Prostaglandins from tumours of human large bowel

Bennett, A. B.; Tacca, M. Del; Stamford, I F; Zebro, T

doi:10.1038/bjc.1977.132

Cited by 178 publications

(47 citation statements)

References 9 publications

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“…THE AMOUNTS OF PROSTAGLANDINS extracted from various tumours, notably from human carcinomas of the breast (Bennett et al, 1975Powles et al, 1976), large intestine (Bennett et al, 1977) and kidney (Atkins et al, 1977) and from certain experimental neoplasms (Powles et al, 1 973;Tashjian et al, 1974;Galasko, 1.976;Galasko & Bennett, 1976) are usually greater than from the corresponding normal tissues. Prostaglandins and other lessclearly defined "tumour-associated" products may be involved in the establishment and growth of metastases in bone and possibly in other sites (Carter, 1978;Bennett, 1979).…”

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confidence: 99%

Prostaglandin-like material extracted from squamous carcinomas of the head and neck

Bennett¹,

Carter²,

Stamford³

et al. 1980

Br J Cancer

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Summary.-Tumour-associated prostaglandin-like material, assessed by bioassay, has been examined in 37 patients with primary and metastatic squamous carcinomas of the head and neck, previously treated by radiotherapy and chemotherapy followed by radical surgery. High amounts of prostaglandin-like material were extracted from tumours excised within 3 months of radiotherapy and chemotherapy. These amounts correlated with necrosis, inflammation and fibrosis, but not with tumour site, size or degree of differentiation. Most of the prostaglandins formed by these treated tumours thus seem to be associated with host stromal and inflammatory cells, rather than the neoplastic cells. The possible roles of prostaglandins in facilitating the spread of squamous carcinomas are discussed.

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confidence: 99%

Prostaglandin-like material extracted from squamous carcinomas of the head and neck

Bennett¹,

Carter²,

Stamford³

et al. 1980

Br J Cancer

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“…An immunological mechanism for this activity has been suggested on the basis of a series of observations, including the inhibition of prostaglandin synthesis by these drugs (Lewis, 1977) the high prostaglandin concentrations in many tumours (Strausser & Humes, 1975;Bennett et al, 1977;Sykes & Maddox, 1972) the immunological unresponsiveness of some tumour-bearing animals and immune "restoration" by indomethacin treatment (Plescia et al, 1975;Strausser & Humes, 1975;Pelus & Strausser, 1976) possibly via effects on "suppressor" cells (Goodwin et al, 1977;Webb & Jamieson, 1976).…”

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confidence: 99%

Mechanism of inhibition of tumour growth by aspirin and indomethacin

Lynch¹,

Castes²,

Astoin³

et al. 1978

Br J Cancer

161

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Summary.-The growth of a 3-methylcholanthrene-induced fibrosarcoma of C3H mice was inhibited by aspirin and indomethacin. While the tumour contained relatively high concentrations of PGE2-like material, that were markedly diminished by indomethacin treatment, our results did not confirm the recently proposed hypothesis that the anti-tumour effect arises from a restoration of depressed immune function. For example, mice that had completely eliminated their tumours under indomethacin administration were not immune to rechallenge. The tumour-bearing animals were not non-specifically immunodepressed, as their splenic PFC responses against SRBC were enhanced. However, while indomethacin augmented the PFC response in normal mice, this adjuvant effect was depressed in tumour-bearing animals. The spleen-cell PHA responses of tumour bearers were severely depressed, and such cells suppressed the PHA response of normal cells. Only after prolonged indomethacin treatment did animals (with comparable tumour burdens) show weak PHA responses and somewhat diminished suppressive activity.Possible alternative mechanisms, such as direct cytotoxicity, or inhibition of inflammation, phosphodiesterase activity, blood coagulation or calcium availability were not implicated (nor definitively excluded) in the anti-tumour effect.

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“…The most obvious possibility is that overexpression of COX-2 leads to high levels of prostaglandins (PGs) in tumor tissue. This hypothesis is supported by the finding of elevated levels of PGs in cancer tissues, compared with corresponding normal tissues [34,35] . PGs produced by COX-2 may subsequently facilitate tumor progression by acting as differentiation and growth factors, immunosuppressors and angiogenic agents [36][37][38] .…”

Section: Discussionmentioning

confidence: 73%