Cyclooxygenase 2: From Inflammation to Carcinogenesis

Tutkimustuotos: Artikkeli kirjassa/raportissa/konferenssijulkaisussaKonferenssiartikkeliTieteellinenvertaisarvioitu

Kuvaus

Cyclooxygenase (COX) is the rate-limiting enzyme in the conversion of arachidonic acid to prostanoids. Two COX isoforms have been cloned, of which COX-1 is constitutively expressed, while the expression of COX-2 is low or nondetectable in most tissues, but can be readily induced in response to cell activation by cytokines, growth factors and tumour promoters. Thus, COX-1 is considered a housekeeping gene and thought to be responsible for the synthesis of prostanoids involved in cytoprotection of the stomach and for the production of the pro-aggregatory prostanoid thromboxane by the platelets. In contrast, COX-2 is an inducible, immediate-early gene, and its role has been related to inflammation, reproduction and carcinogenesis. Expression of COX-2 is elevated in a variety of human malignancies and in their precursor lesions. Furthermore, genetic deletion or pharmacological inhibition of COX-2 suppresses tumour growth in several animal models of carcinogenesis. In humans, elevated COX-2 expression is associated with poor prognosis in adenocarcinomas of the digestive tract and the breast, and a selective inhibitor of COX-2 reduced polyp burden in patients who suffer from familial adenomatous polyposis. Thus, COX-2 seems to be a relevant target in chemoprevention.
Alkuperäiskielienglanti
OtsikkoCancer and Infammation : Novartis Foundation Symposium 256
ToimittajatDerek J. Chadwick, Jamie A. Goode
Julkaisupäivä2004
Sivut215-226
ISBN (painettu)9780470855102
ISBN (elektroninen)9780470856734
DOI - pysyväislinkit
TilaJulkaistu - 2004
OKM-julkaisutyyppiA4 Artikkeli konferenssijulkaisuussa

Julkaisusarja

NimiNovartis Foundation Symposia
KustantajaNovartis Foundation
ISSN (painettu)1935-4657

Lisätietoja


Volume:
Proceeding volume:

Lainaa tätä

Ristimäki, A. (2004). Cyclooxygenase 2: From Inflammation to Carcinogenesis. teoksessa D. J. Chadwick, & J. A. Goode (Toimittajat), Cancer and Infammation: Novartis Foundation Symposium 256 (Sivut 215-226). (Novartis Foundation Symposia). https://doi.org/10.1002/0470856734.ch16
Ristimäki, Ari. / Cyclooxygenase 2: From Inflammation to Carcinogenesis. Cancer and Infammation: Novartis Foundation Symposium 256. Toimittaja / Derek J. Chadwick ; Jamie A. Goode. 2004. Sivut 215-226 (Novartis Foundation Symposia).
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title = "Cyclooxygenase 2: From Inflammation to Carcinogenesis",
abstract = "Cyclooxygenase (COX) is the rate-limiting enzyme in the conversion of arachidonic acid to prostanoids. Two COX isoforms have been cloned, of which COX-1 is constitutively expressed, while the expression of COX-2 is low or nondetectable in most tissues, but can be readily induced in response to cell activation by cytokines, growth factors and tumour promoters. Thus, COX-1 is considered a housekeeping gene and thought to be responsible for the synthesis of prostanoids involved in cytoprotection of the stomach and for the production of the pro-aggregatory prostanoid thromboxane by the platelets. In contrast, COX-2 is an inducible, immediate-early gene, and its role has been related to inflammation, reproduction and carcinogenesis. Expression of COX-2 is elevated in a variety of human malignancies and in their precursor lesions. Furthermore, genetic deletion or pharmacological inhibition of COX-2 suppresses tumour growth in several animal models of carcinogenesis. In humans, elevated COX-2 expression is associated with poor prognosis in adenocarcinomas of the digestive tract and the breast, and a selective inhibitor of COX-2 reduced polyp burden in patients who suffer from familial adenomatous polyposis. Thus, COX-2 seems to be a relevant target in chemoprevention.",
author = "Ari Ristim{\"a}ki",
note = "Volume: Proceeding volume:",
year = "2004",
doi = "10.1002/0470856734.ch16",
language = "English",
isbn = "9780470855102",
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Ristimäki, A 2004, Cyclooxygenase 2: From Inflammation to Carcinogenesis. julkaisussa DJ Chadwick & JA Goode (toim), Cancer and Infammation: Novartis Foundation Symposium 256. Novartis Foundation Symposia, Sivut 215-226. https://doi.org/10.1002/0470856734.ch16

Cyclooxygenase 2: From Inflammation to Carcinogenesis. / Ristimäki, Ari.

