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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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Address |
St. Jude Children's Research Hospital, Memphis, Tennessee, USA |
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English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Series Volume |
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Series Issue |
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Edition |
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ISSN |
1061-4036 |
ISBN |
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Area |
WP6 In vivo |
Expedition |
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Conference |
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Notes |
PMID:19684603 |
Approved |
no |
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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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Abstract |
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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Address |
Section of Haemato-Oncology, Institute of Cancer Research, Sutton, UK |
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English |
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Series Title |
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Series Volume |
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Series Issue |
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Edition |
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ISSN |
0006-4971 |
ISBN |
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Medium |
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Area |
WP6 In vivo |
Expedition |
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Conference |
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Notes |
PMID:21482711 |
Approved |
no |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
49 |
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Author |
Vicente-Duenas, C.; Abollo-Jimenez, F.; Ruiz-Roca, L.; Alonso-Escudero, E.; Jimenez, R.; Cenador, M.B.G.; Criado, F.J.G.; Cobaleda, C.; Sanchez-Garcia, I. |
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Title |
The age of the target cell affects B-cell leukaemia malignancy |
Type |
Journal Article |
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Year |
2010 |
Publication |
Aging |
Abbreviated Journal |
Aging (Albany NY) |
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Volume |
2 |
Issue |
12 |
Pages |
908-913 |
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Keywords |
Age Factors; Animals; Bone Marrow Transplantation; *Cell Aging; Cell Line; Cell Survival; Fusion Proteins, bcr-abl/genetics/metabolism; Genes, abl; Humans; Leukemia, B-Cell/genetics/metabolism/*pathology; Leukemia, Experimental/genetics/metabolism/*pathology; Mice; Mice, Transgenic; Neoplasm Invasiveness; Neoplastic Stem Cells/metabolism/*pathology |
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Abstract |
The incidence, malignancy and treatment resistance of many types of human B-cell leukaemias (B-ALL) are directly related to patient age. A major obstacle to elucidate the contribution of age to the development and evolution of leukaemias is the lack of appropriate mouse models where precise control of the timing of oncogene expression is possible. Here we present proof-of-principle experiments showing how a conditional transgenic mouse model of BCR-ABLp190-driven B-ALL offers the opportunity to test the hypothesis that the age of the leukemic cells-of-origin of B-ALL influences B-ALL malignancy. B-ALLs generated from 12- and 20-month-old progenitors gave rise to a more invasive B-ALL than the one developed from 4-month old precursors. This was evidenced by survival analysis revealing the increased malignancy of B-ALLs generated from 20 or 12-month-old transformed progenitors compared with the 4-month equivalents (median survival of 88 days versus 50.5 and 33 days, respectively). Our study shows that the age of target cells at the time of transformation affects B-ALL malignancy. |
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Address |
Experimental Therapeutics and Translational Oncology Program, Instituto de Biologia Molecular y Celular del Cancer, CSIC/ Universidad de Salamanca, Campus M. de Unamuno s/n, 37007- Salamanca, Spain. cvd@usal.es; isg@usal.es |
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English |
Summary Language |
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Abbreviated Series Title |
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Series Volume |
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Series Issue |
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Edition |
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ISSN |
1945-4589 |
ISBN |
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Area |
WP6 In vivo |
Expedition |
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Conference |
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Notes |
PMID:21164221 |
Approved |
no |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
50 |
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Author |
Vicente-Duenas, C.; Cobaleda, C.; Perez-Losada, J.; Sanchez-Garcia, I. |
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Title |
The evolution of cancer modeling: the shadow of stem cells |
Type |
Journal Article |
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Year |
2010 |
Publication |
Disease Models & Mechanisms |
Abbreviated Journal |
Dis Model Mech |
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Volume |
3 |
Issue |
3-4 |
Pages |
149-155 |
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Keywords |
Animals; *Disease Models, Animal; Embryonic Stem Cells/metabolism; Gene Knock-In Techniques; Humans; Mice; Mutation/genetics; Neoplasms/*pathology; Neoplastic Stem Cells/*pathology; Oncogenes/genetics |
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Abstract |
Cancer is a complex and highly dynamic process. Genetically engineered mouse models (GEMs) that develop cancer are essential systems for dissecting the processes that lead to human cancer. These animal models provide a means to determine the causes of malignancy and to develop new treatments, thus representing a resource of immense potential for medical oncology. The sophistication of modeling cancer in mice has increased to the extent that now we can induce, study and manipulate the cancer disease process in a manner that is impossible to perform in human patients. However, all GEMs described so far have diverse shortcomings in mimicking the hierarchical structure of human cancer tissues. In recent years, a more detailed picture of the cellular and molecular mechanisms determining the formation of cancer has emerged. This Commentary addresses new experimental approaches toward a better understanding of carcinogenesis and discusses the impact of new animal models. |
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Address |
Experimental Therapeutics and Translational Oncology Program, Instituto de Biologia Molecular y Celular del Cancer, CSIC/Universidad de Salamanca, Campus M. Unamuno s/n, 37007-Salamanca, Spain |
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English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Series Volume |
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ISSN |
1754-8403 |
ISBN |
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Area |
WP6 In vivo |
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Notes |
PMID:20212083 |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
51 |
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Author |
Roosli, M.; Jenni, D.; Kheifets, L.; Mezei, G. |
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Title |
Extremely low frequency magnetic field measurements in buildings with transformer stations in Switzerland |
Type |
Journal Article |
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Year |
2011 |
Publication |
The Science of the Total Environment |
Abbreviated Journal |
Sci Total Environ |
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Volume |
409 |
Issue |
18 |
Pages |
3364-3369 |
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Keywords |
*Electrical Equipment and Supplies; *Electromagnetic Fields; Environmental Exposure/*analysis/statistics & numerical data; Housing; Humans; Switzerland |
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Abstract |
The aim of this study was to evaluate an exposure assessment method that classifies apartments in three exposure categories of extremely low frequency magnetic fields (ELF-MF) based on the location of the apartment relative to the transformer room. We completed measurements in 39 apartments in 18 buildings. In each room of the apartments ELF-MF was concurrently measured with 5 to 6 EMDEX II meters for 10 min. Measured arithmetic mean ELF-MF was 0.59 muT in 8 apartments that were fully adjacent to a transformer room, either directly above the transformer or touching the transformer room wall-to-wall. In apartments that only partly touched the transformer room at corners or edges, average ELF-MF level was 0.14 muT. Average exposure in the remaining apartments was 0.10 muT. Kappa coefficient for exposure classification was 0.64 (95%-CI: 0.45-0.82) if only fully adjacent apartments were considered as highly exposed (>0.4 muT). We found a distinct ELF-MF exposure gradient in buildings with transformer. Exposure classification based on the location of the apartment relative to the transformer room appears feasible. Such an approach considerably reduces effort for exposure assessment and may be used to eliminate selection bias in future epidemiologic studies. |
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Address |
Swiss Tropical and Public Health Institute, Basel, Switzerland. martin.roosli@unibas.ch |
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English |
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ISSN |
0048-9697 |
ISBN |
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Area |
WP2 Exposure measurements |
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Notes |
PMID:21684576 |
Approved |
no |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
54 |
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