Prostaglandins and host defense in cancer

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

The whole relationship between prostaglandins and cancer has not received the attention it should from experimental oncologists. This may be because the whole area of prostaglandins is immensely confusing, with different cyclo-oxygenase metabolites having completely opposite results. Thus when one adds a cyclo-oxygenase inhibitor to a system, any result is possible. It is not even settled whether PGE has a physiologic role or is merely a metabolite of an unstable intermediate compound that is the 'real' PG, or whether the effects of cyclo-oxygenase inhibitors are because of inhibition of production of the classic prostaglandins (PGE and PGF) or by inhibition of production of thromboxanes, prostacyclin, etc. This lack of precise definition of the system tends to discourage precision in experimentation, which in turn tends to keep careful investigators out of the area. The investigator studying the effects of PG synthetase inhibitors on cancer growth must accept these limitations.

Original languageEnglish (US)
Pages (from-to)829-844
Number of pages16
JournalMedical Clinics of North America
Volume65
Issue number4
StatePublished - 1981
Externally publishedYes

Fingerprint

Prostaglandins
Cyclooxygenase Inhibitors
Prostaglandins E
Research Personnel
Neoplasms
Thromboxanes
Prostaglandins F
Epoprostenol
Prostaglandin-Endoperoxide Synthases
Ligases
Growth
Oncologists

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Prostaglandins and host defense in cancer. / Goodwin, James.

In: Medical Clinics of North America, Vol. 65, No. 4, 1981, p. 829-844.

Research output: Contribution to journalArticle

@article{73832f7d2be4433f9e420d9be0198496,
title = "Prostaglandins and host defense in cancer",
abstract = "The whole relationship between prostaglandins and cancer has not received the attention it should from experimental oncologists. This may be because the whole area of prostaglandins is immensely confusing, with different cyclo-oxygenase metabolites having completely opposite results. Thus when one adds a cyclo-oxygenase inhibitor to a system, any result is possible. It is not even settled whether PGE has a physiologic role or is merely a metabolite of an unstable intermediate compound that is the 'real' PG, or whether the effects of cyclo-oxygenase inhibitors are because of inhibition of production of the classic prostaglandins (PGE and PGF) or by inhibition of production of thromboxanes, prostacyclin, etc. This lack of precise definition of the system tends to discourage precision in experimentation, which in turn tends to keep careful investigators out of the area. The investigator studying the effects of PG synthetase inhibitors on cancer growth must accept these limitations.",
author = "James Goodwin",
year = "1981",
language = "English (US)",
volume = "65",
pages = "829--844",
journal = "Medical Clinics of North America",
issn = "0025-7125",
publisher = "W.B. Saunders Ltd",
number = "4",

}

TY - JOUR

T1 - Prostaglandins and host defense in cancer

AU - Goodwin, James

PY - 1981

Y1 - 1981

N2 - The whole relationship between prostaglandins and cancer has not received the attention it should from experimental oncologists. This may be because the whole area of prostaglandins is immensely confusing, with different cyclo-oxygenase metabolites having completely opposite results. Thus when one adds a cyclo-oxygenase inhibitor to a system, any result is possible. It is not even settled whether PGE has a physiologic role or is merely a metabolite of an unstable intermediate compound that is the 'real' PG, or whether the effects of cyclo-oxygenase inhibitors are because of inhibition of production of the classic prostaglandins (PGE and PGF) or by inhibition of production of thromboxanes, prostacyclin, etc. This lack of precise definition of the system tends to discourage precision in experimentation, which in turn tends to keep careful investigators out of the area. The investigator studying the effects of PG synthetase inhibitors on cancer growth must accept these limitations.

AB - The whole relationship between prostaglandins and cancer has not received the attention it should from experimental oncologists. This may be because the whole area of prostaglandins is immensely confusing, with different cyclo-oxygenase metabolites having completely opposite results. Thus when one adds a cyclo-oxygenase inhibitor to a system, any result is possible. It is not even settled whether PGE has a physiologic role or is merely a metabolite of an unstable intermediate compound that is the 'real' PG, or whether the effects of cyclo-oxygenase inhibitors are because of inhibition of production of the classic prostaglandins (PGE and PGF) or by inhibition of production of thromboxanes, prostacyclin, etc. This lack of precise definition of the system tends to discourage precision in experimentation, which in turn tends to keep careful investigators out of the area. The investigator studying the effects of PG synthetase inhibitors on cancer growth must accept these limitations.

UR - http://www.scopus.com/inward/record.url?scp=0019794075&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019794075&partnerID=8YFLogxK

M3 - Article

VL - 65

SP - 829

EP - 844

JO - Medical Clinics of North America

JF - Medical Clinics of North America

SN - 0025-7125

IS - 4

ER -