performed interphase multipoint-fluorescence in situ hybridization using 84 chromosome 3-specific probes and detected clonal chromosome 3 aberrations in nine cases, which is of a higher frequency than the previously reported one.
We identified rare structural rearrangements in
childhood acute myeloblastic leukemia
, involving 3q21 and 3q26 loci around RPN1 and MDS1/EVI1 respectively.
The poor outcome in
pediatric
patients with 3q rearrangements appears to be quite uniform.
[MeSH-major]
Chromosome Aberrations. Chromosomes, Human, Pair 3. In Situ Hybridization, Fluorescence / methods. Interphase.
Leukemia
,
Myeloid
/ genetics
[MeSH-minor]
Acute
Disease. Adolescent.
Child
.
Child
, Preschool. Female. Humans. Infant. Male
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(PMID = 16405433.001).
[ISSN]
0902-4441
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
86.
Liang DC, Chan TT, Lin KH, Lin DT, Lu MY, Chen SH, Liu HC, Lin MT, Lee MT, Shu SG, Chang TK, Chen JS, Hsiao CC, Hung IJ, Hsieh YL, Chen RL, Cheng SN, Chang WH, Lee CH, Lin KS:
Improved treatment results for childhood acute myeloid leukemia in Taiwan.
Leukemia
; 2006 Jan;20(1):136-41
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[Title]
Improved treatment results for
childhood acute
myeloid
leukemia
in Taiwan.
To improve treatment results for children with de novo
acute
myeloid
leukemia
(
AML
), we introduced a novel protocol, Taiwan
Pediatric
Oncology Group-
AML
-97A, for
AML
other than
acute
promyelocytic
leukemia
(APL), for which modified conventional protocols were used.
From January 1, 1997, to December 31, 2002, 141 children younger than 17 years old with de novo
AML
were enrolled.
In total, 117 patients with non-APL
AML
were treated with induction therapy of idarubicin and cytarabine (Ara-C), postremission therapy with high-dose Ara-C - containing regimens for four monthly courses, and moderate-dose therapy with idarubicin and Ara-C for four monthly courses.
The remission rate in the
AML
-97A study was 90%, the 5-year survival 51 +/- 5.3% (s.e.) and the 5-year event-free survival 50 +/- 4.8%; for APL, these were 100%, 86 +/- 7.0, and 75 +/- 9.8%.
The
AML
-97A regimen was well tolerated.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ therapy.
Leukemia
, Promyelocytic,
Acute
/ therapy. Stem Cell Transplantation
[MeSH-minor]
Adolescent.
Child
.
Child
, Preschool. Disease-Free Survival. Female. Follow-Up Studies. Humans. Infant. Infant, Newborn. Male. Remission Induction. Taiwan. Treatment Outcome
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(PMID = 16281075.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
87.
Shih LY, Liang DC, Fu JF, Wu JH, Wang PN, Lin TL, Dunn P, Kuo MC, Tang TC, Lin TH, Lai CL:
Characterization of fusion partner genes in 114 patients with de novo acute myeloid leukemia and MLL rearrangement.
Leukemia
; 2006 Feb;20(2):218-23
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[Title]
Characterization of fusion partner genes in 114 patients with de novo
acute
myeloid
leukemia
and MLL rearrangement.
The fusion transcripts of MLL rearrangement [MLL(+)] in
acute
myeloid
leukemia
(
AML
) and their clinicohematologic correlation have not be well characterized in the previous studies.
We used Southern blot analysis to screen MLL(+) in de novo
AML
.
MLL(+) was identified in 114 (98 adults) of 988
AML
patients.
MLL-PTD was rare in
childhood
AML
.
[MeSH-major]
Leukemia
,
Myeloid
/ genetics.
Myeloid
-Lymphoid
Leukemia
Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic / genetics
[MeSH-minor]
Acute
Disease. Adolescent. Adult. Aged. Aged, 80 and over.
Child
, Preschool. Female. Gene Duplication. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Middle Aged. Prospective Studies. Survival Rate. Treatment Outcome
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(PMID = 16341046.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
88.
Sánchez-Medina J, Gonzalez-Ramella O, Gallegos-Castorena S:
The effect of dexrazoxane for clinical and subclinical cardiotoxicity in children with acute myeloid leukemia.
J Pediatr Hematol Oncol
; 2010 May;32(4):294-7
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[Title]
The effect of dexrazoxane for clinical and subclinical cardiotoxicity in children with
acute
myeloid
leukemia
.
Most
acute
myeloid
leukemia
(
AML
) protocols use anthracyclines.
Fifty
pediatric AML
patients were treated with a Medical Research Council
AML
10 modified protocol with dexrazoxane previous to any anthracycline dose.
