The paper reviews the role of prostaglandin (PG) inhibition in tumor g
rowth and radiotherapy. Murine tumors produce PGs and other eicosanoid
s in different quantities, and some tumors do not produce any detectab
le PGs. Synthesis of PGs is inhibited by indomethacin, an inhibitor of
PG-synthase. Tumors that produce PGS respond to indomethacin by slowe
r growth. Inhibition of tumor neoangiogenesis appears as a major mecha
nism for the antitumor effect of indomethacin. Further, inhibition of
production by tumors of PGs potentiates the tumor response to ionizing
radiation; here, however, immune mechanisms stimulated by indomethaci
n play a significant role. While it potentiates the radioresponse in t
umors, indomethacin prevents radiation damage in some normal tissues.
Overall, these studies show that inhibition of tumor PGs can greatly i
mprove radiotherapy Because the effect is limited to PG-producing tumo
rs, the understanding of PG profiles of tumors prior to therapy could
be used for selection of cancer patients likely to benefit from the co
mbination of indomethacin or other PG inhibitors and radiotherapy.