ArticleCancer discovery2020
Relapse-Fated Latent Diagnosis Subclones in Acute B Lineage Leukemia Are Drug Tolerant and Possess Distinct Metabolic Programs.
Article in Cancer discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
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Who cites it
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
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- The chemotherapy-induced senescence-associated secretome promotes cell detachment and metastatic dissemination through metabolic reprogramming.Nature aging · 2026Article
- Relapse in childhood B-cell precursor acute lymphoblastic leukemia: insights from transcriptomic signatures of diagnostic bone marrow.Frontiers in oncology · 2026Review
- Metabolic adaptations in cancer progression.Physiological reviews · 2026Review
- Functional precision approach in patients with very high risk acute lymphoblastic leukaemia in India: a single-centre cohort study.The Lancet regional health. Southeast Asia · 2026Article
- Complex genotype-phenotype relationships shape the response to treatment of down syndrome childhood acute lymphoblastic leukaemia.Scientific reports · 2025Article
- Multipotent lineage potential in B cell acute lymphoblastic leukemia is associated with distinct cellular origins and clinical features.Nature cancer · 2025Article
- High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non-Small Cell Lung Cancer in Patients.Cancer discovery · 2025Article
- Unlocking the Heterogeneity in Acute Leukaemia: Dissection of Clonal Architecture and Metabolic Properties for Clinical Interventions.International journal of molecular sciences · 2024Review
- A regression based approach to phylogenetic reconstruction from multi-sample bulk DNA sequencing of tumors.PLoS computational biology · 2024Article
- Orchard: Building large cancer phylogenies using stochastic combinatorial search.PLoS computational biology · 2024Article
- Mitochondrial dsRNA from B-ALL cells stimulates mesenchymal stromal cells to become cancer-associated fibroblasts.Blood advances · 2024Article
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- Drug tolerant persister cell plasticity in cancer: A revolutionary strategy for more effective anticancer therapies.Signal transduction and targeted therapy · 2024Review
- KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance.Current oncology (Toronto, Ont.) · 2024Review
- Raman Spectroscopy as a Research and Diagnostic Tool in Clinical Hematology and Hematooncology.International journal of molecular sciences · 2024Review
- Relapsed Acute Lymphoblastic Leukemia.Indian journal of pediatrics · 2024Review
- Stem cell-like reprogramming is required for leukemia-initiating activity in B-ALL.The Journal of experimental medicine · 2024Article
- Metabolic heterogeneity in cancer.Nature metabolism · 2024Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
33 authors at 5 institutions in 3 countries.
Funding
Abstract
Disease recurrence causes significant mortality in B-progenitor acute lymphoblastic leukemia (B-ALL). Genomic analysis of matched diagnosis and relapse samples shows relapse often arising from minor diagnosis subclones. However, why therapy eradicates some subclones while others survive and progress to relapse remains obscure. Elucidation of mechanisms underlying these differing fates requires functional analysis of isolated subclones. Here, large-scale limiting dilution xenografting of diagnosis and relapse samples, combined with targeted sequencing, identified and isolated minor diagnosis subclones that initiate an evolutionary trajectory toward relapse [termed diagnosis Relapse Initiating clones (dRI)]. Compared with other diagnosis subclones, dRIs were drug-tolerant with distinct engraftment and metabolic properties. Transcriptionally, dRIs displayed enrichment for chromatin remodeling, mitochondrial metabolism, proteostasis programs, and an increase in stemness pathways. The isolation and characterization of dRI subclones reveals new avenues for eradicating dRI cells by targeting their distinct metabolic and transcriptional pathways before further evolution renders them fully therapy-resistant. SIGNIFICANCE: Isolation and characterization of subclones from diagnosis samples of patients with B-ALL who relapsed showed that relapse-fated subclones had increased drug tolerance and distinct metabolic and survival transcriptional programs compared with other diagnosis subclones. This study provides strategies to identify and target clinically relevant subclones before further evolution toward relapse.
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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.