The biochemical defect in Bloom's syndrome (BS) remains unknown, but two characteristic features of BS cells point to a disturbance of DNA replication, namely, an excessive number of sister-chromatid exchanges (SCEs) in bromodeoxyuridine (BrdU)-substituted cells and an abnormally slow rate of replic
Cancer predisposition in bloom's syndrome
β Scribed by Neil F. Sullivan; Anne E. Willis
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 531 KB
- Volume
- 14
- Category
- Article
- ISSN
- 0265-9247
No coin nor oath required. For personal study only.
β¦ Synopsis
This article focusses upon defining those factors which may contributc to the pathogenesis of cancer. The molecular basis of tumour etiology is discussed with reference to cancer predisposing syndromes, and in particular to the human inherited disease, Bloom's syndrome. In Bloom's syndrome, patients are predisposed to a wide variety of malignant disease. We propose a model in which overexpression of the ubiquitous c-mye proto-oncogene contributes to this process.
π SIMILAR VOLUMES
Cytogenetic studies of an 8-year-old caucasian girl with typical but mild manifestation of Bloom's syndrome showed a characteristic increase of homologous chromatid translocations and prematurely condensed chromosomes. The average frequency of sister chromatid exchanges (SCE) in lymphocytes with 133
A comparison is made between the incidences of sister chromatid exchanges (SCE) per chromosome and group of chromosomes and breakage, visible at metaphase like open gaps, breaks, and breaks involved in chromatid interchange formation (CI) in Bloom's syndrome. It can be shown that the two levels of b