Sister chromatid exchange induction by benzo(a)pryene in cultured peripheral blood lymphocytes of lung cancer patients and healthy individuals with or without familial history of neoplasms

Abstract

The inducibility of sister chromatid exchanges (SCEs) by benzo(a)pyrene (BP) was studied in cultured peripheral blood lymphocytes of 15 untreated lung cancer patients and 25 healthy persons including 11 high- and 14 low-cancer-risk individuals tentatively classified by the familial history of lung cancer and other neoplasms. The baseline SCE frequency in cultured lymphocytes was significantly high in lung cancer patients, as compared with all healthy persons or low-cancer-risk individuals. Following exposure to BP, the lymphocytes of lung-cancer patients and high-cancer-risk individuals exhibited significantly greater SCE yields than those of persons at low risk, although no significant difference was observed in the lymphocyte SCE yields when the levels of lung cancer patients were compared with those of all healthy persons. A comparison of the net SCE increase (delta SCE) in BP-exposed lymphocytes among the study groups, however, revealed a significant difference in delta SCE values only between high- and low-cancer-risk individuals. The present findings on both the observed SCE yields and delta SCE values suggest that lymphocytes of high-risk individuals may be more susceptible to BP-induced DNA damage than those of persons at low risk, and that such a chromosomal hypersensitivity to genotoxins may be associated with a high risk of neoplasms.

Increased frequency of sister chromatid exchanges in lymphocytes of breast cancer patients

“…These include reports on malignant lymphoma (Kurvink et al, 1978), cancer of the breast (Livingston et al, 1983), thyroid (Krizman et al, 1987), and lung (Hopkin and Evans, 1980;Dusaka et al, 1987), acute lymphocytic leukaemia (Otter et al, 1979) and cancer of uterine cervix (Mitra et al, 1982). However, contrary findings have also been reported (Husum et al, 1981;Crossen et al, 1981;Hollander et al, 1978;Cheng et al, 1979).…”

Genetic instability assessed by sister chromatid exchange analysis in the dunning R‐3327 rat prostatic adenocarcinoma model and its relationship to metastatic potential

“…Induced SCEs have been correlated positively with somatic gene mutations [15], chromosomal aberrations [16], and neoplastic transformation [17]. SCE assay has been used successfully to monitor human exposure to occupational and environmental mutagens [HI, and applications for monitoring the effectiveness of cancer chemotherapic agents [19,20] and screening for individuals with high cancer risk [21] have been suggested. Several studies of neoplasia reported increased levels of spontaneous SCEs.…”

“…Several studies of neoplasia reported increased levels of spontaneous SCEs. High SCE rates were observed in lymphocytes from patients with breast cancer [22], cervical cancer [23], lung cancer [21], leukemia [24], and metastatic variants of murine B16 melanoma and human astrocytomas [25]. SCE has occurred with increased frequency in lymphoma cell lines and has been correlated positively with extent of karyotypic abnormalities [26].…”

Evaluation of sister chromatid exchange as an indicator of sensitivity to N‐ethyl‐N‐nitrosourea‐induced carcinogenesis in rats

“…An indication of such a possibility was obtained in a study by Hopkin and Evans [3], who showed that the SCE-response to cigarette smoke condensate in lymphocytes from lung cancer patients was more marked than in cells of those with similar smoking habits but who were without cancer. Following exposure to benzo(a)pyrene in vitro, lymphocytes of lung cancer patients and high-cancerrisk individuals exhibited significantly greater SCE yields than those of persons at low risk [4]. In addition, increased levels of lymphocyte SCEs were observed among breast cancer patients before treatment [5,6].…”