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Hjalgrim, L.L.; Rostgaard, K.; Schmiegelow, K.; Soderhall, S.; Kolmannskog, S.; Vettenranta, K.; Kristinsson, J.; Clausen, N.; Melbye, M.; Hjalgrim, H.; Gustafsson, G. |
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Title |
Age- and sex-specific incidence of childhood leukemia by immunophenotype in the Nordic countries |
Type |
Journal Article |
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Year |
2003 |
Publication |
Journal of the National Cancer Institute |
Abbreviated Journal |
J Natl Cancer Inst |
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Volume |
95 |
Issue |
20 |
Pages |
1539-1544 |
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Keywords |
Adolescent; Age Distribution; Child; Child, Preschool; Female; Finland/epidemiology; Humans; Iceland/epidemiology; Immunophenotyping; Incidence; Infant; Infant, Newborn; Leukemia, Myeloid, Acute/*epidemiology/genetics; Male; Poisson Distribution; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*epidemiology/genetics; Scandinavia/epidemiology; Sex Distribution |
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Abstract |
BACKGROUND: Studies from various countries have found an increasing incidence of childhood leukemia in recent decades. To characterize time trends in the age- and sex-specific incidence of childhood acute leukemia during the last 20 years in the Nordic countries, we analyzed a large set of population-based data from the Nordic Society of Paediatric Haematology and Oncology (NOPHO) in their acute leukemia database covering a population of approximately 5 million children aged 0-14 years. METHODS: Temporal trends in acute myeloid leukemia and acute lymphoblastic leukemia incidence rates overall and for acute lymphoblastic leukemia immunophenotypes and for specific age groups were analyzed by Poisson regression adjusting for age, sex, and country. All statistical tests were two-sided. RESULTS: We identified 1595 girls and 1859 boys diagnosed with acute lymphoblastic leukemia between January 1, 1982, and December 31, 2001, and 260 girls and 224 boys diagnosed with de novo acute myeloid leukemia between January 1, 1985, and December 31, 2001. No statistically significant change was seen in the overall incidence rate for acute lymphoblastic leukemia during the 20-year study (annual change = 0.22%, 95% confidence interval [CI] = -0.36% to 0.80%). The incidence rate of B-precursor acute lymphoblastic leukemia remained unchanged (annual change = 0.30%, 95% CI = -0.57% to 1.18%) from January 1, 1986, through December 31, 2001. A somewhat lower incidence in the first years of the study period indicated an early increasing incidence of B-precursor acute lymphoblastic leukemia that corresponded to a simultaneous decreasing incidence of unclassified acute lymphoblastic leukemia. Incidences of T-cell acute lymphoblastic leukemia (annual change = 1.55%, 95% CI = -1.14% to 4.31%) and acute myeloid leukemia (annual change = 0.58%, 95% CI = -1.24% to 2.44%) were stable during the study period. CONCLUSION: Incidences of acute myeloid leukemia overall, acute lymphoblastic leukemia overall, and specific acute lymphoblastic leukemia immunophenotypes have been stable in the Nordic countries over the past two decades. |
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Department of Epidemiology Research, Danish Epidemiology Science Centre, Statens Serum Institut, Copenhagen, Denmark. lih@ssi.dk |
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0027-8874 |
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WP9 Epidemiology |
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PMID:14559876 |
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Call Number |
CBM.UAM @ ccobaleda @ |
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35 |
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Author |
Hosking, F.J.; Papaemmanuil, E.; Sheridan, E.; Kinsey, S.E.; Lightfoot, T.; Roman, E.; Irving, J.A.E.; Allan, J.M.; Taylor, M.; Tomlinson, I.P.; Greaves, M.; Houlston, R.S. |
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Title |
Genome-wide homozygosity signatures and childhood acute lymphoblastic leukemia risk |
Type |
Journal Article |
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Year |
2010 |
Publication |
Blood |
Abbreviated Journal |
Blood |
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Volume |
115 |
Issue |
22 |
Pages |
4472-4477 |
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Keywords |
Case-Control Studies; Child; Child, Preschool; Chromosome Mapping; European Continental Ancestry Group/genetics; Female; Genes, Recessive; Genome-Wide Association Study; Great Britain; *Homozygote; Humans; Infant; Male; Polymorphism, Single Nucleotide; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/*genetics; Receptors, Erythropoietin/genetics; Risk Factors |
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Abstract |
