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Author |
Greaves, M. |
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Title |
Cancer stem cells: back to Darwin? |
Type |
Journal Article |
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Year |
2010 |
Publication |
Seminars in Cancer Biology |
Abbreviated Journal |
Semin Cancer Biol |
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Volume |
20 |
Issue |
2 |
Pages |
65-70 |
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Keywords |
Animals; *Cell Differentiation; Humans; Mice; Neoplasms/*pathology; Neoplastic Stem Cells/*pathology |
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Abstract |
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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Address |
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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ISSN |
1044-579X |
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WP6 In vivo |
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Notes |
PMID:20359535 |
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CBM.UAM @ ccobaleda @ |
Serial |
31 |
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Author |
Greaves, M.F.; Wiemels, J. |
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Title |
Origins of chromosome translocations in childhood leukaemia |
Type |
Journal Article |
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Year |
2003 |
Publication |
Nature Reviews. Cancer |
Abbreviated Journal |
Nat Rev Cancer |
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Volume |
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 @ |
Serial |
32 |
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Hjalgrim, L.L.; Rostgaard, K.; Schmiegelow, K.; Soderhall, S.; Kolmannskog, S.; Vettenranta, K.; Kristinsson, J.; Clausen, N.; Melbye, M.; Hjalgrim, H.; Gustafsson, G. |
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Title |
Age- and sex-specific incidence of childhood leukemia by immunophenotype in the Nordic countries |
Type |
Journal Article |
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Year |
2003 |
Publication |
Journal of the National Cancer Institute |
Abbreviated Journal |
J Natl Cancer Inst |
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Volume |
95 |
Issue |
20 |
Pages |
1539-1544 |
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Keywords |
Adolescent; Age Distribution; Child; Child, Preschool; Female; Finland/epidemiology; Humans; Iceland/epidemiology; Immunophenotyping; Incidence; Infant; Infant, Newborn; Leukemia, Myeloid, Acute/*epidemiology/genetics; Male; Poisson Distribution; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*epidemiology/genetics; Scandinavia/epidemiology; Sex Distribution |
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Abstract |
BACKGROUND: Studies from various countries have found an increasing incidence of childhood leukemia in recent decades. To characterize time trends in the age- and sex-specific incidence of childhood acute leukemia during the last 20 years in the Nordic countries, we analyzed a large set of population-based data from the Nordic Society of Paediatric Haematology and Oncology (NOPHO) in their acute leukemia database covering a population of approximately 5 million children aged 0-14 years. METHODS: Temporal trends in acute myeloid leukemia and acute lymphoblastic leukemia incidence rates overall and for acute lymphoblastic leukemia immunophenotypes and for specific age groups were analyzed by Poisson regression adjusting for age, sex, and country. All statistical tests were two-sided. RESULTS: We identified 1595 girls and 1859 boys diagnosed with acute lymphoblastic leukemia between January 1, 1982, and December 31, 2001, and 260 girls and 224 boys diagnosed with de novo acute myeloid leukemia between January 1, 1985, and December 31, 2001. No statistically significant change was seen in the overall incidence rate for acute lymphoblastic leukemia during the 20-year study (annual change = 0.22%, 95% confidence interval [CI] = -0.36% to 0.80%). The incidence rate of B-precursor acute lymphoblastic leukemia remained unchanged (annual change = 0.30%, 95% CI = -0.57% to 1.18%) from January 1, 1986, through December 31, 2001. A somewhat lower incidence in the first years of the study period indicated an early increasing incidence of B-precursor acute lymphoblastic leukemia that corresponded to a simultaneous decreasing incidence of unclassified acute lymphoblastic leukemia. Incidences of T-cell acute lymphoblastic leukemia (annual change = 1.55%, 95% CI = -1.14% to 4.31%) and acute myeloid leukemia (annual change = 0.58%, 95% CI = -1.24% to 2.44%) were stable during the study period. CONCLUSION: Incidences of acute myeloid leukemia overall, acute lymphoblastic leukemia overall, and specific acute lymphoblastic leukemia immunophenotypes have been stable in the Nordic countries over the past two decades. |
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Department of Epidemiology Research, Danish Epidemiology Science Centre, Statens Serum Institut, Copenhagen, Denmark. lih@ssi.dk |
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ISSN |
0027-8874 |
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WP9 Epidemiology |
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PMID:14559876 |
