ArticleNature cell biology2021
Dynamic transcriptional reprogramming leads to immunotherapeutic vulnerabilities in myeloma.
Article in Nature cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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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.
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Who cites it
45 citing papers in PubMed, 51 citations in OpenAlex.
- Cell-free DNA for the detection of emerging treatment failure in relapsed/ refractory multiple myeloma.Leukemia · 2022Trial
- Methylation-Associated Differentiation Features Define Biological and Prognostic Heterogeneity in CMS4 Colorectal Cancer.International journal of molecular sciences · 2026Article
- ISGylation-mediated stabilization of CYP4Z1 fuels breast cancer initiation and progression.Experimental & molecular medicine · 2026Article
- Protocol for culture, drug treatment, and dissociation of patient-derived 3D ovarian cancer microspheroids for flow cytometry.STAR protocols · 2026Article
- IL-6-driven POU2AF1 and ELL2 are key regulators of multiple myeloma-distinct transcriptional and splicing programs.Blood advances · 2026Article
- The Shape-Shifting Myeloma: Adaptive Plasticity as a Hallmark of Relapse and Refractoriness.Cancers · 2026Review
- Promoter hypermethylation as a reversible mechanism of resistance to GPRC5D-directed therapy in multiple myeloma.Haematologica · 2026Article
- Article
- Altered immune and treatment response gene expression signatures among poverty-exposed children with B-ALL.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic reprogramming in multiple myeloma-Challenges and opportunities.International journal of cancer · 2026Review
- ID2 Suppresses Multiple Myeloma Cell Proliferation by Repressing the Activity of the Transcription Factor TCF3.Blood cancer discovery · 2026Article
- Pan-cancer bone metastasis atlas at single-cell resolution identifies a distinct tumor-associated macrophage subset for mediating Denosumab-induced immunosensitization in lung cancer bone metastasis.International journal of biological sciences · 2026Article
- Investigation of lncRNA expression in newly diagnosed multiple myeloma reveals a LINC01432-CELF2 axis as an inhibitor of apoptosis.Oncogenesis · 2025Article
- Exploring secondary extramedullary myeloma disease: a five-predictor scoring system with spotlight on double-hit cytogenetics.BMC medicine · 2025Article
- CXCR4/CXCL12 blockade therapy; a new horizon in TNBC therapy.Medical oncology (Northwood, London, England) · 2025Review
- Single-Cell Multiomics Reveals TCR Clonotype-Specific Phenotype and Stemness Heterogeneity of T-ALL Cells.Cell proliferation · 2025Article
- Single-cell analysis of neoplastic plasma cells identifies myeloma pathobiology mediators and potential targets.Cell reports. Medicine · 2025Article
- Single-cell sequencing reveals the mechanisms of multiple myeloma progression: clarity or confusion?Annals of hematology · 2025Review
- Epigenomic heterogeneity as a source of tumour evolution.Nature reviews. Cancer · 2025Review
- To Explore the Key Subgroup and Their Immune Microenvironment During the Formation of Coronary Plaque With scRNA-seq.Cardiology research and practice · 2025Article
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 1 country.
Funding
Abstract
While there is extensive evidence for genetic variation as a basis for treatment resistance, other sources of variation result from cellular plasticity. Using multiple myeloma as an example of an incurable lymphoid malignancy, we show how cancer cells modulate lineage restriction, adapt their enhancer usage and employ cell-intrinsic diversity for survival and treatment escape. By using single-cell transcriptome and chromatin accessibility profiling, we show that distinct transcriptional states co-exist in individual cancer cells and that differential transcriptional regulon usage and enhancer rewiring underlie these alternative transcriptional states. We demonstrate that exposure to standard treatment further promotes transcriptional reprogramming and differential enhancer recruitment while simultaneously reducing developmental potential. Importantly, treatment generates a distinct complement of actionable immunotherapy targets, such as CXCR4, which can be exploited to overcome treatment resistance. Our studies therefore delineate how to transform the cellular plasticity that underlies drug resistance into immuno-oncologic therapeutic opportunities.
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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.