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  • 1
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    BCR-ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-04-15
    Description: The Philadelphia chromosome, a chromosomal abnormality that encodes BCR-ABL1, is the defining lesion of chronic myelogenous leukaemia (CML) and a subset of acute lymphoblastic leukaemia (ALL). To define oncogenic lesions that cooperate with BCR-ABL1 to induce ALL, we performed a genome-wide analysis of diagnostic leukaemia samples from 304 individuals with ALL, including 43 BCR-ABL1 B-progenitor ALLs and 23 CML cases. IKZF1 (encoding the transcription factor Ikaros) was deleted in 83.7% of BCR-ABL1 ALL, but not in chronic-phase CML. Deletion of IKZF1 was also identified as an acquired lesion at the time of transformation of CML to ALL (lymphoid blast crisis). The IKZF1 deletions resulted in haploinsufficiency, expression of a dominant-negative Ikaros isoform, or the complete loss of Ikaros expression. Sequencing of IKZF1 deletion breakpoints suggested that aberrant RAG-mediated recombination is responsible for the deletions. These findings suggest that genetic lesions resulting in the loss of Ikaros function are an important event in the development of BCR-ABL1 ALL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mullighan, Charles G -- Miller, Christopher B -- Radtke, Ina -- Phillips, Letha A -- Dalton, James -- Ma, Jing -- White, Deborah -- Hughes, Timothy P -- Le Beau, Michelle M -- Pui, Ching-Hon -- Relling, Mary V -- Shurtleff, Sheila A -- Downing, James R -- England -- Nature. 2008 May 1;453(7191):110-4. doi: 10.1038/nature06866. Epub 2008 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, 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/18408710" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; Fusion Proteins, bcr-abl/*genetics ; *Gene Deletion ; Humans ; Ikaros Transcription Factor/chemistry/*deficiency/*genetics/metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*genetics/pathology ; Polymorphism, Single Nucleotide/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics/pathology ; Protein Isoforms/chemistry/genetics/metabolism ; Protein Structure, Tertiary
    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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  • 2
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    Genomic analysis of the clonal origins of relapsed acute lymphoblastic leukemia (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-29
    Description: Most children with acute lymphoblastic leukemia (ALL) can be cured, but the prognosis is dismal for the minority of patients who relapse after treatment. To explore the genetic basis of relapse, we performed genome-wide DNA copy number analyses on matched diagnosis and relapse samples from 61 pediatric patients with ALL. The diagnosis and relapse samples typically showed different patterns of genomic copy number abnormalities (CNAs), with the CNAs acquired at relapse preferentially affecting genes implicated in cell cycle regulation and B cell development. Most relapse samples lacked some of the CNAs present at diagnosis, which suggests that the cells responsible for relapse are ancestral to the primary leukemia cells. Backtracking studies revealed that cells corresponding to the relapse clone were often present as minor subpopulations at diagnosis. These data suggest that genomic abnormalities contributing to ALL relapse are selected for during treatment, and they point to new targets for therapeutic intervention.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746051/" 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/PMC2746051/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mullighan, Charles G -- Phillips, Letha A -- Su, Xiaoping -- Ma, Jing -- Miller, Christopher B -- Shurtleff, Sheila A -- Downing, James R -- P30 CA021765/CA/NCI NIH HHS/ -- P30 CA021765-30/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 28;322(5906):1377-80. doi: 10.1126/science.1164266.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19039135" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes ; Cell Cycle/genetics ; Child ; Cyclin-Dependent Kinase Inhibitor p15/genetics ; Gene Deletion ; *Gene Dosage ; Genes, p16 ; *Genome, Human ; Genomics ; Humans ; *Loss of Heterozygosity ; Lymphopoiesis ; Metabolic Networks and Pathways/genetics ; *Mutation ; Oligonucleotide Array Sequence Analysis ; *Polymorphism, Single Nucleotide ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/*genetics/pathology ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/*genetics/pathology ; Proto-Oncogene Proteins c-ets/genetics ; Recurrence ; Repressor Proteins/genetics
    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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