ArticleCancer science2007
Genomic profiling of malignant pleural mesothelioma with array-based comparative genomic hybridization shows frequent non-random chromosomal alteration regions including JUN amplification on 1p32.
Article in Cancer science, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 91 citations in OpenAlex.
- An analysis of succinate dehydrogenase B in pleural mesothelioma.Discover oncology · 2026Article
- A Comprehensive Guide on Epigenetics' Precision Role in Uncommon "Rare" Cancers' Biology and Treatment Frontiers.Sub-cellular biochemistry · 2026Review
- Mesothelioma Mouse Models with Mixed Genomic States of Chromosome and Microsatellite Instability.Cancers · 2022Article
- Three newly established immortalized mesothelial cell lines exhibit morphological phenotypes corresponding to malignant mesothelioma epithelioid, intermediate, and sarcomatoid types, respectively.Cancer cell international · 2021Article
- Malignant pleural mesothelioma: an update.Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia · 2021Review
- Next-generation sequencing implicates oncogenic roles for p53 and JAK/STAT signaling in microcystic adnexal carcinomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Review
- Evaluation of gene expression levels in the diagnosis of lung adenocarcinoma and malignant pleural mesothelioma.Turk gogus kalp damar cerrahisi dergisi · 2020Article
- Circulating biomarkers in malignant pleural mesothelioma.Exploration of targeted anti-tumor therapy · 2020Review
- Mesothelium and Malignant Mesothelioma.Journal of developmental biology · 2019Review
- Establishment and characterization of CRISPR/Cas9-mediated NF2Cancer science · 2019Article
- The hippo pathway provides novel insights into lung cancer and mesothelioma treatment.Journal of cancer research and clinical oncology · 2018Review
- Genomics and Epigenetics of Malignant Mesothelioma.High-throughput · 2018Review
- Large-scale copy number analysis reveals variations in genes not previously associated with malignant pleural mesothelioma.Oncotarget · 2017Article
- Inhibition of the spindle assembly checkpoint kinase Mps-1 as a novel therapeutic strategy in malignant mesothelioma.Oncogene · 2017Article
- E-cadherin expression is correlated with focal adhesion kinase inhibitor resistance in Merlin-negative malignant mesothelioma cells.Oncogene · 2017Article
- Peritoneal Mesothelioma with Residential Asbestos Exposure. Report of a Case with Long Survival (Seventeen Years) Analyzed by Cgh-Array.International journal of molecular sciences · 2017Article
- A Subset of Malignant Mesotheliomas in Young Adults Are Associated With Recurrent EWSR1/FUS-ATF1 Fusions.The American journal of surgical pathology · 2017Article
- High-density array-CGH with targeted NGS unmask multiple noncontiguous minute deletions on chromosome 3p21 in mesothelioma.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Establishment and molecular characterization of cell lines from Japanese patients with malignant pleural mesothelioma.Oncology letters · 2016Article
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
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Abstract
Genome-wide array-based comparative genomic hybridization analysis of malignant pleural mesotheliomas (MPM) was carried out to identify regions that display DNA copy number alterations. Seventeen primary tumors and nine cell lines derived from 22 individuals were studied, some of them originating from the same patients. Regions of genomic aberrations observed in >20% of individuals were 1q, 5p, 7p, 8q24 and 20p with gains, and 1p36.33, 1p36.1, 1p21.3, 3p21.3, 4q22, 4q34-qter, 6q25, 9p21.3, 10p, 13q33.2, 14q32.13, 18q and 22q with losses. Two regions at 1p32.1 and 11q22 showed a high copy gain. The 1p32.1 region contained a protooncogene, JUN, and we further demonstrated overexpression of JUN with real-time polymerase chain reaction analysis. As MPM cell lines did not overexpress JUN, our findings suggested that induction of JUN expression was involved in the development of MPM cells in vivo, which also might result in gene amplification in a subset of MPM. Meanwhile, the most frequent alteration was the 9p21.3 deletion, which includes the p16(INK4a)/p14(ARF) locus. With polymerase chain reaction analysis, we determined the extent of the homozygous deletion regions of the p16(INK4a)/p14(ARF) locus in MPM cell lines, which indicated that the deletion regions varied among cell lines. Our results with array comparative genomic hybridization analysis provide new insights into the genetic background of MPM, and also give some clues to develop a new molecular target therapy for MPM.
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