Transcriptomic classes of BCR-ABL1 lymphoblastic leukemia

In BCR-ABL1 lymphoblastic leukemia, treatment heterogeneity to tyrosine kinase inhibitors (TKIs), especially in the absence of kinase domain mutations in BCR-ABL1 , is poorly understood. Through deep molecular profiling, we uncovered three transcriptomic subtypes of BCR-ABL1 lymphoblastic leukemia,...

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Veröffentlicht in:Nature genetics Jg. 55; H. 7; S. 1186 - 1197
Hauptverfasser: Kim, Jaeseung C., Chan-Seng-Yue, Michelle, Ge, Sabrina, Zeng, Andy G. X., Ng, Karen, Gan, Olga I., Garcia-Prat, Laura, Flores-Figueroa, Eugenia, Woo, Tristan, Zhang, Amy Xin Wei, Arruda, Andrea, Chithambaram, Shivapriya, Dobson, Stephanie M., Khoo, Amanda, Khan, Shahbaz, Ibrahimova, Narmin, George, Ann, Tierens, Anne, Hitzler, Johann, Kislinger, Thomas, Dick, John E., McPherson, John D., Minden, Mark D., Notta, Faiyaz
Format: Journal Article
Sprache:Englisch
Veröffentlicht: New York Nature Publishing Group US 01.07.2023
Nature Publishing Group
Schlagworte:
38/91
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631/67/1990/283/2125
Agriculture
Animal Genetics and Genomics
Antigens
BCR-ABL protein
Biomedical and Life Sciences
Biomedicine
Blood
Cancer Research
Cell cycle
Cell differentiation
Cell Differentiation - genetics
Clinical outcomes
Cloning
Depth profiling
Disease
Flow cytometry
Fusion Proteins, bcr-abl - genetics
Fusion Proteins, bcr-abl - metabolism
Gene expression
Gene Expression Profiling
Gene Function
Genomics
Genotype & phenotype
Heterogeneity
Human Genetics
Humans
Kinases
Kruskal-Wallis test
Leukemia
Lymphatic leukemia
Lymphocytes B
Maturation
Mutation
Patients
Phenotypes
Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics
Progenitor cells
Protein Kinase Inhibitors - pharmacology
Protein Kinase Inhibitors - therapeutic use
Protein-tyrosine kinase
Stem cells
Thermal resistance
Transcriptome - genetics
Transcriptomics
Tyrosine
ISSN:1061-4036, 1546-1718, 1546-1718
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Abstract In BCR-ABL1 lymphoblastic leukemia, treatment heterogeneity to tyrosine kinase inhibitors (TKIs), especially in the absence of kinase domain mutations in BCR-ABL1 , is poorly understood. Through deep molecular profiling, we uncovered three transcriptomic subtypes of BCR-ABL1 lymphoblastic leukemia, each representing a maturation arrest at a stage of B-cell progenitor differentiation. An earlier arrest was associated with lineage promiscuity, treatment refractoriness and poor patient outcomes. A later arrest was associated with lineage fidelity, durable leukemia remissions and improved patient outcomes. Each maturation arrest was marked by specific genomic events that control different transition points in B-cell development. Interestingly, these events were absent in BCR-ABL1 + preleukemic stem cells isolated from patients regardless of subtype, which supports that transcriptomic phenotypes are determined downstream of the leukemia-initialing event. Overall, our data indicate that treatment response and TKI efficacy are unexpected outcomes of the differentiation stage at which this leukemia transforms. Transcriptomic analysis of BCR-ABL1 lymphoblastic leukemia identifies three subgroups, each associated with a maturation arrest at a specific stage of B-cell progenitor differentiation and distinct genetic and clinical features.
AbstractList In BCR-ABL1 lymphoblastic leukemia, treatment heterogeneity to tyrosine kinase inhibitors (TKIs), especially in the absence of kinase domain mutations in BCR-ABL1, is poorly understood. Through deep molecular profiling, we uncovered three transcriptomic subtypes of BCR-ABL1 lymphoblastic leukemia, each representing a maturation arrest at a stage of B-cell progenitor differentiation. An earlier arrest was associated with lineage promiscuity, treatment refractoriness and poor patient outcomes. A later arrest was associated with lineage fidelity, durable leukemia remissions and improved patient outcomes. Each maturation arrest was marked by specific genomic events that control different transition points in B-cell development. Interestingly, these events were absent in BCR-ABL1 preleukemic stem cells isolated from patients regardless of subtype, which supports that transcriptomic phenotypes are determined downstream of the leukemia-initialing event. Overall, our data indicate that treatment response and TKI efficacy are unexpected outcomes of the differentiation stage at which this leukemia transforms.
