Increased frequency of sister chromatid exchanges in lymphocytes of breast cancer patients
β Scribed by Sidharth G. Adhvaryu; Urwashi M. Rawal; Jayesh V. Patel; Devendra D. Patel; Damodar B. Balar
- Publisher
- John Wiley and Sons
- Year
- 1988
- Tongue
- French
- Weight
- 431 KB
- Volume
- 41
- Category
- Article
- ISSN
- 0020-7136
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β¦ Synopsis
Spontaneous and mitomycin-C (MMC)-induced rates of sister chromatid exchanges (SCEs) were studied in peripheral blood lymphocytes (PBLs) of 40 patients with cancer of the breast and 40 healthy female volunteers as controls. Spontaneous SCE per cell value in PBL cultures was 7.72 for the breast cancer patients, which was significantly higher (p < 0.001) than the 6.28 SCEs per cell scored for the controls. Eight of the patients were studied a second time, 3 to 6 months following surgical removal of the tumour. A significant (p < 0.05) reduction in SCE per cell value was observed following mastectomy. MMC-induced frequencies of SCE remained comparable in patients and controls. Cellular kinetics, calculated as average generation time (ACT) from the frequency of cells in M I , M2 and M3 cycles, were comparable in patients and controls.
Increased genomic instability, either inherent or induced by some external mutagen, has been considered as the primary event leading to neoplastic transformation. Cytogenetic endpoints such as the frequency of chromosome aberrations (CA) or sister chromatid exchanges
) offer an opportunity to quantify such genomic instab microscopically. Several authors have reported elevated levels of spontaneous and mutagen-induced CAs and/or SCEs in peripheral blood lymphocytes (PBL) or skin fibroblasts of individuals suffering from various genetic instability syndromes (Ray and German, 1983; Latt et al., 1983) collectively termed "chromosome-breakage syndromes". These individuals are at increased risk of developing cancer at various sites. It has been suggested that, if genetic instability is one of the factors leading to a predisposition to neoplastic transformation, then some cancer pqtients may have higher levels of genetic instability than most other persons, though they may not suffer from one of the genetic instability syndromes (Hsu, 1983).
A number of laboratories have reported increased spontaneous or mutagen-induced CA or SCE frequencies in somatic cells of patients with various cancers. These include reports on malignant lymphoma (
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