ArticleBMC genomics2010
Deletions of immunoglobulin heavy chain and T cell receptor gene regions are uniquely associated with lymphoid blast transformation of chronic myeloid leukemia.
Article in BMC genomics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 50 citations in OpenAlex.
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- Mechanisms of Disease Progression and Resistance to Tyrosine Kinase Inhibitor Therapy in Chronic Myeloid Leukemia: An Update.International journal of molecular sciences · 2019Review
- Overexpression of RNF38 facilitates TGF-β signaling by Ubiquitinating and degrading AHNAK in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2019Article
- Identification of recurrent noncoding mutations in B-cell lymphoma using capture Hi-C.Blood advances · 2019Article
- NovelExperimental hematology & oncology · 2019Article
- Differential genomics and transcriptomics between tyrosine kinase inhibitor-sensitive and -resistant BCR-ABL-dependent chronic myeloid leukemia.Oncotarget · 2018Article
- Expression of RING Finger Protein 38 in Serotonergic Neurons in the Brain of Nile Tilapia,Frontiers in neuroanatomy · 2018Article
- "Chronic myelogenous leukemia in primary blast crisis" rather than "de novoClinical case reports · 2017Article
- RING Finger Protein 38 Is a Neuronal Protein in the Brain of Nile Tilapia,Frontiers in neuroanatomy · 2017Article
- The Philadelphia chromosome in leukemogenesis.Chinese journal of cancer · 2016Review
- Genetic events other than BCR-ABL1.Current hematologic malignancy reports · 2014Review
- RNF38 encodes a nuclear ubiquitin protein ligase that modifies p53.Biochemical and biophysical research communications · 2013Article
- Myeloproliferative neoplasm with ETV6-ABL1 fusion: a case report and literature review.Molecular cytogenetics · 2013Article
- Function of Ikaros as a tumor suppressor in B cell acute lymphoblastic leukemia.American journal of blood research · 2013Article
- Targeted therapy in rare cancers--adopting the orphans.Nature reviews. Clinical oncology · 2012Review
- Epigenetic control and cancer: the potential of histone demethylases as therapeutic targets.Pharmaceuticals (Basel, Switzerland) · 2012Article
- Significance Analysis of Microarrays (SAM) Offers Clues to Differences Between the Genomes of Adult Philadelphia Positive ALL and the Lymphoid Blast Transformation of CML.Cancer informatics · 2012Article
- Imatinib sensitivity in BCR-ABL1-positive chronic myeloid leukemia cells is regulated by the remaining normal ABL1 allele.Cancer research · 2011Article
- Identification of copy number alterations by array comparative genomic hybridization in patients with late chronic or accelerated phase chronic myeloid leukemia treated with imatinib mesylate.International journal of hematology · 2011Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic myelogenous leukemia (CML) results from the neoplastic transformation of a haematopoietic stem cell. The hallmark genetic abnormality of CML is a chimeric BCR/ABL1 fusion gene resulting from the Philadelphia chromosome rearrangement t(9;22)(q34;q11). Clinical and laboratory studies indicate that the BCR/ABL1 fusion protein is essential for initiation, maintenance and progression of CML, yet the event(s) driving the transformation from chronic phase to blast phase are poorly understood.
resultsHere we report multiple genome aberrations in a collection of 78 CML and 14 control samples by oligonucleotide array comparative genomic hybridization. We found a unique signature of genome deletions within the immunoglobulin heavy chain (IGH) and T cell receptor regions (TCR), frequently accompanied by concomitant loss of sequences within the short arm regions of chromosomes 7 and 9, including IKZF1, HOXA7, CDKN2A/2B, MLLT3, IFNA/B, RNF38, PAX5, JMJD2C and PDCD1LG2 genes.
conclusionsNone of these genome losses were detected in any of the CML samples with myeloid transformation, chronic phase or controls, indicating that their presence is obligatory for the development of a malignant clone with a lymphoid phenotype. Notably, the coincidental deletions at IGH and TCR regions appear to precede the loss of IKZF1 and/or p16 genes in CML indicating a possible involvement of RAG in these deletions.
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