Cancer and Infammation: Novartis Foundation Symposium 256. toim. / Derek J. Chadwick; Jamie A. Goode. 2004. s. 215-226 (Novartis Foundation Symposia).

Tutkimustuotos: Artikkeli kirjassa/raportissa/konferenssijulkaisussaKonferenssiartikkeliTieteellinenvertaisarvioitu

TY - GEN

T1 - Cyclooxygenase 2: From Inflammation to Carcinogenesis

AU - Ristimäki, Ari

N1 - Volume: Proceeding volume:

PY - 2004

Y1 - 2004

N2 - Cyclooxygenase (COX) is the rate-limiting enzyme in the conversion of arachidonic acid to prostanoids. Two COX isoforms have been cloned, of which COX-1 is constitutively expressed, while the expression of COX-2 is low or nondetectable in most tissues, but can be readily induced in response to cell activation by cytokines, growth factors and tumour promoters. Thus, COX-1 is considered a housekeeping gene and thought to be responsible for the synthesis of prostanoids involved in cytoprotection of the stomach and for the production of the pro-aggregatory prostanoid thromboxane by the platelets. In contrast, COX-2 is an inducible, immediate-early gene, and its role has been related to inflammation, reproduction and carcinogenesis. Expression of COX-2 is elevated in a variety of human malignancies and in their precursor lesions. Furthermore, genetic deletion or pharmacological inhibition of COX-2 suppresses tumour growth in several animal models of carcinogenesis. In humans, elevated COX-2 expression is associated with poor prognosis in adenocarcinomas of the digestive tract and the breast, and a selective inhibitor of COX-2 reduced polyp burden in patients who suffer from familial adenomatous polyposis. Thus, COX-2 seems to be a relevant target in chemoprevention.

AB - Cyclooxygenase (COX) is the rate-limiting enzyme in the conversion of arachidonic acid to prostanoids. Two COX isoforms have been cloned, of which COX-1 is constitutively expressed, while the expression of COX-2 is low or nondetectable in most tissues, but can be readily induced in response to cell activation by cytokines, growth factors and tumour promoters. Thus, COX-1 is considered a housekeeping gene and thought to be responsible for the synthesis of prostanoids involved in cytoprotection of the stomach and for the production of the pro-aggregatory prostanoid thromboxane by the platelets. In contrast, COX-2 is an inducible, immediate-early gene, and its role has been related to inflammation, reproduction and carcinogenesis. Expression of COX-2 is elevated in a variety of human malignancies and in their precursor lesions. Furthermore, genetic deletion or pharmacological inhibition of COX-2 suppresses tumour growth in several animal models of carcinogenesis. In humans, elevated COX-2 expression is associated with poor prognosis in adenocarcinomas of the digestive tract and the breast, and a selective inhibitor of COX-2 reduced polyp burden in patients who suffer from familial adenomatous polyposis. Thus, COX-2 seems to be a relevant target in chemoprevention.

U2 - 10.1002/0470856734.ch16

DO - 10.1002/0470856734.ch16

M3 - Conference contribution

SN - 9780470855102

T3 - Novartis Foundation Symposia

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BT - Cancer and Infammation

A2 - Chadwick, Derek J.

A2 - Goode, Jamie A.

ER -

Ristimäki A. Cyclooxygenase 2: From Inflammation to Carcinogenesis. julkaisussa Chadwick DJ, Goode JA, toimittajat, Cancer and Infammation: Novartis Foundation Symposium 256. 2004. s. 215-226. (Novartis Foundation Symposia). https://doi.org/10.1002/0470856734.ch16