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  • 1
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    Variable clonal repopulation dynamics influence chemotherapy response in colorectal cancer (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-15
    Description: Intratumoral heterogeneity arises through the evolution of genetically diverse subclones during tumor progression. However, it remains unknown whether cells within single genetic clones are functionally equivalent. By combining DNA copy number alteration (CNA) profiling, sequencing, and lentiviral lineage tracking, we followed the repopulation dynamics of 150 single lentivirus-marked lineages from 10 human colorectal cancers through serial xenograft passages in mice. CNA and mutational analysis distinguished individual clones and showed that clones remained stable upon serial transplantation. Despite this stability, the proliferation, persistence, and chemotherapy tolerance of lentivirally marked lineages were variable within each clone. Chemotherapy promoted the dominance of previously minor or dormant lineages. Thus, apart from genetic diversity, tumor cells display inherent functional variability in tumor propagation potential, which contributes to both cancer growth and therapy tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kreso, Antonija -- O'Brien, Catherine A -- van Galen, Peter -- Gan, Olga I -- Notta, Faiyaz -- Brown, Andrew M K -- Ng, Karen -- Ma, Jing -- Wienholds, Erno -- Dunant, Cyrille -- Pollett, Aaron -- Gallinger, Steven -- McPherson, John -- Mullighan, Charles G -- Shibata, Darryl -- Dick, John E -- R21 CA149990/CA/NCI NIH HHS/ -- R21CA149990-01/CA/NCI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2013 Feb 1;339(6119):543-8. doi: 10.1126/science.1227670. Epub 2012 Dec 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Campbell Family Institute, Ontario Cancer Institute, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23239622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Cell Tracking ; Clonal Evolution/*genetics ; Clone Cells ; Colorectal Neoplasms/*drug therapy/genetics/*pathology ; DNA Copy Number Variations ; Drug Resistance, Neoplasm/*genetics ; Humans ; Lentivirus ; Mice ; Neoplasm Transplantation ; Transcriptome ; Transduction, Genetic ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Evolution of human BCR-ABL1 lymphoblastic leukaemia-initiating cells (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-01-21
    Description: Many tumours are composed of genetically diverse cells; however, little is known about how diversity evolves or the impact that diversity has on functional properties. Here, using xenografting and DNA copy number alteration (CNA) profiling of human BCR-ABL1 lymphoblastic leukaemia, we demonstrate that genetic diversity occurs in functionally defined leukaemia-initiating cells and that many diagnostic patient samples contain multiple genetically distinct leukaemia-initiating cell subclones. Reconstructing the subclonal genetic ancestry of several samples by CNA profiling demonstrated a branching multi-clonal evolution model of leukaemogenesis, rather than linear succession. For some patient samples, the predominant diagnostic clone repopulated xenografts, whereas in others it was outcompeted by minor subclones. Reconstitution with the predominant diagnosis clone was associated with more aggressive growth properties in xenografts, deletion of CDKN2A and CDKN2B, and a trend towards poorer patient outcome. Our findings link clonal diversity with leukaemia-initiating-cell function and underscore the importance of developing therapies that eradicate all intratumoral subclones.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Notta, Faiyaz -- Mullighan, Charles G -- Wang, Jean C Y -- Poeppl, Armando -- Doulatov, Sergei -- Phillips, Letha A -- Ma, Jing -- Minden, Mark D -- Downing, James R -- Dick, John E -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2011 Jan 20;469(7330):362-7. doi: 10.1038/nature09733.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Stem Cell and Developmental Biology, Campbell Family Institute for Cancer Research/Ontario Cancer Institute, Toronto, Ontario M5G 1L7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21248843" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival ; Clone Cells/*metabolism/*pathology ; Cyclin-Dependent Kinase Inhibitor p15/deficiency/genetics ; DNA Copy Number Variations/genetics ; Disease Progression ; *Evolution, Molecular ; Fusion Proteins, bcr-abl/*genetics ; Genes, p16 ; Humans ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Models, Biological ; Neoplasm Transplantation ; Oligonucleotide Array Sequence Analysis ; Philadelphia Chromosome ; Polymorphism, Single Nucleotide/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics/*pathology ; Survival Rate ; Transplantation, Heterologous
