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Author |
Schuz, J.; Ahlbom, A. |
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Title |
Exposure to electromagnetic fields and the risk of childhood leukaemia: a review |
Type |
Journal Article |
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Year |
2008 |
Publication |
Radiation Protection Dosimetry |
Abbreviated Journal |
Radiat Prot Dosimetry |
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Volume |
132 |
Issue |
2 |
Pages |
202-211 |
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Keywords |
Body Burden; Child; *Electromagnetic Fields; Environmental Exposure/*statistics & numerical data; Humans; Incidence; Leukemia, Radiation-Induced/*epidemiology; Radiation Monitoring/statistics & numerical data; Risk Assessment/methods; Risk Factors; Young Adult |
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Abstract |
Extremely low-frequency magnetic fields have been classified as possibly carcinogenic to humans, mainly based on epidemiological studies consistently showing an association between long-term average exposures to magnetic fields above 0.3/0.4 microT and the risk of childhood leukaemia. No mechanism to explain this finding has been established and no support for a causal link emerged from experimental studies. Chance or bias cannot be ruled out with reasonable confidence as an explanation for the observed association. If the association is causal, it explains only a small fraction of childhood leukaemia cases. There were some reports of childhood leukaemia clusters in the vicinity of high-power radio and television broadcast transmitters in studies in Australia and Italy. However, recent large-scale systematic studies in Korea and Germany show no association between exposure to radio frequency electromagnetic fields emitted from broadcast towers and childhood leukaemia risk. Studies on mobile phone use and leukaemia risk in adolescents and young adults may be indicated. |
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Institute of Cancer Epidemiology, Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen, Denmark. joachim@cancer.dk |
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0144-8420 |
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Notes |
PMID:18927133 |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
45 |
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Author |
Sherborne, A.L.; Hosking, F.J.; Prasad, R.B.; Kumar, R.; Koehler, R.; Vijayakrishnan, J.; Papaemmanuil, E.; Bartram, C.R.; Stanulla, M.; Schrappe, M.; Gast, A.; Dobbins, S.E.; Ma, Y.; Sheridan, E.; Taylor, M.; Kinsey, S.E.; Lightfoot, T.; Roman, E.; Irving, J.A.E.; Allan, J.M.; Moorman, A.V.; Harrison, C.J.; Tomlinson, I.P.; Richards, S.; Zimmermann, M.; Szalai, C.; Semsei, A.F.; Erdelyi, D.J.; Krajinovic, M.; Sinnett, D.; Healy, J.; Gonzalez Neira, A.; Kawamata, N.; Ogawa, S.; Koeffler, H.P.; Hemminki, K.; Greaves, M.; Houlston, R.S. |
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Title |
Variation in CDKN2A at 9p21.3 influences childhood acute lymphoblastic leukemia risk |
Type |
Journal Article |
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Year |
2010 |
Publication |
Nature Genetics |
Abbreviated Journal |
Nat Genet |
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Volume |
42 |
Issue |
6 |
Pages |
492-494 |
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Keywords |
Case-Control Studies; *Chromosomes, Human, Pair 9; *Genes, p16; Genetic Predisposition to Disease; Genome-Wide Association Study; Humans; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics |
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Abstract |
Using data from a genome-wide association study of 907 individuals with childhood acute lymphoblastic leukemia (cases) and 2,398 controls and with validation in samples totaling 2,386 cases and 2,419 controls, we have shown that common variation at 9p21.3 (rs3731217, intron 1 of CDKN2A) influences acute lymphoblastic leukemia risk (odds ratio = 0.71, P = 3.01 x 10(-11)), irrespective of cell lineage. |
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Section of Cancer Genetics, Institute of Cancer Research, Sutton, Surrey, UK |
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ISSN |
1061-4036 |
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WP6 In vivo |
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PMID:20453839 |
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CBM.UAM @ ccobaleda @ |
Serial |
46 |
