Il. Hansteen et al., KARYOTYPIC CHANGES IN THE PRECLINICAL AND SUBSEQUENT STAGES OF MALIGNANT MESOTHELIOMA - A CASE-REPORT, Cancer genetics and cytogenetics, 70(2), 1993, pp. 94-98
The karyotypic evolution was evaluated in cells from recurring pleural
effusions in a patient previously exposed to asbestos. Pleural malign
ant mesothelioma (MM) was diagnosed 4 years after the first cytogeneti
c examination. The primary cytogenetic changes consisted of loss of ch
romosomes 1p,14,21, Y, both 22, and derivative chromosomes involving 1
, 2, and 14. The modal chromosome number was 44. Sixty-seven percent o
f the cells had a normal karyotype. After 4 years of spontaneous remis
sion, only 6% of the cells had a normal karyotype, 42% had the same ka
ryotypic changes as found previously, whereas 52% had additional deriv
ative 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 chromos
omal changes are in agreement with the main findings in previous repor
ts. The kazyotype remained quite stable for 7 months in vitro. After 2
3 months in culture, all the cells were near-triploid. Cells establish
ed in culture were cytokeratin positive. All derivative and marker chr
omosomes identified in the cultured cells had previously been observed
in direct preparations from the pleural effusions. We conclude that c
hromosomes 1, 14, 21, and 22 may be involved in the preclinical stage
of development of asbestos-induced mesothelioma, whereas the later chr
omosomal changes may be related to progression of the tumor.