In BCR-ABL1 lymphoblastic leukemia, treatment heterogeneity to tyrosine kinase inhibitors (TKIs), especially in the absence of kinase domain mutations in BCR-ABL1, is poorly understood. Through deep molecular profiling, we uncovered three transcriptomic subtypes of BCR-ABL1 lymphoblastic leukemia, each representing a maturation arrest at a stage of B-cell progenitor differentiation. An earlier arrest was associated with lineage promiscuity, treatment refractoriness and poor patient outcomes. A later arrest was associated with lineage fidelity, durable leukemia remissions and improved patient outcomes. Each maturation arrest was marked by specific genomic events that control different transition points in B-cell development. Interestingly, these events were absent in BCR-ABL1+ preleukemic stem cells isolated from patients regardless of subtype, which supports that transcriptomic phenotypes are determined downstream of the leukemia-initialing event. Overall, our data indicate that treatment response and TKI efficacy are unexpected outcomes of the differentiation stage at which this leukemia transforms.In BCR-ABL1 lymphoblastic leukemia, treatment heterogeneity to tyrosine kinase inhibitors (TKIs), especially in the absence of kinase domain mutations in BCR-ABL1, is poorly understood. Through deep molecular profiling, we uncovered three transcriptomic subtypes of BCR-ABL1 lymphoblastic leukemia, each representing a maturation arrest at a stage of B-cell progenitor differentiation. An earlier arrest was associated with lineage promiscuity, treatment refractoriness and poor patient outcomes. A later arrest was associated with lineage fidelity, durable leukemia remissions and improved patient outcomes. Each maturation arrest was marked by specific genomic events that control different transition points in B-cell development. Interestingly, these events were absent in BCR-ABL1+ preleukemic stem cells isolated from patients regardless of subtype, which supports that transcriptomic phenotypes are determined downstream of the leukemia-initialing event. Overall, our data indicate that treatment response and TKI efficacy are unexpected outcomes of the differentiation stage at which this leukemia transforms.
In BCR-ABL1 lymphoblastic leukemia, treatment heterogeneity to tyrosine kinase inhibitors (TKIs), especially in the absence of kinase domain mutations in BCR-ABL1 , is poorly understood. Through deep molecular profiling, we uncovered three transcriptomic subtypes of BCR-ABL1 lymphoblastic leukemia, each representing a maturation arrest at a stage of B-cell progenitor differentiation. An earlier arrest was associated with lineage promiscuity, treatment refractoriness and poor patient outcomes. A later arrest was associated with lineage fidelity, durable leukemia remissions and improved patient outcomes. Each maturation arrest was marked by specific genomic events that control different transition points in B-cell development. Interestingly, these events were absent in BCR-ABL1 + preleukemic stem cells isolated from patients regardless of subtype, which supports that transcriptomic phenotypes are determined downstream of the leukemia-initialing event. Overall, our data indicate that treatment response and TKI efficacy are unexpected outcomes of the differentiation stage at which this leukemia transforms.
In BCR-ABL1 lymphoblastic leukemia, treatment heterogeneity to tyrosine kinase inhibitors (TKIs), especially in the absence of kinase domain mutations in BCR-ABL1, is poorly understood. Through deep molecular profiling, we uncovered three transcriptomic subtypes of BCR-ABL1 lymphoblastic leukemia, each representing a maturation arrest at a stage of B-cell progenitor differentiation. An earlier arrest was associated with lineage promiscuity, treatment refractoriness and poor patient outcomes. A later arrest was associated with lineage fidelity, durable leukemia remissions and improved patient outcomes. Each maturation arrest was marked by specific genomic events that control different transition points in B-cell development. Interestingly, these events were absent in BCR-ABL1+ preleukemic stem cells isolated from patients regardless of subtype, which supports that transcriptomic phenotypes are determined downstream of the leukemia-initialing event. Overall, our data indicate that treatment response and TKI efficacy are unexpected outcomes of the differentiation stage at which this leukemia transforms.
In BCR-ABL1 lymphoblastic leukemia, treatment heterogeneity to tyrosine kinase inhibitors (TKIs), especially in the absence of kinase domain mutations in BCR-ABL1, is poorly understood. Through deep molecular profiling, we uncovered three transcriptomic subtypes of BCR-ABL1 lymphoblastic leukemia, each representing a maturation arrest at a stage of B-cell progenitor differentiation. An earlier arrest was associated with lineage promiscuity, treatment refractoriness and poor patient outcomes. A later arrest was associated with lineage fidelity, durable leukemia remissions and improved patient outcomes. Each maturation arrest was marked by specific genomic events that control different transition points in B-cell development. Interestingly, these events were absent in BCR-ABL1+ preleukemic stem cells isolated from patients regardless of subtype, which supports that transcriptomic phenotypes are determined downstream of the leukemia-initialing event. Overall, our data indicate that treatment response and TKI efficacy are unexpected outcomes of the differentiation stage at which this leukemia transforms. Transcriptomic analysis of BCR-ABL1 lymphoblastic leukemia identifies three subgroups, each associated with a maturation arrest at a specific stage of B-cell progenitor differentiation and distinct genetic and clinical features.