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Steliarova-Foucher, E.; Stiller, C.; Kaatsch, P.; Berrino, F.; Coebergh, J.-W.; Lacour, B.; Parkin, M. |
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Title |
Geographical patterns and time trends of cancer incidence and survival among children and adolescents in Europe since the 1970s (the ACCISproject): an epidemiological study |
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Journal Article |
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Year |
2004 |
Publication |
Lancet |
Abbreviated Journal |
Lancet |
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Volume |
364 |
Issue |
9451 |
Pages |
2097-2105 |
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Keywords |
Adolescent; Adult; Age of Onset; Child; Child, Preschool; Europe/epidemiology; Humans; Incidence; Infant; Neoplasms/*epidemiology/mortality; Registries; Survival Rate |
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Abstract |
BACKGROUND: Cancer is rare before age 20 years. We aimed to use the European database of childhood and adolescent cancer cases, within the Automated Childhood Cancer Information System project, to estimate patterns and trends of incidence and survival within Europe. METHODS: Comparable, high-quality data from 63 European population-based cancer registries consisted of 113000 tumours in children and 18243 in adolescents diagnosed in 1970-99. Incidence rates and survival were compared by region (east vs west), period, and malignant disease. FINDINGS: In the 1990s, age-standardised incidence rates were 140 per million for children (0-14 years) and 157 per million for ages 0-19 years. Over the three decades, overall incidence increased by 1.0% per year (p<0.0001) in children (increases for most tumour types), and by 1.5% (p<0.0001) in adolescents (15-19 years; notable increases were recorded for carcinomas, lymphomas, and germ-cell tumours). Overall 5-year survival for children in the 1990s was 64% in the east and 75% in the west, with differences between regions for virtually all tumour groups; 5-year survival was much the same in adolescents. Survival has improved dramatically since the 1970s in children and adolescents, more so in the west than in the east. INTERPRETATION: Our results are clear evidence of an increase of cancer incidence in childhood and adolescence during the past decades, and of an acceleration of this trend. Geographical and temporal patterns suggest areas for further study into causes of these neoplasms, as well as providing an indicator of progress of public-health policy in Europe. |
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International Agency for Research on Cancer, Lyon, France. steliarova@iarc.fr |
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ISSN |
0140-6736 |
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Area |
WP9 Epidemiology |
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Notes |
PMID:15589307 |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
47 |
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Author |
Trevino, L.R.; Yang, W.; French, D.; Hunger, S.P.; Carroll, W.L.; Devidas, M.; Willman, C.; Neale, G.; Downing, J.; Raimondi, S.C.; Pui, C.-H.; Evans, W.E.; Relling, M.V. |
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Title |
Germline genomic variants associated with childhood acute lymphoblastic leukemia |
Type |
Journal Article |
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Year |
2009 |
Publication |
Nature Genetics |
Abbreviated Journal |
Nat Genet |
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Volume |
41 |
Issue |
9 |
Pages |
1001-1005 |
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Keywords |
Alleles; Antimetabolites, Antineoplastic/metabolism/therapeutic use; Case-Control Studies; Child; Child, Preschool; Chromosomes, Human, Pair 10; Chromosomes, Human, Pair 7; Cohort Studies; DNA-Binding Proteins/genetics; Dopa Decarboxylase/genetics; European Continental Ancestry Group/genetics; Gene Dosage; Gene Expression Regulation, Neoplastic/drug effects; Gene Frequency; Genetic Predisposition to Disease; *Genetic Variation; Genome-Wide Association Study; *Germ Cells; Germ-Line Mutation; Haplotypes; Humans; Ikaros Transcription Factor/genetics; Linkage Disequilibrium; Methotrexate/metabolism/therapeutic use; Odds Ratio; Oncogene Proteins, Fusion/genetics; Polyglutamic Acid/metabolism; Polymorphism, Single Nucleotide; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*classification/drug therapy/*genetics; Probability; Reproducibility of Results; Risk Factors; Transcription Factors/genetics |
