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
Bloom's syndrome
β Scribed by David Bloom; James German
- Publisher
- Springer
- Year
- 1972
- Tongue
- English
- Weight
- 48 KB
- Volume
- 16
- Category
- Article
- ISSN
- 0340-6717
No coin nor oath required. For personal study only.
π SIMILAR VOLUMES
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
Ethyl methanesulfonate induced several times as many sister. chromatid exchanges (SCEs) in lymphocytes from individuals affected with Bloom's syndrome as in lymphocytes from controls or heterozygotes. In cultures of cells from an individual with Bloom's syndrome who had two populations of lymphocyte
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