Single-cell multiomics analysis of chronic myeloid leukemia links cellular heterogeneity to therapy response
(2024) In eLife 12.- Abstract
The advent of tyrosine kinase inhibitors (TKIs) as treatment of chronic myeloid leukemia (CML) is a paradigm in molecularly targeted cancer therapy. Nonetheless, TKI-insensitive leukemia stem cells (LSCs) persist in most patients even after years of treatment and are imperative for disease progression as well as recurrence during treatment-free remission (TFR). Here, we have generated high-resolution single-cell multiomics maps from CML patients at diagnosis, retrospectively stratified by BCR::ABL1IS (%) following 12 months of TKI therapy. Simultaneous measurement of global gene expression profiles together with >40 surface markers from the same cells revealed that each patient harbored a unique composition of stem and progenitor... (More)
The advent of tyrosine kinase inhibitors (TKIs) as treatment of chronic myeloid leukemia (CML) is a paradigm in molecularly targeted cancer therapy. Nonetheless, TKI-insensitive leukemia stem cells (LSCs) persist in most patients even after years of treatment and are imperative for disease progression as well as recurrence during treatment-free remission (TFR). Here, we have generated high-resolution single-cell multiomics maps from CML patients at diagnosis, retrospectively stratified by BCR::ABL1IS (%) following 12 months of TKI therapy. Simultaneous measurement of global gene expression profiles together with >40 surface markers from the same cells revealed that each patient harbored a unique composition of stem and progenitor cells at diagnosis. The patients with treatment failure after 12 months of therapy had a markedly higher abundance of molecularly defined primitive cells at diagnosis compared to the optimal responders. The multiomic feature landscape enabled visualization of the primitive fraction as a mixture of molecularly distinct BCR::ABL1+ LSCs and BCR::ABL1-hematopoietic stem cells (HSCs) in variable ratio across patients, and guided their prospective isolation by a combination of CD26 and CD35 cell surface markers. We for the first time show that BCR::ABL1+ LSCs and BCR::ABL1- HSCs can be distinctly separated as CD26+CD35- and CD26-CD35+, respectively. In addition, we found the ratio of LSC/HSC to be higher in patients with prospective treatment failure compared to optimal responders, at diagnosis as well as following 3 months of TKI therapy. Collectively, this data builds a framework for understanding therapy response and adapting treatment by devising strategies to extinguish or suppress TKI-insensitive LSCs.
(Less)
- author
- organization
-
- Stem Cells and Leukemia (research group)
- StemTherapy: National Initiative on Stem Cells for Regenerative Therapy
- Center for Translational Genomics (CTG)
- Stem Cell Center
- Developmental lymphopoiesis and leukemia (research group)
- eSSENCE: The e-Science Collaboration
- Conputational Genomics Group (research group)
- Division of Molecular Medicine and Gene Therapy
- publishing date
- 2024-11-06
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy, Humans, Single-Cell Analysis/methods, Protein Kinase Inhibitors/pharmacology, Neoplastic Stem Cells/metabolism, Retrospective Studies, Male, Female, Gene Expression Profiling, Middle Aged, Multiomics
- in
- eLife
- volume
- 12
- publisher
- eLife Sciences Publications
- external identifiers
-
- pmid:39503729
- scopus:85208603370
- ISSN
- 2050-084X
- DOI
- 10.7554/eLife.92074
- language
- English
- LU publication?
- yes
- additional info
- © 2023, Warfvinge et al.
- id
- d6e13a5b-5786-4781-b112-b2cc39452fab
- date added to LUP
- 2024-12-11 14:21:20
- date last changed
- 2025-01-09 05:31:59
@article{d6e13a5b-5786-4781-b112-b2cc39452fab, abstract = {{<p>The advent of tyrosine kinase inhibitors (TKIs) as treatment of chronic myeloid leukemia (CML) is a paradigm in molecularly targeted cancer therapy. Nonetheless, TKI-insensitive leukemia stem cells (LSCs) persist in most patients even after years of treatment and are imperative for disease progression as well as recurrence during treatment-free remission (TFR). Here, we have generated high-resolution single-cell multiomics maps from CML patients at diagnosis, retrospectively stratified by BCR::ABL1IS (%) following 12 months of TKI therapy. Simultaneous measurement of global gene expression profiles together with >40 surface markers from the same cells revealed that each patient harbored a unique composition of stem and progenitor cells at diagnosis. The patients with treatment failure after 12 months of therapy had a markedly higher abundance of molecularly defined primitive cells at diagnosis compared to the optimal responders. The multiomic feature landscape enabled visualization of the primitive fraction as a mixture of molecularly distinct BCR::ABL1+ LSCs and BCR::ABL1-hematopoietic stem cells (HSCs) in variable ratio across patients, and guided their prospective isolation by a combination of CD26 and CD35 cell surface markers. We for the first time show that BCR::ABL1+ LSCs and BCR::ABL1- HSCs can be distinctly separated as CD26+CD35- and CD26-CD35+, respectively. In addition, we found the ratio of LSC/HSC to be higher in patients with prospective treatment failure compared to optimal responders, at diagnosis as well as following 3 months of TKI therapy. Collectively, this data builds a framework for understanding therapy response and adapting treatment by devising strategies to extinguish or suppress TKI-insensitive LSCs.</p>}}, author = {{Warfvinge, Rebecca and Geironson Ulfsson, Linda and Dhapola, Parashar and Safi, Fatemeh and Sommarin, Mikael and Soneji, Shamit and Hjorth-Hansen, Henrik and Mustjoki, Satu and Richter, Johan and Thakur, Ram Krishna and Karlsson, Göran}}, issn = {{2050-084X}}, keywords = {{Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy; Humans; Single-Cell Analysis/methods; Protein Kinase Inhibitors/pharmacology; Neoplastic Stem Cells/metabolism; Retrospective Studies; Male; Female; Gene Expression Profiling; Middle Aged; Multiomics}}, language = {{eng}}, month = {{11}}, publisher = {{eLife Sciences Publications}}, series = {{eLife}}, title = {{Single-cell multiomics analysis of chronic myeloid leukemia links cellular heterogeneity to therapy response}}, url = {{http://dx.doi.org/10.7554/eLife.92074}}, doi = {{10.7554/eLife.92074}}, volume = {{12}}, year = {{2024}}, }