[Frontiers in Bioscience 2, d482-500, October 1, 1997]

	[Frontiers in Bioscience 2, d482-500, October 1, 1997] Reprints PubMed CAVEAT LECTOR
	PROSTAGLANDINS AND CANCER Susan M. Fischer The University of Texas M. D. Anderson Cancer Center, Science Park-Research Division, Smithville, TX 78957 Received 9/3/97 Accepted 9/23/97 6. SUMMARY The study of involvement of PGs in the pathogenesis and progression of cancer is currently a lively field of research. The evidence weighs heavily in favor of such a role in many types of cancer. This is based on the observation of high PG levels and elevated expression of synthetic enzymes in various types of tumors. Such a role for PGs is also supported by the numerous animal investigations and human epidemiological studies showing that NSAIDs prevent development of cancer. However, the recent demonstration that these drugs cause apoptosis, and that related anti-cancer drugs that also cause apoptosis do not inhibit PG synthesis, suggest that the story is far from clear. Hopefully, the recently developed knockout and transgenic mouse models will provide the definitive information that is needed. A clearer demonstration that PG synthesis contributes to the development and/or growth of several types of malignancies offers the opportunity for improved approaches to the prevention of cancer.

[Frontiers in Bioscience 2, d482-500, October 1, 1997]
Reprints
PubMed
CAVEAT LECTOR

PROSTAGLANDINS AND CANCER

Susan M. Fischer

The University of Texas M. D. Anderson Cancer Center, Science Park-Research Division, Smithville, TX 78957

Received 9/3/97 Accepted 9/23/97

6. SUMMARY

The study of involvement of PGs in the pathogenesis and progression of cancer is currently a lively field of research. The evidence weighs heavily in favor of such a role in many types of cancer. This is based on the observation of high PG levels and elevated expression of synthetic enzymes in various types of tumors. Such a role for PGs is also supported by the numerous animal investigations and human epidemiological studies showing that NSAIDs prevent development of cancer. However, the recent demonstration that these drugs cause apoptosis, and that related anti-cancer drugs that also cause apoptosis do not inhibit PG synthesis, suggest that the story is far from clear. Hopefully, the recently developed knockout and transgenic mouse models will provide the definitive information that is needed. A clearer demonstration that PG synthesis contributes to the development and/or growth of several types of malignancies offers the opportunity for improved approaches to the prevention of cancer.