Assessment of the Mutations of p53 Suppressor Gene and Ha- and Ki-ras Oncogenes in Malignant Mesothelioma in Relation to Asbestos Exposure: A Study of 12 American Patients.

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  • KITAMURA Fumihiko
    Department of Public Health and Occupational Medicine, Graduate School of Medicine, The University of Tokyo National Institute of Industrial Health
  • ARAKI Shunichi
    Department of Public Health and Occupational Medicine, Graduate School of Medicine, The University of Tokyo National Institute of Industrial Health
  • SUZUKI Yasunosuke
    Deparment of Community Medicine, Mount Sinai School of Medicine
  • YOKOYAMA Kazuhito
    Department of Public Health and Occupational Medicine, Graduate School of Medicine, The University of Tokyo
  • TANIGAWA Takeshi
    Department of Public Health and Occupational Medicine, Graduate School of Medicine, The University of Tokyo Institute of Community Medicine, University of Tsukuba
  • IWASAKI Ryu
    Department of Gene Analysis, Mitsubishi Kagaku Bio-Clinical-Laboratories, Inc.

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In our previous study, we found no genetic alteration in exons 1 and 2 of Ha- and Ki-ras oncogenes nor in exons 5 to 9 of the p53 suppressor gene in seven Japanese malignant mesothelioma patients exposed to asbestos. To examine further whether malignant mesothelioma due to asbestos has genetic alterations in the p53 suppressor gene and in Ha- and Ki-ras oncogenes, we analyzed point mutations of these genes in paraffin embedded operative open biopsied samples of the primary tumor of malignant mesothelioma in twelve American patients. The genetic analysis was conducted by the PCR-SSCP (polymerase chain reaction single-strand conformation polymorphism) method in all patients and by sequencing analysis of DNA bases in the two patients with suspected gene mutation. The analysis of the p53 suppressor gene showed an amino acid converting mutation of exon 7 in one patient and a polymorphism of exon 6 in another patient; the former patient was a heavy smoker with a biphasic cell type. No genetic alteration was found in exons 1 and 2 of Ha- and Ki-ras oncogenes in any of the patients. The results suggest that the effects of asbestos on the p53 suppressor gene and Ha- and Ki-ras oncogenes in malignant mesothelioma are negligible. Further studies are needed to examine whether the observed mutation of the p53 suppressor gene is due to the combined effects of asbestos and smoking or to other unknown factors.

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