Recent studies have reported that regions of homozygosity (ROH) in the genome are detectable in outbred populations and can be associated with an increased risk of malignancy. To examine whether homozygosity is associated with an increased risk of developing childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL), we analyzed 824 ALL cases and 2398 controls genotyped for 292 200 tagging SNPs. Across the genome, cumulative distribution of ROH was not significantly different between cases and controls. Four common ROH at 10p11.2-10q11.21, 1p31.1, 19p13.2-3, and 20q11.1-23 were, however, associated with ALL risk at P less than .01 (including 1 ROH to which the erythropoietin receptor [EPOR] gene maps, P = .005) but were nonsignificant after adjusting for multiple testing. Our findings make it unlikely that levels of measured homozygosity, caused by autozygosity, uniparental isodisomy, or hemizygosity, play a major role in defining BCP-ALL risk in predominantly outbred populations. |
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Section of Cancer Genetics, Institute of Cancer Research, Sutton, Surrey, United Kingdom |
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0006-4971 |
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WP6 In vivo |
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PMID:20231427 |
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CBM.UAM @ ccobaleda @ |
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36 |
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Lausten-Thomsen, U.; Madsen, H.O.; Vestergaard, T.R.; Hjalgrim, H.; Nersting, J.; Schmiegelow, K. |
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Title |
Prevalence of t(12;21)[ETV6-RUNX1]-positive cells in healthy neonates |
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Journal Article |
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Year |
2011 |
Publication |
Blood |
Abbreviated Journal |
Blood |
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117 |
Issue |
1 |
Pages |
186-189 |
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Keywords |
Adult; Chromosomes, Human, Pair 12/*genetics; Chromosomes, Human, Pair 21/*genetics; Cross-Sectional Studies; Female; Fetal Blood/cytology/*metabolism; Humans; Infant; Infant, Newborn; Oncogene Proteins, Fusion/*genetics; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*diagnosis/genetics; Prognosis; Sensitivity and Specificity; Translocation, Genetic/*genetics |
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t(12;21)(p13;q22)[ETV6-RUNX1] is the most common chromosomal translocation in childhood acute lymphoblastic leukemia, and it can often be backtracked to Guthrie cards supporting prenatal initiation and high levels of circulating t(12;21)-positive cells at birth. To explore the prevalence of ETV6-RUNX1-positive cells in healthy neonates, mononuclear cells from 1417 umbilical cord blood samples were isolated within 24 hours from birth and subsequently screened for ETV6-RUNX1 transcripts using a highly sensitive real-time reverse transcription polymerase chain reaction assay. In first-run polymerase chain reaction, 14 samples were positive at levels below 10(-5), of which specific hybridization reflecting the relevant genetic region was positive in 9 cases. Repeated analyses using stored mRNA and flowcytometric sorting of a CD19(+), CD8(+), and CD19(-)/CD8(-) subpopulations from cryopreserved mononuclear cells from the same cord blood samples (mean sorted: 18 x 10(6) cells) revealed no positive findings, which demonstrates that the level and/or frequency of ETV6-RUNX1-positive cells is markedly lower than suggested in previous studies. |
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Department of Paediatrics, The University Hospital Rigshospitalet, Copenhagen, Denmark |
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0006-4971 |
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WP6 In vivo |
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PMID:20713965 |
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CBM.UAM @ ccobaleda @ |
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37 |
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Mori, H.; Colman, S.M.; Xiao, Z.; Ford, A.M.; Healy, L.E.; Donaldson, C.; Hows, J.M.; Navarrete, C.; Greaves, M. |
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Title |
Chromosome translocations and covert leukemic clones are generated during normal fetal development |
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Journal Article |
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Year |
2002 |
Publication |
Proceedings of the National Academy of Sciences of the United States of America |
Abbreviated Journal |
Proc Natl Acad Sci U S A |
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Volume |
99 |
Issue |
12 |
Pages |
8242-8247 |
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Keywords |
Base Sequence; Core Binding Factor Alpha 2 Subunit; DNA/blood; DNA Primers; *Embryonic and Fetal Development; Fetal Blood/chemistry; Humans; In Situ Hybridization, Fluorescence; Infant, Newborn; Leukemia/embryology/*genetics; Molecular Sequence Data; Oncogene Proteins, Fusion/*genetics; Polymerase Chain Reaction; RNA, Messenger/genetics; Reverse Transcriptase Polymerase Chain Reaction; Transcription Factors/*genetics; *Translocation, Genetic |