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Abstract |
Using the Affymetrix 500K Mapping array and publicly available genotypes, we identified 18 SNPs whose allele frequency differed significantly(P < 1 x 10(-5)) between pediatric acute lymphoblastic leukemia (ALL) cases (n = 317) and non-ALL controls (n = 17,958). Two SNPs in ARID5B not only differed between ALL and non-ALL groups (rs10821936, P = 1.4 x 10(-15), odds ratio (OR) = 1.91; rs10994982, P = 5.7 x 10(-9), OR = 1.62) but also distinguished B-hyperdiploid ALL from other subtypes (rs10821936, P = 1.62 x 10(-5), OR = 2.17; rs10994982, P = 0.003, OR 1.72). These ARID5B SNPs also distinguished B-hyperdiploid ALL from other subtypes in an independent validation cohort (n = 124 children with ALL; P = 0.003 and P = 0.0008, OR 2.45 and 2.86, respectively) and were associated with methotrexate accumulation and gene expression pattern in leukemic lymphoblasts. We conclude that germline variants affect susceptibility to, and characteristics of, specific ALL subtypes. |
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St. Jude Children's Research Hospital, Memphis, Tennessee, USA |
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1061-4036 |
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WP6 In vivo |
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Notes |
PMID:19684603 |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
48 |
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Author |
van Delft, F.W.; Horsley, S.; Colman, S.; Anderson, K.; Bateman, C.; Kempski, H.; Zuna, J.; Eckert, C.; Saha, V.; Kearney, L.; Ford, A.; Greaves, M. |
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Title |
Clonal origins of relapse in ETV6-RUNX1 acute lymphoblastic leukemia |
Type |
Journal Article |
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Year |
2011 |
Publication |
Blood |
Abbreviated Journal |
Blood |
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Volume |
117 |
Issue |
23 |
Pages |
6247-6254 |
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Keywords |
Child; Child, Preschool; Chromosomes, Human, Pair 16/*genetics/metabolism; Chromosomes, Human, Pair 6/*genetics/metabolism; Cyclin C; Cyclin-Dependent Kinase Inhibitor p15/genetics/metabolism; Cyclin-Dependent Kinase Inhibitor p16/genetics/metabolism; Female; Humans; Male; Oncogene Proteins, Fusion/*genetics/metabolism; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics/metabolism/mortality/therapy; Recurrence; *Sequence Deletion; *Translocation, Genetic |
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B-cell precursor childhood acute lymphoblastic leukemia with ETV6-RUNX1 (TEL-AML1) fusion has an overall good prognosis, but relapses occur, usually after cessation of treatment and occasionally many years later. We have investigated the clonal origins of relapse by comparing the profiles of genomewide copy number alterations at presentation in 21 patients with those in matched relapse (12-119 months). We identified, in total, 159 copy number alterations at presentation and 231 at relapse (excluding Ig/TCR). Deletions of CDKN2A/B or CCNC (6q16.2-3) or both increased from 38% at presentation to 76% in relapse, suggesting that cell-cycle deregulation contributed to emergence of relapse. A novel observation was recurrent gain of chromosome 16 (2 patients at presentation, 4 at relapse) and deletion of plasmocytoma variant translocation 1 in 3 patients. The data indicate that, irrespective of time to relapse, the relapse clone was derived from either a major or minor clone at presentation. Backtracking analysis by FISH identified a minor subclone at diagnosis whose genotype matched that observed in relapse approximately 10 years later. These data indicate subclonal diversity at diagnosis, providing a variable basis for intraclonal origins of relapse and extended periods (years) of dormancy, possibly by quiescence, for stem cells in ETV6-RUNX1(+) acute lymphoblastic leukemia. |
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Section of Haemato-Oncology, Institute of Cancer Research, Sutton, UK |
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ISSN |
0006-4971 |
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WP6 In vivo |
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Notes |
PMID:21482711 |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
49 |
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