C. Bacova et al., The single cell gel electrophoresis: A potential tool for DNA analysis of the patients with hematological malignancies, NEOPLASMA, 45(6), 1998, pp. 349-359
Single cell gel electrophoresis (SCGE) was used to evaluate the level of DN
A damage in peripheral blood (PB), bone marrow (BM), and lymphatic node (LN
) cells of patients with acute lymphoblastic leukemia (ALL), acute myeloid
leukemia (AML), chronic lymphocytic leukemia (CLL), chronic myeloid leukemi
a (CML) and non-Hodgkin's lymphoma (NHL). The level of DNA damage was compa
red with the level of basal DNA damage in control group, represented by hea
lthy donors.
Statistically significant increase of basal DNA damage was found in leukemi
a/lymphoma cells of patients suffered from AML, CML, ALL of T-cell subtype
(T-ALL), and NHL, however, no difference in basal DNA damage was found in p
atients with ALL of early B-cell subtype (B-ALL) and CLL in comparison to c
ontrol group. The mean basal DNA damage increased in the order CLL< early B
-ALL<T-ALL<AML<CML<NHL (5.6, 7.2, 10.7, 11.9, 16.9, and 23.4% of tail DNA,
respectively) what correlated with survival prediction of patients with par
ticular hematological disease. A large heterogeneity was found in the level
of basal DNA damage among patients with AML. By sorting this group accordi
ng to the immunophenotypic markers and cell maturity a good correlation was
found between the level of basal DNA damage and French-American-British (F
AB) classification for AML M-1-M-2 vs. M-4-M-5). Though T-ALL group manifes
ted larger homogeneity in comparison with AML, the value of basal DNA damag
e was also dependent on T-cells maturity and coexpression of surface marker
CD10.
Chemotherapy resulted in a significant but variable increase of DNA damage
in leukemia/lymphoma cells. No increase of DNA damage was repeatedly observ
ed in leukemia/lymphoma cells of patient who did not respond to therapy. Th
e level of DNA damage in cells of patients in remission decreased more or l
ess to the basal level in control cells.