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Chung, M. - K., Yu, W. - J., Kim, Y. - B., & Myung, S. - H. (2010). Lack of a co-promotion effect of 60 Hz circularly polarized magnetic fields on spontaneous development of lymphoma in AKR mice. Bioelectromagnetics, 31(2), 130–139.
Abstract: The present study was conducted to investigate the possible effect of 60 Hz circularly polarized magnetic fields (MFs) as promoters of genetically initiated lymphoma in AKR mice. One hundred sixty female animals were divided into four different groups. They were exposed to four different intensities of circularly polarized MFs. Animals received exposure to 60 Hz circularly polarized MF at field strengths (rms-value) of 0 microT (sham control, T1, Group I), 5 microT(T2, Group II), 83.3 microT (T3, Group III), or 500 microT(T4, Group IV), for 21 h/day from the age of 4-6 weeks to the age of 44-46 weeks. There were no exposure-related changes in mean survival time, clinical signs, body weights, hematological values, micronucleus assay, gene expression arrays, analysis of apoptosis, and necropsy findings. At histopathological examination, lymphoma was seen in all the groups. The tumor incidence was 31/40(78%), 30/40(75%), 32/40(80%), and 31/40(78%) in sham control, 5, 83.3, and 500 microT groups, respectively. However, there were no differences in the tumor incidence between the sham control (T1) and circularly polarized MF exposure groups (T2-T4). In conclusion, there was no evidence that exposure to 60 Hz circularly polarized MF strengths up to 500 microT promoted lymphoma in AKR mice.
Keywords: Animals; Apoptosis/physiology/radiation effects; Body Weight/physiology/radiation effects; *Electromagnetic Fields; Female; Gene Expression/radiation effects; Incidence; Lymphoma/epidemiology/pathology/*physiopathology; Mice; Mice, Inbred AKR; Micronucleus Tests; Necrosis/pathology/physiopathology; Spleen/pathology/physiopathology/radiation effects; Thymus Gland/pathology/physiopathology/radiation effects; Time Factors
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Cid, M. A., Ubeda, A., Hernández-Bule, M. L., MartÃnez, M. A., & Trillo, M. Ã. . (2012). Antagonistic effects of a 50 Hz magnetic field and melatonin in the proliferation and differentiation of hepatocarcinoma cells. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 30(6), 1502–1516.
Abstract: BACKGROUND/AIMS: Epidemiological and experimental evidence exists indicating that exposure to weak, extremely low frequency magnetic fields (ELF – MF) could affect cancer progression. It has been proposed that such hypothetical action could be mediated by MF-induced effects on the cellular response to melatonin (MEL), a potentially oncostatic neurohormone. The present study investigates the response of HepG2 cells to intermittent exposure to a 50 Hz, 10 µT MF, in the presence or absence of MEL at physiological (10 nM) or pharmacological doses (1 µM). METHODS: The Trypan blue cell exclusion test, BrdU incorporation and PCNA expression assays were carried out to assess the cellular response in terms of viability and proliferation. In addition, albumin and alpha-fetoprotein, were analyzed as specific hepatocellular differentiation markers. RESULTS: The results indicate that the MF exerts significant cytoproliferative and dedifferentiating effects that can be prevented by 10 nM MEL. Conversely, MEL exerts cytostatic and differentiating effects on HepG2 that are abolished by simultaneous exposure to MF. CONCLUSION: As a whole, these results support the hypothesis that ELF – MF and MEL exert opposite, mutually counteracting effects on cell proliferation and differentiation.
Keywords: Albumins; Albumins: metabolism; Antineoplastic Agents; Antineoplastic Agents: pharmacology; Carcinoma, Hepatocellular; Cell Differentiation; Cell Differentiation: drug effects; Cell Proliferation; Cell Proliferation: drug effects; Cell Survival; DNA Replication; Hep G2 Cells; Humans; Magnetic Fields; Melatonin; Melatonin: pharmacology; Melatonin: physiology; Proliferating Cell Nuclear Antigen; Proliferating Cell Nuclear Antigen: metabolism; alpha-Fetoproteins; alpha-Fetoproteins: metabolism
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Close, J. (2012). Are stress responses to geomagnetic storms mediated by the cryptochrome compass system? Proceedings of the Royal Society B: Biological Sciences, 279(1736), 2081–2090.
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Cobaleda, C., Gutierrez-Cianca, N., Perez-Losada, J., Flores, T., Garcia-Sanz, R., Gonzalez, M., et al. (2000). A primitive hematopoietic cell is the target for the leukemic transformation in human philadelphia-positive acute lymphoblastic leukemia. Blood, 95(3), 1007–1013.
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.
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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Cobaleda, C., & Sanchez-Garcia, I. (2009). B-cell acute lymphoblastic leukaemia: towards understanding its cellular origin. Bioessays, 31(6), 600–609.
Abstract: B-cell acute lymphoblastic leukaemia (B-ALL) is a clonal malignant disease originated in a single cell and characterized by the accumulation of blast cells that are phenotypically reminiscent of normal stages of B-cell differentiation. B-ALL origin has been a subject of continuing discussion, given the fact that human disease is diagnosed at late stages and cannot be monitored during its natural evolution from its cell of origin, although most B-ALLs probably start off with chromosomal changes in haematopoietic stem cells. However, the cells responsible for maintaining the disease appear to differ between the different types of B-ALLs and this remains an intriguing and exciting topic of research, since these cells have been posited to be responsible for resistance to conventional therapies, recurrence and dissemination. During the last years this problem has been addressed primarily by transplantation of purified subpopulations of human B-ALL cells into immunodeficient mice. The results from these different reconstitution experiments and their interpretations are compared in this review in the context of normal B-cell developmental plasticity. While the results from different research groups might appear mutually exclusive, we discuss how they could be reconciled with the biology of normal B-cells and propose research avenues for addressing these issues in the future.
Keywords: Animals; B-Lymphocytes/cytology/*physiology; Cell Differentiation/physiology; Humans; Leukemia, B-Cell/*etiology/genetics/pathology; Neoplastic Stem Cells/cytology/physiology; Phenotype; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*etiology/genetics/pathology/physiopathology; Tumor Markers, Biological/metabolism
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