In vivo characterization by means of digital cell image analysis of early-induced fractionated radiotherapy effects on the MXT mouse mammary tumor.
OBJECTIVE
To study the cell kinetics and chromatin modifications occurring in function of the fractionated irradiation administered to the MXT mouse mammary adenocarcinoma.


METHODS
The MXT tumor cells were submitted to three fractions of a 4.8 Gy dose delivered at 24-h intervals. MXT tumor cells were collected by means of fine needle aspirations (between 5 and 10 samples were obtained after each irradiation) during treatment and submitted to the computer-assisted microscope analysis of Feulgen-stained specimens. Three groups of parameters has been described: i.e., the geometry of the nucleus, the nuclear DNA content, and the chromatin texture. Furthermore, cell cycle parameters were studied in the aim to know the distribution of the cells within the cell cycle.


RESULTS
The mean values relating to geometric parameters (i.e., the nuclear area and its standard deviation) decreased during treatment. Variations in the nuclear DNA content appeared as being cyclical and could be explained in terms of the modifications in the distribution of the cells within the cell cycle. The quantitative analysis of the cell cycle parameters revealed that the percentage of S cells increased regularly after each irradiation. In contrast, the percentage of G2 cells decreased between each irradiation. The parameters describing nuclear texture showed regular variations between each irradiation. These variations consisted in two cycles constituted by a decrease in chromatin condensation, followed by an increase.


CONCLUSIONS
The development of the geometric parameters indicates that fractionated radiotherapy leads to the emergence of a more homogeneous population. The effects of the radiotherapy on the distribution of the cells within the cell cycle could be explained through the phenomenon of repopulation and by the high degree of radiosensitivity of the G2 cells (decrease in the percentage of G2 cells). Last, the variations observed at chromatin pattern level could be explained through DNA repair processes.
El-Khattabi
O
O
Département de Radio-Oncologie, Service de Radiothérapie, Institut Jules Bordet, Brussels, Belgium.
Pauwels
O
O
Simon
S
S
Gasperin
P
P
Frühling
J
J
Kiss
R
R
Van Houtte
P
P
D000818:Animals; D002453:Cell Cycle / Q000528:radiation effects; D002467:Cell Nucleus / Q000473:pathology / Q000528:radiation effects*; D002843:Chromatin / Q000528:radiation effects; D004273:DNA, Neoplasm / Q000032:analysis / Q000528:radiation effects*; D005260:Female; D008325:Mammary Neoplasms, Experimental / Q000235:genetics / Q000532:radiotherapy* / Q000648:ultrastructure; D051379:Mice; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA
D002843:Chromatin; D004273:DNA, Neoplasm