ArticleCancer research2008
Disruption of NAD(P)H:quinone oxidoreductase 1 gene in mice leads to radiation-induced myeloproliferative disease.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Navigating redox imbalance: the role of oxidative stress in embryonic development and long-term health outcomes.Frontiers in cell and developmental biology · 2025Review
- Effect of naturally-occurring mutations on the stability and function of cancer-associated NQO1: Comparison of experiments and computation.Frontiers in molecular biosciences · 2022Article
- NQO1 Deficiency Aggravates Renal Injury by Dysregulating Vps34/ATG14L Complex during Autophagy Initiation in Diabetic Nephropathy.Antioxidants (Basel, Switzerland) · 2021Article
- Article
- An Overview of Nrf2 Signaling Pathway and Its Role in Inflammation.Molecules (Basel, Switzerland) · 2020Review
- Radiation-induced tissue damage and response.The Journal of pathology · 2020Review
- NAD(P)H Quinone Dehydrogenase 1 Ablation Inhibits Activation of the Phosphoinositide 3-Kinase/Akt Serine/Threonine Kinase and Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Pathways and Blocks Metabolic Adaptation in Hepatocellular Carcinoma.Hepatology (Baltimore, Md.) · 2020Article
- Comparative Assessment of Tungsten Toxicity in the Absence or Presence of Other Metals.Toxics · 2018Review
- Retraction: NRH:Quinone Oxidoreductase 2-Deficient Mice Are Highly Susceptible to Radiation-induced B-Cell Lymphomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- A functional pseudogene, NMRAL2P, is regulated by Nrf2 and serves as a coactivator of NQO1 in sulforaphane-treated colon cancer cells.Molecular nutrition & food research · 2017Article
- Tungsten-induced carcinogenesis in human bronchial epithelial cells.Toxicology and applied pharmacology · 2015Article
- Methylation-independent repression of Dnmt3b contributes to oncogenic activity of Dnmt3a in mouse MYC-induced T-cell lymphomagenesis.Oncogene · 2015Article
- Increased NQO1 but not c-MET and survivin expression in non-small cell lung carcinoma with KRAS mutations.International journal of environmental research and public health · 2014Article
- Regulation of Nrf2-an update.Free radical biology & medicine · 2014Review
- NRH:quinone oxidoreductase 2 (NQO2) protein competes with the 20 S proteasome to stabilize transcription factor CCAAT enhancer-binding protein α (C/EBPα), leading to protection against γ radiation-induced myeloproliferative disease.The Journal of biological chemistry · 2013Article
- NAD(P)H:quinone oxidoreductase 1 (NQO1) competes with 20S proteasome for binding with C/EBPα leading to its stabilization and protection against radiation-induced myeloproliferative disease.The Journal of biological chemistry · 2012Article
- Benzene toxicity: The role of the susceptibility factor NQO1 in bone marrow endothelial cell signaling and function.Chemico-biological interactions · 2011Article
- NRH:quinone oxidoreductase 2-deficient mice are highly susceptible to radiation-induced B-cell lymphomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
NAD(P)H:quinone oxidoreductase 1 null (NQO1(-/-)) mice exposed to 3 Gy of gamma-radiation showed an increase in neutrophils, bone marrow hypercellularity, and enlarged lymph nodes and spleen. The spleen showed disrupted follicular structure, loss of red pulp, and granulocyte and megakarocyte invasion. Blood and histologic analysis did not show any sign of infection in mice. These results suggested that exposure of NQO1(-/-) mice to gamma-radiation led to myeloproliferative disease. Radiation-induced myeloproliferative disease was observed in 74% of NQO1(-/-) mice as compared with none in wild-type (WT) mice. NQO1(-/-) mice exposed to gamma-radiation also showed lymphoma tissues (32%) and lung adenocarcinoma (84%). In contrast, only 11% WT mice showed lymphoma and none showed lung adenocarcinoma. Exposure of NQO1(-/-) mice to gamma-radiation resulted in reduced apoptosis in granulocytes and lack of induction of p53, p21, and Bax. NQO1(-/-) mice also showed increased expression of myeloid differentiation factors CCAAT/enhancer binding protein alpha (C/EBPalpha) and Pu.1. Intriguingly, exposure of NQO1(-/-) mice to gamma-radiation failed to induce C/EBPalpha and Pu.1, as was observed in WT mice. These results suggest that decreased p53/apoptosis and increased Pu.1 and C/EBPalpha led to myeloid hyperplasia in NQO1(-/-) mice. The lack of induction of apoptosis and differentiation contributed to radiation-induced myeloproliferative disease in NQO1(-/-) mice.
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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.