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Author |
Kuster, N. |
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Comments on the Brief Communication “Security considerations in blinded exposure experiments using electromagnetic waves†by Christian Wolf |
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Journal Article |
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Year |
2008 |
Publication |
Bioelectromagnetics |
Abbreviated Journal |
Bioelectromagnetics |
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29 |
Issue |
8 |
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660-661 |
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0197-8462 |
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Call Number |
IT'IS @ kuster @ |
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25 |
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Author |
Cobaleda, C.; Sanchez-Garcia, I. |
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Title |
B-cell acute lymphoblastic leukaemia: towards understanding its cellular origin |
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Journal Article |
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Year |
2009 |
Publication |
BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology |
Abbreviated Journal |
Bioessays |
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31 |
Issue |
6 |
Pages |
600-609 |
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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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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. |
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Departamento de Fisiologia y Farmacologia, Universidad de Salamanca, Campus M. de Unamuno s/n, 37007-SALAMANCA, Spain. ccobalhz@usal.es |
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0265-9247 |
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WP6 In vivo |
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PMID:19444834 |
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CBM.UAM @ ccobaleda @ |
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29 |
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Author |
Greaves, M. |
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Title |
In utero origins of childhood leukaemia |
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Journal Article |
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Year |
2005 |
Publication |
Early Human Development |
Abbreviated Journal |
Early Hum Dev |
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81 |
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1 |
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123-129 |
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Child; Diseases in Twins; Female; Fetal Diseases/*genetics; Genes/genetics; Humans; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*embryology/*genetics; Pregnancy; Preleukemia/*blood; Translocation, Genetic/*genetics; Twins, Monozygotic |
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Chimaeric fusion genes derived by chromosome translocation are common molecular abnormalities in paediatric leukaemia and provide unique markers for the malignant clone. They have been especially informative in studies with twins concordant for leukaemia and in retrospective scrutiny of archived neonatal blood spots. These data have indicated that, in paediatric leukaemia, the majority of chromosome translocations arise in utero during foetal haemopoiesis. Chromosomal translocations and preleukaemic clones arise at a substantially higher frequency ( approximately 100x) before birth than the cumulative incidence or risk of disease, reflecting the requirement for complementary and secondary genetic events that occur postnatally. A consequence of the latter is a very variable and occasionally protracted postnatal latency of disease (1-15 years). These natural histories provide an important framework for consideration of key aetiological events in paediatric leukaemia. |
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Address |
Chester Beatty Laboratories, Institute of Cancer Research, Section of Haemato-Oncology, 237 Fulham Road, London SW3 6JB, United Kingdom. mel.greaves@icr.ac.uk |
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0378-3782 |
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WP6 In vivo |
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PMID:15707724 |
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CBM.UAM @ ccobaleda @ |
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30 |
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Author |
Greaves, M. |
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Title |
Cancer stem cells: back to Darwin? |
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Journal Article |
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2010 |
Publication |
Seminars in Cancer Biology |
Abbreviated Journal |
Semin Cancer Biol |
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20 |
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2 |
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65-70 |
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Animals; *Cell Differentiation; Humans; Mice; Neoplasms/*pathology; Neoplastic Stem Cells/*pathology |
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Current models of cancer propagation or 'stem' cells pay scant attention to the evolutionary dynamics of cancer or to the underlying genetic, mutational drivers. Recent genetic studies on acute lymphoblastic leukaemia at the single cell level reveal a complex non-linear, branching clonal architecture-with sub-clones having distinctive genetic signatures. Most cancers appropriately interrogated are found to have intra-clonal genetic heterogeneity indicative of divergent clonal evolution. These data further suggest that clonal architecture might be driven by genetic heterogeneity of propagating or 'stem' cells. When assayed for leukaemic regeneration in NOD/SCID/gamma mice, genetically diverse 'stem' cells read-out, broadly reflecting the clonal architecture. This has suggested a 'back to Darwin' model for cancer propagation. In this, cells with self-renewal potency or 'stem-ness' provide genetically diverse units of evolutionary selection in cancer progression. The model has significant implications for targeted cancer therapy. |
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Section of Haemato-Oncology, The Institute of Cancer Research, Brookes Lawley Building, 15 Cotswold Road, Sutton, Surrey SM2 5NG, United Kingdom. mel.greaves@icr.ac.uk <mel.greaves@icr.ac.uk> |
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1044-579X |
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WP6 In vivo |
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Notes |
PMID:20359535 |
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CBM.UAM @ ccobaleda @ |
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31 |
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Author |
Greaves, M.F.; Wiemels, J. |
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Title |
Origins of chromosome translocations in childhood leukaemia |
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Journal Article |
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Year |
2003 |
Publication |
Nature Reviews. Cancer |
Abbreviated Journal |
Nat Rev Cancer |
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3 |
Issue |
9 |
Pages |
639-649 |
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Keywords |
Child; Fetal Diseases/embryology; Hematopoiesis/*genetics; Humans; Leukemia/etiology/*genetics/physiopathology; Translocation, Genetic/*genetics |
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Abstract |
Chromosome translocations are often early or initiating events in leukaemogenesis, occurring prenatally in most cases of childhood leukaemia. Although these genetic changes are necessary, they are usually not sufficient to cause leukaemia. How, when and where do translocations arise? And can these insights aid our understanding of the natural history, pathogenesis and causes of leukaemia? |
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Address |
LRF Centre for Cell and Molecular Biology, Institute of Cancer Research, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, UK. mel.greaves@icr.ac.uk |
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1474-175X |
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WP6 In vivo |
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PMID:12951583 |
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CBM.UAM @ ccobaleda @ |
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32 |
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