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Title |
NTP Toxicology and Carcinogenesis Studies of 60-HZ Magnetic Fields IN F344/N Rats and B6C3F1 Mice (Whole-body Exposure Studies) |
Type |
Journal Article |
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Year |
1999 |
Publication |
National Toxicology Program Technical Report Series |
Abbreviated Journal |
Natl Toxicol Program Tech Rep Ser |
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Volume |
488 |
Issue |
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Pages |
1-168 |
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Abstract |
Electric and magnetic fields (EMF) are associated with the production, transmission, and use of electricity; thus, the potential for human exposure is high. These electric and magnetic fields are predominantly of low frequency (60 Hz in the United States and 50 Hz in Europe) and generally of low intensity. Epidemiology studies have suggested a potential for increased breast cancer, brain cancer, and leukemia rates with increasing magnetic field exposure. Therefore, given the widespread exposure to low-intensity, 60-Hz magnetic fields in industrialized societies, standard toxicology studies and long-term carcinogenesis studies were conducted using traditional rodent models. Male and female F344/N rats and B6C3F1mice were exposed to 60-Hz magnetic fields by whole-body exposure for 2 years. 2-YEAR STUDY IN RATS: Groups of 100 male and 100 female rats were exposed to 60-Hz magnetic fields at intensities of 0.02, 2, or 10 G for 18.5 hours per day, 7 days per week, for 106 weeks. Groups of 100 male and 100 female control rats were housed in the same exposure chambers without applied magnetic fields. Additional groups of 100 male and 100 female rats were intermittently exposed (1 hour on and 1 hour off) to a 10 G 60-Hz field 18.5 hours per day, 7 days per week, for 106 weeks. The highest field intensity (10 G) is approximately 5,000-fold greater than what was considered high intensity for homes in epidemiology studies in humans. Survival and Body Weights: Survival and mean body weights of exposed groups of male and female rats was similar to those of the control groups. Pathology Findings: The incidences of thyroid gland C-cell adenoma and carcinoma in 0.02 G male rats, adenoma in 2 G males, and adenoma or carcinoma (combined) in 0.02 and 2 G males were significantly greater than in the control group. The incidence of mononuclear cell leukemia in males in the 10 G intermittent group was significantly less than in the control group. 2-YEAR STUDY IN MICE: Groups of 100 male and 100 female mice were exposed to 60-Hz magnetic fields at intensities of 0.02, 2, or 10 G for 18.5 hours per day, 7 days per week, for 106 weeks. Groups of 100 male and 100 female control mice were housed in the same exposure chambers without applied magnetic fields. Additional groups of 100 male and 100 female mice were intermittently exposed (1 hour on and 1 hour off) to a 10 G 60-Hz field 18.5 hours per day, 7 days per week, for 106 weeks. Survival and Body Weights: Survival of male mice exposed to 10 G was significantly less than that of control mice after 2 years; survival of all other exposed groups of mice was similar to that of control mice. Mean body weights of exposed groups of male and female mice were similar to those of the control groups throughout the study. Pathology Findings: The incidences of alveolar/bronchiolar adenoma were significantly decreased in 0.02 and 2 G male mice and 2 G female mice relative to the control groups; the incidences of alveolar/bronchiolar adenoma or carcinoma (combined) were significantly less in males and females exposed to 2 G than in the control groups. In female mice, the incidence of malignant lymphoma in the 10 G intermittent group was significantly less than in the controls. CONCLUSIONS: Under the conditions of these 2-year whole-body exposure studies, there was equivocal evidence of carcinogenic activity of 60-Hz magnetic fields in male F344/N rats based on increased incidences of thyroid gland C-cell neoplasms in the 0.02 and 2G groups. There was no evidence of carcinogenic activity in female F344/N rats or male or female B6C3F1 mice exposed to 0.02, 2, or 10 G, or 10 G intermittent 60-Hz magnetic fields. In exposed rats and mice there were no increased incidences of neoplasms at sites for which epidemiology studies have suggested an association with magnetic fields (brain, mammary gland, leukemia). |
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National Toxicology Program |
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English |
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ISSN |
0888-8051 |
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WP6 In vivo |
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Notes |
PMID:12563343 |
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Call Number |
ITEM @ geertje.lewin @ |
Serial |
110 |
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Title |
Non-ionizing radiation, Part 1: static and extremely low-frequency (ELF) electric and magnetic fields |
Type |
Journal Article |
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Year |
2002 |
Publication |
IARC Monographs on the Evaluation of Carcinogenic Risks to Humans / World Health Organization, International Agency for Research on Cancer |
Abbreviated Journal |
IARC Monogr Eval Carcinog Risks Hum |
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Volume |
80 |
Issue |
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Pages |
1-395 |
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Keywords |
Developed Countries; Dose-Response Relationship, Radiation; Electromagnetic Fields/*adverse effects; Environmental Exposure/*adverse effects; Europe; Female; Humans; Male; Neoplasms, Radiation-Induced/*etiology; Occupational Exposure; Pregnancy; Radiation, Nonionizing/*adverse effects; *Risk Assessment |
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Corporate Author |
IARC Working Group on the Evaluation of Carcinogenic Risks to Humans |
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English |
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Edition |
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ISSN |
1017-1606 |
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WP6 In vivo |
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Notes |
PMID:12071196 |
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Call Number |
ITEM @ geertje.lewin @ |
Serial |
111 |
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Author |
Steliarova-Foucher, E.; Stiller, C.; Kaatsch, P.; Berrino, F.; Coebergh, J.-W. |
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Title |
Trends in childhood cancer incidence in Europe, 1970-99 |
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Journal Article |
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Year |
2005 |
Publication |
Lancet |
Abbreviated Journal |
Lancet |
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Volume |
365 |
Issue |
9477 |
Pages |
2088 |
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Keywords |