The event-free survival was 53%, 15.7% died of disease, and 11.8% died free of
leukemia
.
[MeSH-major]
Anthracyclines / adverse effects. Cardiovascular Agents / therapeutic use. Heart Diseases / chemically induced.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Razoxane / therapeutic use
[MeSH-minor]
Adolescent.
Child
.
Child
, Preschool. Female. Follow-Up Studies. Humans. Infant. Male. Prospective Studies. Survival Rate. Treatment Outcome
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(PMID = 20404753.001).
[ISSN]
1536-3678
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Anthracyclines; 0 / Cardiovascular Agents; 5AR83PR647 / Razoxane
89.
Meshinchi S, Arceci RJ:
Prognostic factors and risk-based therapy in pediatric acute myeloid leukemia.
Oncologist
; 2007 Mar;12(3):341-55
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[Title]
Prognostic factors and risk-based therapy in
pediatric
acute
myeloid
leukemia
.
Acute
myeloid
leukemia
(
AML
) has posed significant therapeutic challenges to
pediatric
oncologists.
Despite intensive therapy, half of the children with
AML
relapse and die from their disease.
Efforts to identify risk factors in
AML
are directed toward defining populations who may benefit from alternative therapies.
Management of high-risk patients may prove more difficult, as the nearly myeloablative nature of
AML
therapy leaves little room for therapy escalation short of stem cell transplantation.
This review evaluates prognostic factors in
pediatric AML
and discusses the feasibility of using these factors in risk-adapted therapy regimens.
[MeSH-major]
Leukemia
,
Myeloid
/ therapy
[MeSH-minor]
Acute
Disease. Antineoplastic Agents / therapeutic use.
Child
. Humans. Neoplasm Recurrence, Local. Prognosis. Risk Assessment. Risk Factors. Stem Cell Transplantation
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(PMID = 17405900.001).
[ISSN]
1083-7159
[Journal-full-title]
The oncologist
[ISO-abbreviation]
Oncologist
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents
[Number-of-references]
133
90.
Ünal E, Sahdev I:
Use of gemtuzumab ozogamicin in the treatment of pediatric relapsed/ refractory Acute Myeloid Leukemia.
Turk J Haematol
; 2008 Mar 5;25(1):36-41
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[Title]
Use of gemtuzumab ozogamicin in the treatment of
pediatric
relapsed/ refractory
Acute
Myeloid
Leukemia
.
[Transliterated title]
Pediatrik relaps/refraktor akut
myeloid
lösemi tedavisinde gemtuzumab ozogamisin kullanımı.
Gemtuzumab ozogamicin (GO, MylotargTM) is an antibody-targeted chemotherapy agent that has been studied in
acute
myeloid
leukemia
(
AML
) at first relapse in adults.
There is limited experience in
pediatric
patients.
We report six patients with refractory/relapsed CD33+
AML
who were treated with GO on compassionate-use basis.
GO should be used cautiously in chemotherapy-refractory
AML pediatric
patients due to the high incidence of VOD.
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(PMID = 27264148.001).
[ISSN]
1300-7777
[Journal-full-title]
Turkish journal of haematology : official journal of Turkish Society of Haematology
[ISO-abbreviation]
Turk J Haematol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Turkey
91.
Gesundheit B, Shapira MY, Resnick IB, Amar A, Kristt D, Dray L, Budowski E, Or R:
Successful cell-mediated cytokine-activated immunotherapy for relapsed acute myeloid leukemia after hematopoietic stem cell transplantation.
Am J Hematol
; 2009 Mar;84(3):188-90
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[Title]
Successful cell-mediated cytokine-activated immunotherapy for relapsed
acute
myeloid
leukemia
after hematopoietic stem cell transplantation.
Acute
myeloid
leukemia
(
AML
) is an extremely aggressive disease with a high relapse rate even after allogeneic hematopoietic stem cell transplantation (HSCT).
We report the successful outcome of cell-mediated cytokine-activated immunotherapy in a high-risk
pediatric AML
patient who relapsed shortly after allogeneic HSCT.
Donor lymphocyte infusion along with interferon induced a graft-versus-
leukemia
effect, presenting as a reversible episode of graft-versus-host disease, which led to stable complete donor chimerism and total eradication of
AML
for over 24 months, at the time of this report.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ immunology.
Leukemia
,
Myeloid
,
Acute
/ therapy. Lymphocyte Transfusion. Neoplasm Recurrence, Local / immunology. Neoplasm Recurrence, Local / therapy
[MeSH-minor]
Child
. Graft vs Host Disease. Graft vs
Leukemia
Effect. Hematopoietic Stem Cell Transplantation. Humans. Immunologic Factors / administration & dosage. Immunotherapy. Interferon-alpha / administration & dosage. Male. Recombinant Proteins
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(PMID = 19105234.001).