In BCR-ABL1 lymphoblastic leukemia, treatment heterogeneity to tyrosine kinase inhibitors (TKIs), especially in the absence of kinase domain mutations in BCR-ABL1 , is poorly understood. Through deep molecular profiling, we uncovered three transcriptomic subtypes of BCR-ABL1 lymphoblastic leukemia, each representing a maturation arrest at a stage of B-cell progenitor differentiation. An earlier arrest was associated with lineage promiscuity, treatment refractoriness and poor patient outcomes. A later arrest was associated with lineage fidelity, durable leukemia remissions and improved patient outcomes. Each maturation arrest was marked by specific genomic events that control different transition points in B-cell development. Interestingly, these events were absent in BCR-ABL1 + preleukemic stem cells isolated from patients regardless of subtype, which supports that transcriptomic phenotypes are determined downstream of the leukemia-initialing event. Overall, our data indicate that treatment response and TKI efficacy are unexpected outcomes of the differentiation stage at which this leukemia transforms. Transcriptomic analysis of BCR-ABL1 lymphoblastic leukemia identifies three subgroups, each associated with a maturation arrest at a specific stage of B-cell progenitor differentiation and distinct genetic and clinical features.
Author Zeng, Andy G. X.
McPherson, John D.
Dick, John E.
Notta, Faiyaz
Kim, Jaeseung C.
Khoo, Amanda
Chithambaram, Shivapriya
Tierens, Anne
Arruda, Andrea
Khan, Shahbaz
Kislinger, Thomas
Flores-Figueroa, Eugenia
Gan, Olga I.
Woo, Tristan
Ng, Karen
Hitzler, Johann
Zhang, Amy Xin Wei
Ge, Sabrina
Garcia-Prat, Laura
Minden, Mark D.
Dobson, Stephanie M.
Ibrahimova, Narmin
Chan-Seng-Yue, Michelle
George, Ann
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  orcidid: 0000-0001-8049-9347
  surname: McPherson
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  givenname: Faiyaz
  orcidid: 0000-0002-5748-3985
  surname: Notta
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  email: faiyaz.notta@gmail.com
  organization: Princess Margaret Cancer Centre, Ontario Institute for Cancer Research, Department of Medical Biophysics, University of Toronto
BackLink https://www.ncbi.nlm.nih.gov/pubmed/37337105$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright The Author(s) 2023
2023. The Author(s).
Copyright Nature Publishing Group Jul 2023
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Snippet In BCR-ABL1 lymphoblastic leukemia, treatment heterogeneity to tyrosine kinase inhibitors (TKIs), especially in the absence of kinase domain mutations in...
In BCR-ABL1 lymphoblastic leukemia, treatment heterogeneity to tyrosine kinase inhibitors (TKIs), especially in the absence of kinase domain mutations in...
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StartPage 1186
SubjectTerms 38/91
45
45/23
631/208/199
631/67/1990/283/2125
Agriculture
Animal Genetics and Genomics
Antigens
BCR-ABL protein
Biomedical and Life Sciences
Biomedicine
Blood
Cancer Research
Cell cycle
Cell differentiation
Cell Differentiation - genetics
Clinical outcomes
Cloning
Depth profiling
Disease
Flow cytometry
Fusion Proteins, bcr-abl - genetics
Fusion Proteins, bcr-abl - metabolism
Gene expression
Gene Expression Profiling
Gene Function
Genomics
Genotype & phenotype
Heterogeneity
Human Genetics
Humans
Kinases
Kruskal-Wallis test
Leukemia
Lymphatic leukemia
Lymphocytes B
Maturation
Mutation
Patients
Phenotypes
Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics
Progenitor cells
Protein Kinase Inhibitors - pharmacology
Protein Kinase Inhibitors - therapeutic use
Protein-tyrosine kinase
Stem cells
Thermal resistance
Transcriptome - genetics
Transcriptomics
Tyrosine
Title Transcriptomic classes of BCR-ABL1 lymphoblastic leukemia
URI https://link.springer.com/article/10.1038/s41588-023-01429-4
https://www.ncbi.nlm.nih.gov/pubmed/37337105
https://www.proquest.com/docview/2837483219
https://www.proquest.com/docview/2827921412
https://pubmed.ncbi.nlm.nih.gov/PMC10335939
Volume 55
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