ArticleThe American journal of pathology2002
Specific allelic loss of p16 (INK4A) tumor suppressor gene after weeks of iron-mediated oxidative damage during rat renal carcinogenesis.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 62 citations in OpenAlex.
- Ferroptosis and cancer: when iron turns against tumors.Cellular and molecular life sciences : CMLS · 2025Review
- Environmental impact on carcinogenesis under BRCA1 haploinsufficiency.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023Review
- Iron as spirit of life to share under monopoly.Journal of clinical biochemistry and nutrition · 2022Article
- BRCA1 haploinsufficiency promotes chromosomal amplification under Fenton reaction-based carcinogenesis through ferroptosis-resistance.Redox biology · 2022Article
- The Role of Ferric Nitrilotriacetate in Renal Carcinogenesis and Cell Death: From Animal Models to Clinical Implications.Cancers · 2022Review
- Ferroptosis resistance determines high susceptibility of murine A/J strain to iron-induced renal carcinogenesis.Cancer science · 2022Article
- Acquired Evolution of Mitochondrial Metabolism Regulated by HNF1B in Ovarian Clear Cell Carcinoma.Cancers · 2021Review
- Carcinogenesis as Side Effects of Iron and Oxygen Utilization: From the Unveiled Truth toward Ultimate Bioengineering.Cancers · 2020Review
- Asbestos conceives Fe(II)-dependent mutagenic stromal milieu through ceaseless macrophage ferroptosis and β-catenin induction in mesothelium.Redox biology · 2020Article
- MAPKs' status at early stages of renal carcinogenesis and tumors induced by ferric nitrilotriacetate.Molecular and cellular biochemistry · 2015Article
- Iron and thiols as two major players in carcinogenesis: friends or foes?Frontiers in pharmacology · 2014Review
- Iron and cancer: more ore to be mined.Nature reviews. Cancer · 2013Review
- Bovine lactoferrin ameliorates ferric nitrilotriacetate-induced renal oxidative damage in rats.Journal of clinical biochemistry and nutrition · 2012Article
- Identification of nitration sites by peroxynitrite on p16 protein.The protein journal · 2012Article
- Fenton reaction induced cancer in wild type rats recapitulates genomic alterations observed in human cancer.PloS one · 2012Article
- p16(Ink4a) overexpression in cancer: a tumor suppressor gene associated with senescence and high-grade tumors.Oncogene · 2011Review
- A beverage containing fermented black soybean ameliorates ferric nitrilotriacetate-induced renal oxidative damage in rats.Journal of clinical biochemistry and nutrition · 2010Article
- Role of iron in carcinogenesis: cancer as a ferrotoxic disease.Cancer science · 2009Review
- Article
- Chronic oxidative stress causes amplification and overexpression of ptprz1 protein tyrosine phosphatase to activate beta-catenin pathway.The American journal of pathology · 2007Article
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7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative tissue damage has been shown to be associated with carcinogenesis. In human cancers p16(INK4A) is one of the most frequently mutated tumor suppressor genes. The present study used the ferric nitrilotriacetate (Fe-NTA)-induced rat renal carcinogenesis model to determine whether oxidative damage can cause specific allelic loss of p16 (INK4A). By the use of fluorescent in situ hybridization in combination with imprint cytology at single-cell resolution, we found that the number of renal tubular cells with aneuploidy (1 or 3 signals) at the p16(INK4A) locus was significantly and specifically increased (1 week, 37.2 +/- 2.3%; 3 weeks, 37.8 +/- 1.3% vs control, 22.5 +/- 1.9%; mean +/- SE, N = 8; P < 0.001 and P < 0.0001, respectively) after repeated intraperitoneal administration of 5 to10 mg of iron/kg in the form of Fe-NTA for 3 weeks. No increase in aneuploidy was observed at the loci of either the p53 or vhl tumor suppressor gene. Furthermore, the increase in the cells with 3 signals was followed by a continuous increase in those with 1 signal. Therefore, the p16 (INK4A) locus is specifically vulnerable to oxidative damage, leading to its allelic loss within weeks, presumably due to a deficiency in the replication of both the alleles.
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