I. Zusman et al., The immune system, apoptosis and apoptosis-related proteins in human ovarian tumors (A review), INT J ONCOL, 18(5), 2001, pp. 965-972
Our studies on the relationships among the lymphoid system, apoptosis and a
poptosis-related proteins (ARP) in human ovarian benign cysts, borderline t
umors, and carcinomas are reviewed and analyzed. Fas and Fas ligand are exp
ressed in 50% to 80% of the epithelial cells in all studied tumors. Many bc
l-2-positive tumor epithelial cells are seen in benign cysts and they disap
pear as tumorigenesis progresses, whereas p53 protein is found only in bord
erline tumors and in carcinomas. Many exceptions to the opinion that bcl-2
inhibits apoptosis and p53 promotes it are encountered. Bcl-2 is lacking in
epithelial cells of mucoid tumors of all grades, and its absence does not
stimulate their apoptosis. P53 protein is absent from most lymphocytes, mac
rophages and epithelial tumor cells, nevertheless, they undergo apoptosis.
Indeed, in many tumors apoptosis is regulated without the participation of
bcl-2 and p53. Different components of the immune system become active duri
ng different stages of tumor development. The weak reaction of T-cell kille
rs and macrophages is typical in benign cysts. In borderline tumors, the ac
tivity of T-cell killers increases in the parenchyma, and that of T helpers
and macrophages in the stroma. In carcinomas with high lymphoid infiltrati
on, a strong reaction of macrophages and T cell killers in the tumoral pare
nchyma as well high reaction of T helpers and B lymphocytes in the stroma a
re typical. Apoptosis that should protect against tumor also stimulates apo
ptotic death of lymphocytes and macrophages, and this has catastrophic cons
equences, as seen in weakly infiltrated carcinomas. In conclusion, our stud
ies indicate that during malignancy the major task of the immune system is
curtailment and control of tumorigenesis.