ArticlePloS one2011
Losses of both products of the Cdkn2a/Arf locus contribute to asbestos-induced mesothelioma development and cooperate to accelerate tumorigenesis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 65 citations in OpenAlex.
- Cellular defense mechanisms against asbestos fibers.Frontiers in public health · 2025Review
- Modeling Malignant Mesothelioma in Genetically Engineered Mice.Current protocols · 2025Article
- GermlineProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Asbestos accelerates disease onset in a genetic model of malignant pleural mesothelioma.Frontiers in toxicology · 2023Article
- The Rocky Road from Preclinical Findings to Successful Targeted Therapy in Pleural Mesothelioma.International journal of molecular sciences · 2022Review
- Medical and Surgical Care of Patients With Mesothelioma and Their Relatives Carrying Germline BAP1 Mutations.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2022Review
- Mesothelioma Mouse Models with Mixed Genomic States of Chromosome and Microsatellite Instability.Cancers · 2022Article
- DNA repair and damage pathways in mesothelioma development and therapy.Cancer cell international · 2022Review
- Review
- Mouse models for mesothelioma drug discovery and development.Expert opinion on drug discovery · 2021Review
- P14/ARF-Positive Malignant Pleural Mesothelioma: A Phenotype With Distinct Immune Microenvironment.Frontiers in oncology · 2021Article
- Asbestos conceives Fe(II)-dependent mutagenic stromal milieu through ceaseless macrophage ferroptosis and β-catenin induction in mesothelium.Redox biology · 2020Article
- Combined deletion of Bap1, Nf2, and Cdkn2ab causes rapid onset of malignant mesothelioma in mice.The Journal of experimental medicine · 2020Article
- Preclinical Models of Malignant Mesothelioma.Frontiers in oncology · 2020Review
- Inactivation ofCancer research · 2019Article
- CDKN2A copy number and p16 expression in malignant pleural mesothelioma in relation to asbestos exposure.BMC cancer · 2019Article
- Chrysotile effects on the expression of anti-oncogene P53 and P16 and oncogene C-jun and C-fos in Wistar rats' lung tissues.Environmental science and pollution research international · 2018Article
- Mesotheliomas in Genetically Engineered Mice Unravel Mechanism of Mesothelial Carcinogenesis.International journal of molecular sciences · 2018Review
- Heterogeneous Contributing Factors in MPM Disease Development and Progression: Biological Advances and Clinical Implications.International journal of molecular sciences · 2018Review
- New Perspectives on Diagnosis and Therapy of Malignant Pleural Mesothelioma.Frontiers in oncology · 2018Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
The CDKN2A/ARF locus encompasses overlapping tumor suppressor genes p16(INK4A) and p14(ARF), which are frequently co-deleted in human malignant mesothelioma (MM). The importance of p16(INK4A) loss in human cancer is well established, but the relative significance of p14(ARF) loss has been debated. The tumor predisposition of mice singly deficient for either Ink4a or Arf, due to targeting of exons 1α or 1β, respectively, supports the idea that both play significant and nonredundant roles in suppressing spontaneous tumors. To further test this notion, we exposed Ink4a(+/-) and Arf(+/-) mice to asbestos, the major cause of MM. Asbestos-treated Ink4a(+/-) and Arf(+/-) mice showed increased incidence and shorter latency of MM relative to wild-type littermates. MMs from Ink4a(+/-) mice exhibited biallelic inactivation of Ink4a, loss of Arf or p53 expression and frequent loss of p15(Ink4b). In contrast, MMs from Arf(+/-) mice exhibited loss of Arf expression, but did not require loss of Ink4a or Ink4b. Mice doubly deficient for Ink4a and Arf, due to deletion of Cdkn2a/Arf exon 2, showed accelerated asbestos-induced MM formation relative to mice deficient for Ink4a or Arf alone, and MMs exhibited biallelic loss of both tumor suppressor genes. The tumor suppressor function of Arf in MM was p53-independent, since MMs with loss of Arf retained functional p53. Collectively, these in vivo data indicate that both CDKN2A/ARF gene products suppress asbestos carcinogenicity. Furthermore, while inactivation of Arf appears to be crucial for MM pathogenesis, the inactivation of both p16(Ink4a) and p19(Arf) cooperate to accelerate asbestos-induced tumorigenesis.
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