ArticleBlood2012
Enforced expression of Lin28b leads to impaired T-cell development, release of inflammatory cytokines, and peripheral T-cell lymphoma.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 75 citations in OpenAlex.
- Reexpression of Let-7g microRNA inhibits the proliferation and migration via K-Ras/HMGA2/snail axis in hepatocellular carcinoma.BioMed research international · 2014Trial
- LIN28B Aggravates the Inflammation in Sepsis-Induced Lung Injury by Stabilizing GATA6 mRNA and Upregulating TRAF6.Pulmonary circulation · 2026Article
- LncRNA HOTAIR promotes aerobic glycolysis by recruiting Lin28 to induce inflammation and apoptosis in acute lung injury.RNA biology · 2025Review
- LIN28B promotes the progression of endometrial cancer through upregulating MYC and correlates with immune microenvironment.Frontiers in oncology · 2025Article
- Downregulation ofeLife · 2024Article
- Downregulation ofbioRxiv : the preprint server for biology · 2024Article
- LIN28 upregulation in primary human T cells impaired CAR T antitumoral activity.Frontiers in immunology · 2024Article
- Nephron-SpecificInternational journal of biological sciences · 2024Article
- Cell-based assay to detect small molecules restoring levels of let-7 miRNAs.American journal of cancer research · 2024Article
- LncRNA CDKN2B-AS1 interacts with LIN28B to exacerbate sepsis-induced acute lung injury by inducing HIF-1α/NLRP3-mediated pyroptosis.The Kaohsiung journal of medical sciences · 2023Article
- Shaping immunity for life: Layered development of CD8Immunological reviews · 2023Review
- Article
- LIN28B Enhanced STAT3 Signaling Regulates Inflammatory Response and Chemotherapeutic Resistance in Cholangiocytes.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- LncRNA HOTAIR Promotes LPS-Induced Inflammation and Apoptosis of Cardiomyocytes via Lin28-Mediated PDCD4 Stability.Inflammation · 2021Article
- LIN28B regulates transcription and potentiates MYCN-induced neuroblastoma through binding to ZNF143 at target gene promotors.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- RNA Regulators in Leukemia and Lymphoma.Cold Spring Harbor perspectives in medicine · 2020Review
- High activation of STAT5A drives peripheral T-cell lymphoma and leukemia.Haematologica · 2020Article
- Thymic precursor cells generate acute myeloid leukemia in NUP98-PHF23/NUP98-HOXD13 double transgenic mice.Scientific reports · 2019Article
- Cancer the'RBP'eutics-RNA-binding proteins as therapeutic targets for cancer.Pharmacology & therapeutics · 2019Review
- The efficiency of murine MLL-ENL-driven leukemia initiation changes with age and peaks during neonatal development.Blood advances · 2019Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
LIN28A and LIN28B, the mammalian homologs of lin-28, are implicated in malignant transformation in part because of their ability to promote degradation of the let-7 family of miRs. In the present study, we show that overexpression of Lin28b in vivo leads to an aggressive peripheral T-cell lymphoma (PTCL) characterized by widespread infiltration of parenchymal organs with malignant CD4(+) cells. Similar to patients with PTCL, Lin28b-transgenic mice show signs of inflammation such as eosinophilia, increased C-reactive protein, release of inflammatory cytokines, and pleural effusion. The PTCLs that develop in Lin28b mice are derived from activated T cells and show decreased let-7 expression, increased Il6 expression, activation of NF-κB, and infiltration of B cells, all resulting in an inflammatory microenvironment. In addition, LIN28B is overexpressed 7.5-fold in PTCL patient samples compared with activated CD4(+) cells. The results of the present study demonstrate for the first time that Lin28b can transform primary cells in vivo, identify a previously unsuspected link between Lin28b and PTCL, and provide a unique animal model for the study of PTCL biology and therapy.
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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.