Data from previous studies published on the induction by mutagens of sister chromatid exchanges (SCEs) and structural chromosome damage were compared qualitatively and quantitatively. Although a good correlation between the incidence of both cytogenetic phenomena has been pointed out in many previous publications, about 30% of the agents for which comparable data were available yielded non-corresponding qualitative results concerning both indicator effects. However, even in the group with good qualitative agreement distinct quantitative differences indicated different molecular mechanisms of the formation of SCEs and breaks. Additional information supporting the importance of these differences for the validity of both indicator systems has been derived from the results obtained using strong clastogens exhibiting a low or no SCE-inducing activity and vice versa, from special observations on chromosomal breakage syndromes, and from studies on the action of known co- and anti-clastogens on SCE-induction by chemical mutagens. As a result, it has been suggested that the SCE-technique should be considered as a valuable additional method for cytogenetic mutagenicity testing, which, however, is not adequate to replace the classical methods of analysis of structural chromosome damage.

Sister chromatid exchange (SCE) and structural chromosome aberration in mutagenicity testing.

The sister chromatid exchange (SCE) frequencies of six freshly established and two old cell lines derived from patients with lymphatic tumors or leukemia were compared to the SCE rates of lymphoblastoid cell lines of normal controls. All cell lines from malignant tumors displayed significantly higher SCE values than the control lines. In general, the SCE rates seem to be correlated to the number of chromosomal markers and the degree of karyotypic instability of each line.

A possible correlation between the degree of karyotype aberrations and the rate of sister chromatid exchanges in lymphoma lines.

Statistical analysis of cytogenetic abnormalities in human cancer cells

Sister chromatid exchange (SCE) frequency has been analyses after short-term culture of leukemic bone marrow cells of eight untreated patients with acute leukemia. Compared to normal bone marrow, results show a statistically significant decrease of SCE (p less than 0.001) in euploid as well as in aneuploid leukemias, ranging from 2.11 to 2.97 SCE per metaphase. The different SCE values were not related to contraction status of chromosomes and could not be explained by the age of patients. Therefore, low SCE may be a typical feature of leukemic cells. An examination of growth rates by the SCE technique revealed a high turnover of normal bone marrow cells. About 80% of the cells did not need more than 50 h to run two or three cell cycles. Leukemic cells, however, apparently divided more slowly, which is in good agreement with data obtained by autoradiographic methods.

Sister chromatid exchange and growth kinetics in untreated acute leukemia.

It is known that cigarette smoking induces leukocytosis and increased genetic instability in normal individuals. Therefore, a retrospective review was conducted of 173 patients with chronic myelogenous leukemia to detect a possible influence of cigarette smoking on initial characteristics at the time of presentation and on the course of this disease. Thirty-nine patients (23%) were smoking 5 cigarettes/d or more at time of diagnosis. Cigarette smoking was significantly related to male sex (P = 0.0005) and younger age at diagnosis (P = 0.02) and smokers tended to have lower leukocyte counts (P = 0.07) than nonsmokers. Cigarette smoking was significantly associated with early blast crisis (P less than 0.0001) and short survival (P less than 0.0001). Other characteristics associated with a poor prognosis included hepatomegaly, anemia, and a high percentage of peripheral blast cells at time of diagnosis. When studied in a multivariate analysis, cigarette smoking remained the strongest prognostic factor for both occurrence of blast crisis (P = 0.0003) and overall survival (P = 0.0001). Other poor prognosis factors found in the multivariate analysis included a high percentage of blasts in the peripheral blood at time of diagnosis and high platelet count. It is possible that cigarette smoke may act as a promoter or cocarcinogen in the transformation of chronic myelogenous leukemia.

https://acsjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/1097-0142%2819890515%2963%3A10%3C2060%3A%3AAID-CNCR2820631031%3E3.0.CO%3B2-2

Influence of cigarette smoking on the presentation and course of chronic myelogenous leukemia.

The sister chromatid exchange (SCE) frequency in bone-marrow cells of 12 untreated patients with chronic myelocytic leukemia (CML) was analysed and compared with the SCE frequency in bone-marrow cells of nine healthy persons. In normal persons the SCE ranged from 3.64 to 5.15 per cell. In CML patients the SCE was significantly lower, ranging from 2.32 to 3.44 per cell. The differences found were unrelated to patients' age and contraction state of the chromosomes. It is suggested that the leukemic process could account for the low SCE rate.

Gabriele Theis

Papers

Sister chromatid exchange in PH1-positive chronic myelocytic leukemia