ArticleBlood2010
SNP array analysis of tyrosine kinase inhibitor-resistant chronic myeloid leukemia identifies heterogeneous secondary genomic alterations.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Pooled it
- Clonal evolution and clinical implications of genetic abnormalities in blastic transformation of chronic myeloid leukaemia.Nature communications · 2021Article
- Genomic Copy Number Variants in CML Patients With the Philadelphia Chromosome (Ph+): An Update.Frontiers in genetics · 2021Article
- Mechanisms of Disease Progression and Resistance to Tyrosine Kinase Inhibitor Therapy in Chronic Myeloid Leukemia: An Update.International journal of molecular sciences · 2019Review
- SNP Array in Hematopoietic Neoplasms: A Review.Microarrays (Basel, Switzerland) · 2015Review
- Use of single nucleotide polymorphism array technology to improve the identification of chromosomal lesions in leukemia.Current cancer drug targets · 2013Review
- Genomic instability may originate from imatinib-refractory chronic myeloid leukemia stem cells.Blood · 2013Article
- Genetic mechanisms of chronic myeloid leukemia blastic transformation.Current hematologic malignancy reports · 2012Review
- Selection of therapy: rational decisions based on molecular events.Hematology/oncology clinics of North America · 2011Review
- Article
- 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
- Chronic myeloid leukemia patients sensitive and resistant to imatinib treatment show different metabolic responses.PloS one · 2010Article
- Chronic myeloid leukemia: mechanisms of blastic transformation.The Journal of clinical investigation · 2010Review
Corrections and comments
- Erratum issuedThoenissen, Nils H [corrected to Thoennissen, Nils H]
Authors and funding
20 authors at 10 institutions in 4 countries.
Funding
Abstract
To elucidate whether tyrosine kinase inhibitor (TKI) resistance in chronic myeloid leukemia is associated with characteristic genomic alterations, we analyzed DNA samples from 45 TKI-resistant chronic myeloid leukemia patients with 250K single nucleotide polymorphism arrays. From 20 patients, matched serial samples of pretreatment and TKI resistance time points were available. Eleven of the 45 TKI-resistant patients had mutations of BCR-ABL1, including 2 T315I mutations. Besides known TKI resistance-associated genomic lesions, such as duplication of the BCR-ABL1 gene (n = 8) and trisomy 8 (n = 3), recurrent submicroscopic alterations, including acquired uniparental disomy, were detectable on chromosomes 1, 8, 9, 17, 19, and 22. On chromosome 22, newly acquired and recurrent deletions of the IGLC1 locus were detected in 3 patients, who had previously presented with lymphoid or myeloid blast crisis. This may support a hypothesis of TKI-induced selection of subclones differentiating into immature B-cell progenitors as a mechanism of disease progression and evasion of TKI sensitivity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.