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Author Cobaleda, C.; Gutierrez-Cianca, N.; Perez-Losada, J.; Flores, T.; Garcia-Sanz, R.; Gonzalez, M.; Sanchez-Garcia, I. url  openurl
  Title A primitive hematopoietic cell is the target for the leukemic transformation in human philadelphia-positive acute lymphoblastic leukemia Type Journal Article
  Year 2000 Publication Blood Abbreviated Journal Blood  
  Volume 95 Issue 3 Pages 1007-1013  
  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  
  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.  
  Address Departamento de Proliferacion y Diferenciacion Celular, Instituto de Microbiologia Bioquimica, Universidad de Salamanca, Salamanca, Spain  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0006-4971 ISBN Medium  
  Area WP6 In vivo Expedition Conference  
  Notes PMID:10648416 Approved no  
  Call Number (up) CBM.UAM @ ccobaleda @ Serial 34  
Permanent link to this record
 

 
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. url  openurl
  Title Mechanism of relapse in pediatric acute lymphoblastic leukemia Type Journal Article
  Year 2008 Publication Cell Cycle (Georgetown, Tex.) Abbreviated Journal Cell Cycle  
  Volume 7 Issue 10 Pages 1315-1320  
  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  
  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.  
  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  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1551-4005 ISBN Medium  
  Area WP6 In vivo Expedition Conference  
  Notes PMID:18418081 Approved no  
  Call Number (up) CBM.UAM @ ccobaleda @ Serial 33  
Permanent link to this record
 

 
Author Anderson, K.; Lutz, C.; van Delft, F.W.; Bateman, C.M.; Guo, Y.; Colman, S.M.; Kempski, H.; Moorman, A.V.; Titley, I.; Swansbury, J.; Kearney, L.; Enver, T.; Greaves, M. url  doi
openurl 
  Title Genetic variegation of clonal architecture and propagating cells in leukaemia Type Journal Article
  Year 2011 Publication Nature Abbreviated Journal Nature  
  Volume 469 Issue 7330 Pages 356-361  
  Keywords Animals; Clone Cells/metabolism/*pathology; DNA Copy Number Variations/genetics; DNA Mutational Analysis; Disease Progression; Genetic Variation/*genetics; Genotype; Humans; Immunophenotyping; In Situ Hybridization, Fluorescence; Interleukin Receptor Common gamma Subunit/deficiency/genetics; Mice; Mice, Inbred NOD; Mice, SCID; Neoplasm Transplantation; Oncogene Proteins, Fusion/genetics; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics/*pathology  
  Abstract Little is known of the genetic architecture of cancer at the subclonal and single-cell level or in the cells responsible for cancer clone maintenance and propagation. Here we have examined this issue in childhood acute lymphoblastic leukaemia in which the ETV6-RUNX1 gene fusion is an early or initiating genetic lesion followed by a modest number of recurrent or 'driver' copy number alterations. By multiplexing fluorescence in situ hybridization probes for these mutations, up to eight genetic abnormalities can be detected in single cells, a genetic signature of subclones identified and a composite picture of subclonal architecture and putative ancestral trees assembled. Subclones in acute lymphoblastic leukaemia have variegated genetics and complex, nonlinear or branching evolutionary histories. Copy number alterations are independently and reiteratively acquired in subclones of individual patients, and in no preferential order. Clonal architecture is dynamic and is subject to change in the lead-up to a diagnosis and in relapse. Leukaemia propagating cells, assayed by serial transplantation in NOD/SCID IL2Rgamma(null) mice, are also genetically variegated, mirroring subclonal patterns, and vary in competitive regenerative capacity in vivo. These data have implications for cancer genomics and for the targeted therapy of cancer.  
  Address Section of Haemato-Oncology, The Institute of Cancer Research, Sutton SM2 5NG, UK  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0028-0836 ISBN Medium  
  Area WP6 In vivo Expedition Conference  
  Notes PMID:21160474 Approved no  
  Call Number (up) CBM.UAM @ ccobaleda @ Serial 28  
Permanent link to this record
 

 
Author Cobaleda, C.; Sanchez-Garcia, I. url  doi
openurl 
  Title B-cell acute lymphoblastic leukaemia: towards understanding its cellular origin Type Journal Article
  Year 2009 Publication BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology Abbreviated Journal Bioessays  
  Volume 31 Issue 6 Pages 600-609  
  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  
  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.  
  Address Departamento de Fisiologia y Farmacologia, Universidad de Salamanca, Campus M. de Unamuno s/n, 37007-SALAMANCA, Spain. ccobalhz@usal.es  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0265-9247 ISBN Medium  
  Area WP6 In vivo Expedition Conference  
  Notes PMID:19444834 Approved no  
  Call Number (up) CBM.UAM @ ccobaleda @ Serial 29  
Permanent link to this record
 

 
Author Greaves, M. url  doi
openurl 
  Title In utero origins of childhood leukaemia Type Journal Article
  Year 2005 Publication Early Human Development Abbreviated Journal Early Hum Dev  
  Volume 81 Issue 1 Pages 123-129  
  Keywords 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  
  Abstract 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.  
  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  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0378-3782 ISBN Medium  
  Area WP6 In vivo Expedition Conference  
  Notes PMID:15707724 Approved no  
  Call Number (up) CBM.UAM @ ccobaleda @ Serial 30  
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