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no |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
35 |
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Author |
Hosking, F.J.; Papaemmanuil, E.; Sheridan, E.; Kinsey, S.E.; Lightfoot, T.; Roman, E.; Irving, J.A.E.; Allan, J.M.; Taylor, M.; Tomlinson, I.P.; Greaves, M.; Houlston, R.S. |
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Title |
Genome-wide homozygosity signatures and childhood acute lymphoblastic leukemia risk |
Type |
Journal Article |
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Year |
2010 |
Publication |
Blood |
Abbreviated Journal |
Blood |
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Volume |
115 |
Issue |
22 |
Pages |
4472-4477 |
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Keywords |
Case-Control Studies; Child; Child, Preschool; Chromosome Mapping; European Continental Ancestry Group/genetics; Female; Genes, Recessive; Genome-Wide Association Study; Great Britain; *Homozygote; Humans; Infant; Male; Polymorphism, Single Nucleotide; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/*genetics; Receptors, Erythropoietin/genetics; Risk Factors |
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Abstract |
Recent studies have reported that regions of homozygosity (ROH) in the genome are detectable in outbred populations and can be associated with an increased risk of malignancy. To examine whether homozygosity is associated with an increased risk of developing childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL), we analyzed 824 ALL cases and 2398 controls genotyped for 292 200 tagging SNPs. Across the genome, cumulative distribution of ROH was not significantly different between cases and controls. Four common ROH at 10p11.2-10q11.21, 1p31.1, 19p13.2-3, and 20q11.1-23 were, however, associated with ALL risk at P less than .01 (including 1 ROH to which the erythropoietin receptor [EPOR] gene maps, P = .005) but were nonsignificant after adjusting for multiple testing. Our findings make it unlikely that levels of measured homozygosity, caused by autozygosity, uniparental isodisomy, or hemizygosity, play a major role in defining BCP-ALL risk in predominantly outbred populations. |
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Section of Cancer Genetics, Institute of Cancer Research, Sutton, Surrey, United Kingdom |
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0006-4971 |
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WP6 In vivo |
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Notes |
PMID:20231427 |
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CBM.UAM @ ccobaleda @ |
Serial |
36 |
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Author |
Lausten-Thomsen, U.; Madsen, H.O.; Vestergaard, T.R.; Hjalgrim, H.; Nersting, J.; Schmiegelow, K. |
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Title |
Prevalence of t(12;21)[ETV6-RUNX1]-positive cells in healthy neonates |
Type |
Journal Article |
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Year |
2011 |
Publication |
Blood |
Abbreviated Journal |
Blood |
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117 |
Issue |
1 |
Pages |
186-189 |
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Keywords |
Adult; Chromosomes, Human, Pair 12/*genetics; Chromosomes, Human, Pair 21/*genetics; Cross-Sectional Studies; Female; Fetal Blood/cytology/*metabolism; Humans; Infant; Infant, Newborn; Oncogene Proteins, Fusion/*genetics; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*diagnosis/genetics; Prognosis; Sensitivity and Specificity; Translocation, Genetic/*genetics |
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Abstract |
t(12;21)(p13;q22)[ETV6-RUNX1] is the most common chromosomal translocation in childhood acute lymphoblastic leukemia, and it can often be backtracked to Guthrie cards supporting prenatal initiation and high levels of circulating t(12;21)-positive cells at birth. To explore the prevalence of ETV6-RUNX1-positive cells in healthy neonates, mononuclear cells from 1417 umbilical cord blood samples were isolated within 24 hours from birth and subsequently screened for ETV6-RUNX1 transcripts using a highly sensitive real-time reverse transcription polymerase chain reaction assay. In first-run polymerase chain reaction, 14 samples were positive at levels below 10(-5), of which specific hybridization reflecting the relevant genetic region was positive in 9 cases. Repeated analyses using stored mRNA and flowcytometric sorting of a CD19(+), CD8(+), and CD19(-)/CD8(-) subpopulations from cryopreserved mononuclear cells from the same cord blood samples (mean sorted: 18 x 10(6) cells) revealed no positive findings, which demonstrates that the level and/or frequency of ETV6-RUNX1-positive cells is markedly lower than suggested in previous studies. |
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Department of Paediatrics, The University Hospital Rigshospitalet, Copenhagen, Denmark |
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0006-4971 |
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WP6 In vivo |
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PMID:20713965 |
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CBM.UAM @ ccobaleda @ |
Serial |
37 |
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