[ISSN]
1096-8652
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Immunologic Factors; 0 / Interferon-alpha; 0 / Recombinant Proteins; 76543-88-9 / interferon alfa-2a
92.
Lafiura KM, Bielawski DM, Posecion NC Jr, Ostrea EM Jr, Matherly LH, Taub JW, Ge Y:
Association between prenatal pesticide exposures and the generation of leukemia-associated T(8;21).
Pediatr Blood Cancer
; 2007 Oct 15;49(5):624-8
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[Title]
Association between prenatal pesticide exposures and the generation of
leukemia
-associated T(8;21).
BACKGROUND: This study was designed to investigate the relationship between prenatal pesticide exposures and the generation of
leukemia
-associated t(8;21)(q22;q22), one of the most common cytogenetic abnormalities in
childhood acute
myeloid
leukemia
(
AML
).
Similar heterogeneity in the fusion transcripts was detected in the t(8;21) positive cord blood samples as in our previous study with t(8;21)
AML
patients.
They suggest that prenatal pesticide exposures may be causal factors for the generation of
leukemia
-associated chromosomal translocations.
[MeSH-major]
Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8.
Leukemia
/ etiology. Propoxur / analysis. Translocation, Genetic
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[Copyright]
(c) 2007 Wiley-Liss, Inc.
[CommentIn]
Pediatr Blood Cancer. 2007 Oct 15;49(5):607-8
[
17712841.001
]
(PMID = 17610268.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA92308; United States / NICHD NIH HHS / HD / HD039428
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Pesticides; BFH029TL73 / Propoxur
93.
de Jonge HJ, Weidenaar AC, Ter Elst A, Boezen HM, Scherpen FJ, Bouma-Ter Steege JC, Kaspers GJ, Goemans BF, Creutzig U, Zimmermann M, Kamps WA, de Bont ES:
Endogenous vascular endothelial growth factor-C expression is associated with decreased drug responsiveness in childhood acute myeloid leukemia.
Clin Cancer Res
; 2008 Feb 1;14(3):924-30
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[Title]
Endogenous vascular endothelial growth factor-C expression is associated with decreased drug responsiveness in
childhood acute
myeloid
leukemia
.
PURPOSE: We hypothesized that downstream effects of endogenous vascular endothelial growth factor (VEGF)/VEGF receptor signaling on
acute
myelogenous
leukemia
(
AML
) cell survival resulted in increased in vitro cellular drug resistance and a longer time to kill most leukemic cells in vivo upon drug exposure.
EXPERIMENTAL DESIGN: In primary
AML
cells from
pediatric
patients, VEGFA and VEGFC mRNA expression and in vitro cellular resistance to nine cytotoxic drugs were studied.
As in vivo equivalents for in vitro drug resistance, in vivo
AML
blast reduction upon drug exposure, measured as blast cell reduction on day 15 in the bone marrow and as time in days from diagnosis to complete remission (CR) were used.
RESULTS: Increased endogenous VEGFC levels significantly correlated with increased in vitro resistance for six typical
AML
drugs in primary
AML
cells from
pediatric
patients.
CONCLUSIONS: These results suggest for the first time that higher endogenous VEGFC levels of
AML
cells are related to decreased in vitro and in vivo drug responsiveness.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics. Vascular Endothelial Growth Factor C / genetics
[MeSH-minor]
Adolescent. Adult. Antineoplastic Agents / therapeutic use.
Child
.
Child
, Preschool. Female. Humans. Infant. Karyotyping. Male. RNA, Messenger / genetics. Risk Assessment. Treatment Outcome. Vascular Endothelial Growth Factor A / genetics
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(PMID = 18245556.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C
94.
Abdelhaleem M:
Frequent but nonrandom expression of lymphoid markers on de novo childhood acute myeloid leukemia.
Exp Mol Pathol
; 2007 Oct;83(2):259-63
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[Title]
Frequent but nonrandom expression of lymphoid markers on de novo
childhood acute
myeloid
leukemia
.
Lymphoid marker expression in 59 cases of de novo
childhood acute
myeloid
leukemia
(
AML
) was as follows: CD2 (15.5%), CD4 (73.8%), CD7 (25.8%), CD19 (22%) and CD56 (28.9%).
Individual marker expression, as well as co-expression with other lymphoid markers, could be correlated with the FAB subtype of
leukemia
and the presence and type of certain
leukemia
fusion gene transcripts.
The data showed that the expression of lymphoid markers in
childhood
de novo
AML
was common but nonrandom and was likely a reflection of the biological differences between various types of
leukemia
.