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Studies on monozygotic twins with concordant leukemia and retrospective scrutiny of neonatal blood spots of patients with leukemia indicate that chromosomal translocations characteristic of pediatric leukemia often arise prenatally, probably as initiating events. The modest concordance rate for leukemia in identical twins ( approximately 5%), protracted latency, and transgenic modeling all suggest that additional postnatal exposure and/or genetic events are required for clinically overt leukemia development. This notion leads to the prediction that chromosome translocations, functional fusion genes, and preleukemic clones should be present in the blood of healthy newborns at a rate that is significantly greater than the cumulative risk of the corresponding leukemia. Using parallel reverse transcriptase-PCR and real-time PCR (Taqman) screening, we find that the common leukemia fusion genes, TEL-AML1 or AML1-ETO, are present in cord bloods at a frequency that is 100-fold greater than the risk of the corresponding leukemia. Single-cell analysis by cell enrichment and immunophenotype/fluorescence in situ hybridization multicolor staining confirmed the presence of translocations in restricted cell types corresponding to the B lymphoid or myeloid lineage of the leukemias that normally harbor these fusion genes. The frequency of positive cells (10(-4) to 10(-3)) indicates substantial clonal expansion of a progenitor population. These data have significant implications for the pathogenesis, natural history, and etiology of childhood leukemia. |
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Leukaemia Research Fund Centre for Cell and Molecular Biology, Institute of Cancer Research, Chester Beatty Laboratories, London SW3 6JB, UK |
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0027-8424 |
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PMID:12048236 |
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CBM.UAM @ ccobaleda @ |
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38 |
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Mullighan, C.G.; Goorha, S.; Radtke, I.; Miller, C.B.; Coustan-Smith, E.; Dalton, J.D.; Girtman, K.; Mathew, S.; Ma, J.; Pounds, S.B.; Su, X.; Pui, C.-H.; Relling, M.V.; Evans, W.E.; Shurtleff, S.A.; Downing, J.R. |
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Genome-wide analysis of genetic alterations in acute lymphoblastic leukaemia |
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Journal Article |
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2007 |
Publication |
Nature |
Abbreviated Journal |
Nature |
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446 |
Issue |
7137 |
Pages |
758-764 |
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Keywords |
Alleles; B-Cell-Specific Activator Protein/genetics; B-Lymphocytes/metabolism/pathology; Child; DNA-Binding Proteins/genetics; Gene Amplification/genetics; Genome, Human/*genetics; Genomics; Humans; Molecular Sequence Data; Mutation/*genetics; Point Mutation/genetics; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics/pathology; Sequence Deletion/genetics; Trans-Activators/genetics; Translocation, Genetic/genetics |
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Chromosomal aberrations are a hallmark of acute lymphoblastic leukaemia (ALL) but alone fail to induce leukaemia. To identify cooperating oncogenic lesions, we performed a genome-wide analysis of leukaemic cells from 242 paediatric ALL patients using high-resolution, single-nucleotide polymorphism arrays and genomic DNA sequencing. Our analyses revealed deletion, amplification, point mutation and structural rearrangement in genes encoding principal regulators of B lymphocyte development and differentiation in 40% of B-progenitor ALL cases. The PAX5 gene was the most frequent target of somatic mutation, being altered in 31.7% of cases. The identified PAX5 mutations resulted in reduced levels of PAX5 protein or the generation of hypomorphic alleles. Deletions were also detected in TCF3 (also known as E2A), EBF1, LEF1, IKZF1 (IKAROS) and IKZF3 (AIOLOS). These findings suggest that direct disruption of pathways controlling B-cell development and differentiation contributes to B-progenitor ALL pathogenesis. Moreover, these data demonstrate the power of high-resolution, genome-wide approaches to identify new molecular lesions in cancer. |
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Department of Pathology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA |
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0028-0836 |
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WP6 In vivo |
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PMID:17344859 |
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CBM.UAM @ ccobaleda @ |
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39 |
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