ArticleBlood2023
C1Q labels a highly aggressive macrophage-like leukemia population indicating extramedullary infiltration and relapse.
Article in Blood, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- LDLRAD2 drives glycolysis and angiogenesis to promote extramedullary infiltration in acute myeloid leukemia.iScience · 2026Article
- Differential expression of CD74 and C1QB in jaw versus long bone osteosarcoma: Insights from animal models, public datasets and clinical cohorts.Journal of bone oncology · 2026Article
- Frequent NPM1 mutation, monoblastic/monocytic origin and prognostic significance of organ and system involvement in myeloid sarcoma: a multicenter study.The journal of pathology. Clinical research · 2026Article
- Diagnosis of pulmonary infiltration by acute monocytic leukemia via routine cytological examination of bronchoalveolar lavage fluid: A case report.CytoJournal · 2026Article
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- Lipid accumulation in foam cells drives C1q-dependent synaptic loss and impairs motor function recovery after spinal cord injury.Communications biology · 2025Article
- Infiltrating macrophages replace Kupffer cells and play diverse roles in severe alcohol-associated hepatitis.Cellular & molecular immunology · 2025Article
- New insights into extracellular vesicles in metastatic cancer: From mechanisms to diagnostics and targeted therapies.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- IGSF9-targeted therapy inhibits the progression of acute myeloid leukemia.Blood advances · 2025Article
- Innovative evaluation of selinexor and JQ1 synergy in leukemia therapy via C-MYC inhibition.Journal of translational medicine · 2025Article
- C1QMolecular cancer · 2025Article
- Diagnostic Approaches in Myeloid Sarcoma.Current issues in molecular biology · 2025Review
- Cancer stem cells and post-therapy tumour recurrence: a systematic review of mechanistic pathways and translational gaps.Ecancermedicalscience · 2025Review
- Intervention effect of regulating GABA-A receptor activity on the formation of experimental abdominal aortic aneurysm in rats.Scientific reports · 2024Article
- CDK9 recruits HUWE1 to degrade RARα and offers therapeutic opportunities for cutaneous T-cell lymphoma.Nature communications · 2024Article
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- Complement or insult: the emerging link between complement cascade deficiencies and pathology of myeloid malignancies.Journal of leukocyte biology · 2024Review
- Myeloid Sarcoma: Novel Advances Regarding Molecular Pathogenesis, Presentation and Therapeutic Options.Journal of clinical medicine · 2024Review
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Authors and funding
19 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extramedullary infiltration (EMI) is a concomitant manifestation that may indicate poor outcome of acute myeloid leukemia (AML). The underlying mechanism remains poorly understood and therapeutic options are limited. Here, we employed single-cell RNA sequencing on bone marrow (BM) and EMI samples from a patient with AML presenting pervasive leukemia cutis. A complement C1Q+ macrophage-like leukemia subset, which was enriched within cutis and existed in BM before EMI manifestations, was identified and further verified in multiple patients with AML. Genomic and transcriptional profiling disclosed mutation and gene expression signatures of patients with EMI that expressed high levels of C1Q. RNA sequencing and quantitative proteomic analysis revealed expression dynamics of C1Q from primary to relapse. Univariate and multivariate analysis demonstrated adverse prognosis significance of C1Q expression. Mechanistically, C1Q expression, which was modulated by transcription factor MAF BZIP transcription factor B, endowed leukemia cells with tissue infiltration ability, which could establish prominent cutaneous or gastrointestinal EMI nodules in patient-derived xenograft and cell line-derived xenograft models. Fibroblasts attracted migration of the C1Q+ leukemia cells through C1Q-globular C1Q receptor recognition and subsequent stimulation of transforming growth factor β1. This cell-to-cell communication also contributed to survival of C1Q+ leukemia cells under chemotherapy stress. Thus, C1Q served as a marker for AML with adverse prognosis, orchestrating cancer infiltration pathways through communicating with fibroblasts and represents a compelling therapeutic target for EMI.
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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.