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Effectively Targeting Treatment-Naïve CML Stem/Progenitor Cells From Imatinib-Nonresponders With Combination Treatments Of JAK2 and ABL Inhibitors In Vitro and In Vivo

2013· article· en· W2547251167 on OpenAlexaff
Hanyang Lin, Min Chen, Katharina Rothe, Matthew V. Lorenzi, Adrian Woolfson, Xiaoyan Jiang

Bibliographic record

VenueBlood · 2013
Typearticle
Languageen
FieldMedicine
TopicChronic Myeloid Leukemia Treatments
Canadian institutionsUniversity of British ColumbiaBC Cancer Agency
Fundersnot available
KeywordsStem cellImatinib mesylateProgenitor cellDasatinibNilotinibCancer researchImatinibTyrosine kinaseCD34HaematopoiesisK562 cellsTyrosine-kinase inhibitorMyeloid leukemiaMedicineBiologyImmunologyLeukemiaInternal medicineCell biologyReceptorCancer

Abstract

fetched live from OpenAlex

Abstract The hallmark of chronic myeloid leukemia (CML) is the presence of a BCR-ABL fusion gene that originates in hematopoietic stem cells. The BCR-ABL oncoprotein has constitutively elevated tyrosine kinase (TK) activity and drives CML pathogenesis. Introduction of Imatinib Mesylate (IM) and other tyrosine kinase inhibitor (TKI) therapies has had a major impact on the treatment of chronic phase CML, but early relapses and persistence of leukemic stem cells remain problematic. We have recently identified an AHI-1–BCR-ABL–JAK2 protein complex that contributes to the transforming activity of BCR-ABL and to IM-resistance of CML stem/progenitor cells. We therefore hypothesized that combined suppression of BCR-ABL and JAK2 activities might more effectively eliminate CML stem/progenitor cells in vitro and in vivo. Several JAK2 inhibitors are currently in various stages of clinical trials, but their off-target effects on normal primitive hematopoietic cells remain a concern. We have now examined the biological effects of an orally bioavailable, selective JAK2 inhibitor (BMS-911543) in combination with TKIs, including IM, dasatinib (DA) and nilotinib, both on CML cells lines and CD34+ treatment-naïve IM-nonresponder cells, which were obtained at diagnosis from CML patients who were classified subsequently, after initiation of IM therapy, as IM-nonresponders. In cell line studies, Western blot analysis showed that combination treatment was more effective at reducing pSTAT5 levels in K562 cells and IM-resistant K562 cells than single agents. In colony-forming cell (CFC) assays, combination treatment resulted in a greater reduction in colonies produced from these cells compared to single agents (2-3 fold, p<0.05). Similarly, intracellular staining analyses showed that combined exposure of CD34+ CML cells (n=4) to BMS-911543 and a TKI produced a deeper, more prolonged suppression of pSTAT5 and pCRKL activity than single agents (40-46% suppression for the combinations vs. 15-20% suppression for the single agents at 72 hrs, p<0.05). Combination treatments also resulted in greater inhibition of colony growth of CD34+ CML cells compared to single agents (n=7, 74-86% vs. 40-50%, p<0.05). Interestingly, the combination of BMS-911543 and a TKI almost completely inhibited BFU-E colony formation as compared to treatment with TKI alone (92-100% vs.63-66%, p<0.01). CFU-GM colonies were also more significantly reduced as a result of combination treatment, compared to single agents (49-71% vs. 30-39%, p<0.01). Long-term culture-initiating cell assays showed that more primitive cells were also more significantly eliminated by combination treatments (n=3, 2-3 fold, p<0.05). Importantly, our CFC data indicate that BMS-911543 is less toxic to normal bone marrow (BM) CD34+ cells (n=7) than the same cells from CML samples (n=7, 2-3 fold, p<0.05). To test the ability of combination treatments to eliminate primitive CML cells with in vivo leukemia propagating activity, we injected primitive CML cells intravenously into NSG mice and treated mice with inhibitors by oral gavage for two weeks. Mice undergoing combination treatment showed significantly reduced weight loss and engraftment levels in peripheral blood, BM , spleen, and liver compared to mice treated with single agents (0.14% vs. 6.14%, 1.17% vs. 26.3%, 2.46% vs. 51.5%, and 77.8% vs. 92.9%, respectively, p<0.05). H&E histology staining revealed that mice treated with DA and BMS-911543 had less infiltration of leukemic cells into their spleens and livers than mice treated with DA alone. Quantitative RT-PCR analysis further demonstrated a statistically significant reduction in BCR-ABL transcript levels in spleen, liver, and BM of mice treated with a combination of DA and BMS-911543 compared to mice treated with single agents (15-20 fold, p<0.05). Most importantly, combination treatments significantly enhanced survival of leukemic mice compared to mice treated with single agents (median survival of IM + BMS-911543 vs. IM: 70 days vs. 60.5 days, p<0.05; DA + BMS-911543 vs. DA: 96.5 days vs. 81 days, p<0.001). This study suggests that simultaneously targeting BCR-ABL and JAK2 activities in CML stem/progenitor cells may improve outcomes in patients, especially those destined to develop TKI resistance. Disclosures: No relevant conflicts of interest to declare.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.006

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0020.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.008
GPT teacher head0.221
Teacher spread0.214 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

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Citations0
Published2013
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