Background. p53 acts as a tumor suppressor gene because of to its nega
tive control of the cell cycle and its central role in programmed cell
death. It frequently is mutated, as observed in a variety of human ne
oplasms. The mutations inhibit tumor-suppressor activities of p53, whi
ch may gain a new function of tumor promotion. In this study, p53 was
investigated in various components of dedifferentiated chondrosarcoma
and correlated with their proliferative activities. Methods. Immunohis
tochemical assays for p53, Ki-67, and proliferating cell nuclear antig
en (PCNA) were used in a series of eight dedifferentiated chondrosarco
mas of bone. The cartilaginous component was low grade (Grade I-II) in
five cases. It was predominantly low grade with foci of a high grade
(Grade III) chondrosarcoma in the remaining three cases. The noncartil
aginous (dedifferentiated) high grade component consisted of malignant
fibrous histiocytoma in five cases and osteosarcoma in three. Results
. Regardless of the histological type, diffuse strong nuclear staining
for p53 occurred in the high grade noncartilaginous component of all
eight of the tumors. The low grade cartilaginous component of six case
s was negative for p53, with focal weak staining in the two remaining
cases. The high grade cartilaginous component showed strong positive s
taining for this protein in all three cases. Ki-67 and PCNA expression
were similar to that of p53. Conclusions. The percentage of p53 posit
ive staining roughly was parallel to the proliferating fraction of cel
ls in various components of dedifferentiated chondrosarcoma. Moreover,
p53 overexpression was consistently present in the high grade noncart
ilaginous (dedifferentiated) component of the tumor and was accompanie
d by increased proliferative activity.