ArticleBlood cancer discovery2022
Genetic and Transcriptional Contributions to Relapse in Normal Karyotype Acute Myeloid Leukemia.
Article in Blood cancer discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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
19 citing papers in PubMed, 29 citations in OpenAlex.
- An Immune Dysfunction Signature Score Predicts Survival in MDS Patients: Insights From a Longitudinal, Multicenter Study.Cancer science · 2026Article
- A unique malignant cell type per patient tumor encoded in each cancer cell transcriptome.iScience · 2026Article
- Dynamic heterogeneity towards drug resistance in AML cells is primarily driven by epigenomic mechanism unveiled by multi-omics analysis.Journal of advanced research · 2026Article
- Intra-Leukemic Interferon Signaling Suppresses Expansion and Mediates Chemoresistance in Human AML.Blood cancer discovery · 2026Article
- Dual relevance ofFrontiers in oncology · 2026Article
- Immune monitoring for relapse of acute myeloid leukemia after allogeneic stem cell transplantation in clinical laboratories.Frontiers in immunology · 2026Review
- Clonal Evolution of Pediatric Acute Myeloid Leukemia and Its Contribution to Disease Relapse.medRxiv : the preprint server for health sciences · 2025Article
- A heterozygous CEBPA mutation disrupting the bZIP domain in a RUNX1 and SRSF2 mutational background causes MDS disease progression.Nature communications · 2025Article
- Mesenchymal stem cells in the bone marrow microenvironment: a double-edged sword for AML.Journal of cancer research and clinical oncology · 2025Review
- Breaking the Bone Marrow Barrier: Peripheral Blood as a Gateway to Measurable Residual Disease Detection in Acute Myelogenous Leukemia.American journal of hematology · 2025Review
- High-dimensional Immune Profiles and Machine Learning May Predict Acute Myeloid Leukemia Relapse Early following Transplant.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- SHP-1 inhibition targets leukaemia stem cells to restore immunosurveillance and enhance chemosensitivity by metabolic reprogramming.Nature cell biology · 2024Article
- Comprehensive characterization of IFNγ signaling in acute myeloid leukemia reveals prognostic and therapeutic strategies.Nature communications · 2024Article
- Mitochondrial abnormalities as a target of intervention in acute myeloid leukemia.Frontiers in oncology · 2024Review
- Description of a novel subtype of acute myeloid leukemia defined by recurrent CBFB insertions.Blood · 2023Article
- Article
- Transcriptional Plasticity Drives Leukemia Immune Escape.Blood cancer discovery · 2022Article
- Longitudinal single-cell transcriptomics reveals distinct patterns of recurrence in acute myeloid leukemia.Molecular cancer · 2022Article
- Recurrent transcriptional responses in AML and MDS patients treated with decitabine.Experimental hematology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
To better understand clonal and transcriptional adaptations after relapse in patients with acute myeloid leukemia (AML), we collected presentation and relapse samples from six normal karyotype AML cases. We performed enhanced whole-genome sequencing to characterize clonal evolution, and deep-coverage single-cell RNA sequencing on the same samples, which yielded 142,642 high-quality cells for analysis. Identifying expressed mutations in individual cells enabled us to discriminate between normal and AML cells, to identify coordinated changes in the genome and transcriptome, and to identify subclone-specific cell states. We quantified the coevolution of genetic and transcriptional heterogeneity during AML progression, and found that transcriptional changes were significantly correlated with genetic changes. However, transcriptional adaptation sometimes occurred independently, suggesting that clonal evolution does not represent all relevant biological changes. In three cases, we identified cells at diagnosis that likely seeded the relapse. Finally, these data revealed a conserved relapse-enriched leukemic cell state bearing markers of stemness, quiescence, and adhesion. SIGNIFICANCE: These data enabled us to identify a relapse-enriched leukemic cell state with distinct transcriptional properties. Detailed case-by-case analyses elucidated the complex ways in which the AML genome, transcriptome, and immune microenvironment interact to evade chemotherapy. These analyses provide a blueprint for evaluating these factors in larger cohorts.
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.