Child; Europe/epidemiology; Humans; Incidence; Neoplasms/*epidemiology; Registries |
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Corporate Author |
ACCIS Scientific Committee |
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English |
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Edition |
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ISSN |
0140-6736 |
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Area |
WP9 Epidemiology |
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Notes |
PMID:15964441 |
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no |
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Call Number |
IARC @ ErdmannF @ |
Serial |
101 |
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Author |
Cobaleda, C.; Gutierrez-Cianca, N.; Perez-Losada, J.; Flores, T.; Garcia-Sanz, R.; Gonzalez, M.; Sanchez-Garcia, I. |
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Title |
A primitive hematopoietic cell is the target for the leukemic transformation in human philadelphia-positive acute lymphoblastic leukemia |
Type |
Journal Article |
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Year |
2000 |
Publication |
Blood |
Abbreviated Journal |
Blood |
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Volume |
95 |
Issue |
3 |
Pages |
1007-1013 |
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Keywords |
ADP-ribosyl Cyclase; Animals; Antigens, CD/analysis; Antigens, CD34/analysis; Antigens, CD38; Antigens, Differentiation/analysis; Antigens, Neoplasm/analysis; Cell Differentiation; Cell Division; Cell Transformation, Neoplastic/*pathology; Fusion Proteins, bcr-abl/physiology; Hematopoietic Stem Cells/classification/*pathology; Humans; Immunophenotyping; Membrane Glycoproteins; Mice; Mice, Inbred NOD; Mice, SCID; NAD+ Nucleosidase/analysis; Neoplasm Transplantation; Neoplastic Stem Cells/classification/*pathology/transplantation; Philadelphia Chromosome; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*pathology |
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Abstract |
BCR-ABL is a chimeric oncogene generated by translocation of sequences from the chromosomal counterpart (c-ABL gene) on chromosome 9 into the BCR gene on chromosome 22. Alternative chimeric proteins, BCR-ABL(p190) and BCR-ABL(p210), are produced that are characteristic of chronic myelogenous leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph(1)-ALL). In CML, the transformation occurs at the level of pluripotent stem cells. However, Ph(1)-ALL is thought to affect progenitor cells with lymphoid differentiation. Here we demonstrate that the cell capable of initiating human Ph(1)-ALL in non-obese diabetic mice with severe combined immunodeficiency disease (NOD/SCID), termed SCID leukemia-initiating cell (SL-IC), possesses the differentiative and proliferative capacities and the potential for self-renewal expected of a leukemic stem cell. The SL-ICs from all Ph(1)-ALL analyzed, regardless of the heterogeneity in maturation characteristics of the leukemic blasts, were exclusively CD34(+ )CD38(-), which is similar to the cell-surface phenotype of normal SCID-repopulating cells. This indicates that normal primitive cells, rather than committed progenitor cells, are the target for leukemic transformation in Ph(1)-ALL. |
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Address |
Departamento de Proliferacion y Diferenciacion Celular, Instituto de Microbiologia Bioquimica, Universidad de Salamanca, Salamanca, Spain |
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English |
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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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Area |
WP6 In vivo |
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Notes |
PMID:10648416 |
Approved |
no |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
34 |
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Author |
Henderson, M.J.; Choi, S.; Beesley, A.H.; Sutton, R.; Venn, N.C.; Marshall, G.M.; Kees, U.R.; Haber, M.; Norris, M.D. |
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Title |
Mechanism of relapse in pediatric acute lymphoblastic leukemia |
Type |
Journal Article |
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Year |
2008 |
Publication |
Cell Cycle (Georgetown, Tex.) |
Abbreviated Journal |
Cell Cycle |
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Volume |
7 |
Issue |
10 |
Pages |
1315-1320 |
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Keywords |
Child; *Drug Resistance, Neoplasm; Gene Rearrangement/*genetics; Genetic Markers/genetics; Humans; Models, Biological; Polymerase Chain Reaction; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*diagnosis/drug therapy/*prevention & control; Receptors, Antigen/genetics; Recurrence; Time Factors |
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Abstract |
Relapse following initial chemotherapy remains a barrier to survival in approximately 20% of children suffering from acute lymphoblastic leukemia (ALL). Recently, to investigate the mechanism of relapse, we analysed clonal populations in 27 pairs of matched diagnosis and relapse ALL samples using PCR-based detection of multiple antigen receptor gene rearrangements. These clonal markers revealed the emergence of apparently new populations at relapse in 13 patients. In those cases where the new 'relapse clone' could be detected in the diagnosis population, there was a close correlation between length of first remission and quantity of the relapse clone in the diagnosis sample. A shorter length of time to first relapse correlated with a higher quantity of the relapsing clone at diagnosis. This observation, together with demonstrated differential chemosensitivity between sub-clones at diagnosis, indicates that relapse in ALL patients may commonly involve selection of a minor intrinsically resistant sub-clone that is undetectable by routine PCR-based methods. From a clinical perspective, relapse prediction may be improved with strategies to detect minor potentially resistant sub-clones early during treatment, hence allowing intensification of therapy. Together with the availability of relevant in vivo experimental models and powerful technology for detailed analysis of patient specimens, this new information will help shape future experimentation towards targeted therapy for high-risk ALL. |
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Address |
Children's Cancer Institute Australiafor Medical Research, Experimental Therapeutics Program, PO Box 81 (HighSt), Randwick, Sydney, NSW 2031 Australia. mhenderson@ccia.unsw.edu.au |
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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 |
1551-4005 |
ISBN |
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Area |
WP6 In vivo |
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Notes |
PMID:18418081 |
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no |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
33 |
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