ArticleBlood2021
Unexpected suppression of tumorigenesis by c-MYC via TFAP4-dependent restriction of stemness in B lymphocytes.
Article in Blood, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
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- Latent Regulatory Programs Generate Synthetic T Cell States with Enhanced Therapeutic Potential.bioRxiv : the preprint server for biology · 2026Article
- Deep Proteomics Analysis Unravels the Molecular Signatures of Tonsillar B Cells in PFAPA and OSAS in the Pediatric Population.International journal of molecular sciences · 2025Article
- Audit of B-cell cancer genes.Blood advances · 2025Review
- Advancing the genetic engineering toolbox by combining AsCas12a knock-in mice with ultra-compact screening.Nature communications · 2025Article
- Single cell-spatial transcriptomics and bulk multi-omics analysis of heterogeneity and ecosystems in hepatocellular carcinoma.NPJ precision oncology · 2024Article
- Aging, oxidative stress and degenerative diseases: mechanisms, complications and emerging therapeutic strategies.Biogerontology · 2023Review
- Deletion of the transcriptional regulator TFAP4 accelerates c-MYC-driven lymphomagenesis.Cell death and differentiation · 2023Article
- Targeting NK-1R attenuates renal fibrosisFrontiers in immunology · 2023Article
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The proliferative burst of B lymphocytes is essential for antigen receptor repertoire diversification during the development and selective expansion of antigen-specific clones during immune responses. High proliferative activity inevitably promotes oncogenesis, the risk of which is further elevated in B lymphocytes by endogenous gene rearrangement and somatic mutations. However, B-cell-derived cancers are rare, perhaps owing to putative intrinsic tumor-suppressive mechanisms. We show that c-MYC facilitates B-cell proliferation as a protumorigenic driver and unexpectedly coengages counteracting tumor suppression through its downstream factor TFAP4. TFAP4 is mutated in human lymphoid malignancies, particularly in >10% of Burkitt lymphomas, and reduced TFAP4 expression was associated with poor survival of patients with MYC-high B-cell acute lymphoblastic leukemia. In mice, insufficient TFAP4 expression accelerated c-MYC-driven transformation of B cells. Mechanistically, c-MYC suppresses the stemness of developing B cells by inducing TFAP4 and restricting self-renewal of proliferating B cells. Thus, the pursuant transcription factor cascade functions as a tumor suppressor module that safeguards against the transformation of developing B cells.
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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.