Karyotypic changes in the preclinical and subsequent stages of malignant mesothelioma: a case report

Our plain-English summary of Karyotypic changes in the preclinical and subsequent stages of malignant mesothelioma: a case report, by I.L. Hansteen, B. Hilt, J.T. Lien, et al (Cancer Genetics and Cytogenetics, 1993).

The study

• Authors: I.L. Hansteen, B. Hilt, J.T. Lien, V. Skaug, A. Haugen
• Journal: Cancer Genetics and Cytogenetics
• Published: 1993;70(2):94-8
• Type of article: Case report
• Cited by: 14 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The karyotypic evolution was evaluated in cells from recurring pleural effusions in a patient previously exposed to asbestos. Pleural malignant mesothelioma (MM) was diagnosed 4 years after the first cytogenetic examination. The primary cytogenetic changes consisted of loss of chromosomes 1p,14,21, Y, both 22, and derivative chromosomes involving 1, 2, and 14. The modal chromosome number was 44. Sixty-seven percent of the cells had a normal karyotype. After 4 years of spontaneous remission, only 6% of the cells had a normal karyotype, 42% had the same karyotypic changes as found previously, whereas 52% had additional derivative chromosomes involving chromosomes 1, 3, 5, 7, 8, and 12, trisomy 7, 7p, and 11, and partial or whole monosomy 3, 8, and 9. The chromosomal changes are in agreement with the main findings in previous reports. The karyotype remained quite stable for 7 months in vitro. After 23 months in culture, all the cells were near-triploid. Cells established in culture were cytokeratin positive. All derivative and marker chromosomes identified in the cultured cells had previously been observed in direct preparations from the pleural effusions. We conclude that chromosomes 1, 14, 21, and 22 may be involved in the preclinical stage of development of asbestos-induced mesothelioma, whereas the later chromosomal changes may be related to progression of the tumor.

In plain English

This case report tracked chromosome changes in chest-fluid cells from one man. From 1953 to 1963 he worked at a factory making fire-proof doors, where he was exposed to asbestos dust used to insulate the doors. The article did not name a fiber type. In 1984 he had a pleural effusion (fluid around the lung) whose cells allowed no diagnosis, and it cleared on its own. It returned in March 1988, and an August 1988 biopsy showed pleural malignant mesothelioma of epithelial type. He died in April 1989. In 1984, 67% of the dividing cells were normal. The rest had 44 chromosomes, with losses involving chromosomes 1p, 14, 21, 22 and Y. In the March 1988 sample, 6% were normal, 42% had the same changes, and 52% had further changes. Some 1988 cells had an extra chromosome 7 or 11. Cultured cells were all near-triploid (about three chromosome sets) after 23 months and never formed tumors in mice. The authors concluded that changes in chromosomes 1, 14, 21 and 22 might be early, and later changes might relate to tumor progression.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: case report: repeated chromosome (karyotype) analysis of pleural effusion cells over time, plus long-term cell culture
• Who was studied: One man born in 1918, in Norway. He had a pleural effusion in 1984 that resolved spontaneously and recurred in March 1988. He was diagnosed by biopsy in August 1988 with epithelial-type pleural malignant mesothelioma, which the Norwegian Mesothelioma Panel confirmed. He died in April 1989.
• Exposure: Asbestos dust used for insulation of fire-proof doors, at a door factory where he worked from 1953 to 1963. No fiber type is stated.
• Main results:
  • In the first (1984) effusion sample, 67% of the dividing cells had a normal male karyotype.
  • The early abnormal cells showed loss of chromosomes 1p, 14, 21, Y and both chromosomes 22.
  • When the effusion recurred in March 1988, about 4 years later, 6% of cells in that sample were normal, 42% had the same changes as in 1984, and 52% had additional derivative chromosomes.
  • Of the cells karyotyped after 4 years, 42% had one extra chromosome 7 and 33% had one extra chromosome 11.
  • In the last in vivo sample (May 1988), no cells were normal and 79% had the same changes found in 1984.
  • The patient's lymphocytes (blood cells) had a normal male karyotype.
  • In laboratory culture, all examined cells were near-triploid after 23 months and 45 passages.
  • The cultured cells were cytokeratin positive.
  • When injected into nude mice followed for 6 months, the cultured cells never produced tumors.
  • Survival from histologic diagnosis to death was 8 months.
• The authors' conclusion: The authors concluded that involvement of chromosomes 1, 14, 21 and 22 might be primary (early) changes in malignant mesothelioma. They suggested that trisomy 7, 7p and 11 and whole or partial loss of chromosomes 3, 8 and 9 might be secondary changes related to tumor progression.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Mesothelioma.

Medical terms in this study, explained in our Lexicon: Malignant Mesothelioma, Pleural Effusion, Mesothelioma.

Related studies

• An early, nonrandom karyotypic change in immortal Syrian hamster cell lines transformed by asbestos: trisomy of chromosome 11 — M. Oshimura, T.W. Hesterberg, et al. (1986)
• Identification of specific gene copy number changes in asbestos-related lung cancer — P. Nymark, H. Wikman, et al. (2006)
• DNA copy number changes in familial malignant mesothelioma — V. Ascoli, Y. Aalto, et al. (2001)
• Cytogenetic analysis of malignant mesothelioma — A. Hagemeijer, M.A. Versnel, et al. (1990)
• Specificity of asbestos-induced chromosomal aberrations in short-term cultured human mesothelial cells — K. Olofsson, J. Mark (1989)
• Cytogenetic findings in an effusion secondary from pleural mesothelioma — M.J. Bello, J.A. Rey, et al. (1987)

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