[MeSH-major]
Antigens, CD / genetics.
Leukemia
,
Myeloid
/ pathology. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / pathology
[MeSH-minor]
Antigens, CD19 / genetics. Antigens, CD2 / genetics. Antigens, CD4 / genetics. Antigens, CD56 / genetics. Antigens, CD7 / genetics.
Child
. Gene Expression Regulation, Neoplastic. Humans
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(PMID = 17662713.001).
[ISSN]
0014-4800
[Journal-full-title]
Experimental and molecular pathology
[ISO-abbreviation]
Exp. Mol. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD19; 0 / Antigens, CD2; 0 / Antigens, CD4; 0 / Antigens, CD56; 0 / Antigens, CD7
95.
Cheng J, Sakamot KM:
Topics in pediatric leukemia--acute myeloid leukemia.
MedGenMed
; 2005;7(1):20
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[Title]
Topics in
pediatric
leukemia
--
acute
myeloid
leukemia
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ diagnosis.
Leukemia
,
Myeloid
,
Acute
/ therapy
[MeSH-minor]
Acute
Disease.
Child
. Humans
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[ISSN]
1531-0132
[Journal-full-title]
MedGenMed : Medscape general medicine
[ISO-abbreviation]
MedGenMed
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
29
[Other-IDs]
NLM/ PMC1681379
96.
Jain M, Bakhshi S, Shukla AA, Chauhan SS:
Cathepsins B and L in peripheral blood mononuclear cells of pediatric acute myeloid leukemia: potential poor prognostic markers.
Ann Hematol
; 2010 Dec;89(12):1223-32
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[Title]
Cathepsins B and L in peripheral blood mononuclear cells of
pediatric
acute
myeloid
leukemia
: potential poor prognostic markers.
However, their significance in
acute
leukemias is lacking.
This study was planned to investigate expression and significance of these proteases in peripheral blood mononuclear cells (PBMCs) of patients with
pediatric
acute
myeloid
leukemia
(
AML
).
CTSL and CTSB activities were assayed in PBMCs of 24 children with
AML
and ten healthy controls by spectrofluorimetry.
CTSL and CTSB protease activity and their mRNA expression were significantly higher in
AML
patients compared to controls (p ≤ 0.001).
Cystatin expression though significantly high (p ≤ 0.001) in
AML
was negatively correlated with CTSL (r = -0.920; p ≤ 0.001) and CTSB (r = -0.580, p ≤ 0.001) expression.
AML
patients with higher CTSL and CTSB activity exhibited an inferior EFS (CTSL: p = 0.045; CTSB: p = 0.002) and overall survival (OS; CTSL: p = 0.05; CTSB: p = 0.004) compared to patients with lower levels of these proteases.
This is the first report demonstrating increased expression of CTSL and CTSB in
AML
, mechanism of their increased expression in relation to VEGF, and their association with poor EFS and OS.
[MeSH-major]
Cathepsin B / metabolism. Cathepsin L / metabolism.
Leukemia
,
Myeloid
/ enzymology. Leukocytes, Mononuclear / enzymology
[MeSH-minor]
Acute
Disease. Adolescent. Biomarkers, Tumor / blood. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism.
Child
.
Child
, Preschool. Cystatin C / genetics. Female. Gene Expression Regulation, Leukemic. Humans. Infant. Kaplan-Meier Estimate. Male. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Vascular Endothelial Growth Factor A / genetics
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(PMID = 20567828.001).
[ISSN]
1432-0584
[Journal-full-title]
Annals of hematology
[ISO-abbreviation]
Ann. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Cystatin C; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 3.4.22.1 / Cathepsin B; EC 3.4.22.15 / Cathepsin L
97.
Horan JT, Alonzo TA, Lyman GH, Gerbing RB, Lange BJ, Ravindranath Y, Becton D, Smith FO, Woods WG, Children's Oncology Group:
Impact of disease risk on efficacy of matched related bone marrow transplantation for pediatric acute myeloid leukemia: the Children's Oncology Group.
J Clin Oncol
; 2008 Dec 10;26(35):5797-801
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[Title]
Impact of disease risk on efficacy of matched related bone marrow transplantation for
pediatric
acute
myeloid
leukemia
: the Children's Oncology Group.
PURPOSE: There is considerable variation in the use of HLA-matched related bone marrow transplantation (BMT) for the treatment of
pediatric
patients with newly diagnosed
acute
myeloid
leukemia
(
AML
).
METHODS: We combined data from four cooperative group clinical trials:
Pediatric
Oncology Group 8821, Children's Cancer Group (CCG) 2891, CCG 2961, and Medical Research Council 10.
RESULTS: The data set included 1,373
pediatric