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    The genetic basis of early T-cell precursor acute lymphoblastic leukaemia (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-01-13
    Description: Early T-cell precursor acute lymphoblastic leukaemia (ETP ALL) is an aggressive malignancy of unknown genetic basis. We performed whole-genome sequencing of 12 ETP ALL cases and assessed the frequency of the identified somatic mutations in 94 T-cell acute lymphoblastic leukaemia cases. ETP ALL was characterized by activating mutations in genes regulating cytokine receptor and RAS signalling (67% of cases; NRAS, KRAS, FLT3, IL7R, JAK3, JAK1, SH2B3 and BRAF), inactivating lesions disrupting haematopoietic development (58%; GATA3, ETV6, RUNX1, IKZF1 and EP300) and histone-modifying genes (48%; EZH2, EED, SUZ12, SETD2 and EP300). We also identified new targets of recurrent mutation including DNM2, ECT2L and RELN. The mutational spectrum is similar to myeloid tumours, and moreover, the global transcriptional profile of ETP ALL was similar to that of normal and myeloid leukaemia haematopoietic stem cells. These findings suggest that addition of myeloid-directed therapies might improve the poor outcome of ETP ALL.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267575/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267575/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jinghui -- Ding, Li -- Holmfeldt, Linda -- Wu, Gang -- Heatley, Sue L -- Payne-Turner, Debbie -- Easton, John -- Chen, Xiang -- Wang, Jianmin -- Rusch, Michael -- Lu, Charles -- Chen, Shann-Ching -- Wei, Lei -- Collins-Underwood, J Racquel -- Ma, Jing -- Roberts, Kathryn G -- Pounds, Stanley B -- Ulyanov, Anatoly -- Becksfort, Jared -- Gupta, Pankaj -- Huether, Robert -- Kriwacki, Richard W -- Parker, Matthew -- McGoldrick, Daniel J -- Zhao, David -- Alford, Daniel -- Espy, Stephen -- Bobba, Kiran Chand -- Song, Guangchun -- Pei, Deqing -- Cheng, Cheng -- Roberts, Stefan -- Barbato, Michael I -- Campana, Dario -- Coustan-Smith, Elaine -- Shurtleff, Sheila A -- Raimondi, Susana C -- Kleppe, Maria -- Cools, Jan -- Shimano, Kristin A -- Hermiston, Michelle L -- Doulatov, Sergei -- Eppert, Kolja -- Laurenti, Elisa -- Notta, Faiyaz -- Dick, John E -- Basso, Giuseppe -- Hunger, Stephen P -- Loh, Mignon L -- Devidas, Meenakshi -- Wood, Brent -- Winter, Stuart -- Dunsmore, Kimberley P -- Fulton, Robert S -- Fulton, Lucinda L -- Hong, Xin -- Harris, Christopher C -- Dooling, David J -- Ochoa, Kerri -- Johnson, Kimberly J -- Obenauer, John C -- Evans, William E -- Pui, Ching-Hon -- Naeve, Clayton W -- Ley, Timothy J -- Mardis, Elaine R -- Wilson, Richard K -- Downing, James R -- Mullighan, Charles G -- CA114766/CA/NCI NIH HHS/ -- CA98413/CA/NCI NIH HHS/ -- CA98543/CA/NCI NIH HHS/ -- P30 CA021765/CA/NCI NIH HHS/ -- P30 CA021765-33/CA/NCI NIH HHS/ -- P30CA021765/CA/NCI NIH HHS/ -- U01GM92666/GM/NIGMS NIH HHS/ -- U54 HG003079/HG/NHGRI NIH HHS/ -- England -- Nature. 2012 Jan 11;481(7380):157-63. doi: 10.1038/nature10725.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Computational Biology and Bioinformatics, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22237106" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Child ; DNA Copy Number Variations/genetics ; Genes, ras/genetics ; Genetic Predisposition to Disease/*genetics ; Genome, Human/genetics ; Genomics ; Hematopoiesis/genetics ; Histones/metabolism ; Humans ; Janus Kinases/genetics/metabolism ; Leukemia, Myeloid, Acute/drug therapy/genetics/pathology ; Molecular Sequence Data ; Mutation/*genetics ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/drug therapy/*genetics/pathology ; Receptors, Interleukin-7/genetics ; Sequence Analysis, DNA ; Signal Transduction/genetics ; Stem Cells/metabolism/pathology ; T-Lymphocytes/metabolism/pathology ; Translocation, Genetic/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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