ArticleHuman genetics1987
Loss of heterozygosity in hypotriploid cell cultures from testicular tumours.
Article in Human genetics, 1987. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 24 citations in OpenAlex.
- Molecular cytogenetic analysis of adult testicular germ cell tumours and identification of regions of consensus copy number change.British journal of cancer · 1998Article
- Molecular biologic investigations of proto-oncogenes and growth factors in human testicular tumors.World journal of urology · 1994Review
- Correlation between retinoblastoma gene expression and differentiation in human testicular tumors.Proceedings of the National Academy of Sciences of the United States of America · 1991Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have established cell lines with a hypotriploid chromosome number from four testicular tumours. Each line had at least one Y chromosome and most of the informative centrosome and enzyme markers were heterozygous implying that the tumours originated from germ cells before the first meiotic division. The small metacentric marker chromosome (i12p), specific for testicular tumours, was present in all tumour cell lines and up to three copies were found in some lines. Rearrangements of chromosome 1 and 11 were each found in three out of four tumours. The rearrangements of chromosome 1 all resulted in duplication of 1q and deletion of short-arm material from the same chromosome giving loss of heterozygosity for enzyme markers on 1p. Loss of satellite material from chromosome 13 and the centromere region of chromosome 9 were found in single cases. This study shows that even where the chromosome number of tumour cells is near triploid, regions of the genome can be deleted. The chromosomes most frequently involved in rearrangements, 1, 11, and 12 all contain sites of ras oncogenes and it is suggested that loss of normal alleles could result in homozygosity for mutant oncogenes which may play a part in tumour progression.
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