Promotion of Growth of Tumour Cells in Acutely Inflamed Tissues

Section: Discussionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Reactions of the tumour bed to lethally irradiated tumour cells, and the Révész effect

Brenk¹,

Crowe²,

Stone³

1977

“…(Bennett, 1979(Bennett, , 1982(Bennett, , 1989. Furthermore, some PGs are involved in inflammation, which has a variable effect on tumour spread, a small inflammatory reaction causing enhancement and a large one causing inhibition (Van den Brenk et al, 1974).…”

Section: Resultsmentioning

confidence: 99%

Breast cancer, prostaglandins and patient survival

Bennett

Stamford²,

Berstock³

et al. 1989

Summary Prostaglandins may have both undesirable and desirable effects in malignant disease. Their possible roles in breast cancer were studied by examining the relationships between different variables and the amounts of prostaglandin-like material (PG-LM) extracted from 141 breast carcinomas. Univariate analysis indicates a direct correlation with patient age and menopausal status, with a greater yield from cancers of post-compared with pre-menopausal women. Tumours up to 2cm diameter yielded more PG-LM than those measuring >2-5cm. Although there was also a direct correlation with bone metastasis near to the time of surgery, this was because no positive bone scans occurred in patients whose tumours yielded little total PG-LM (<16ng PGE2 equivalents per g tissue). Since tumour PG-LM did not predict later spread to bone, and yields of > 16 ng g -' were similar in the positive and negative bone scan groups, tumour PG-LM appears to be unimportant for skeletal metastasis. There was no obvious relationship of tumour PG-LM to the grade of malignancy, tumour type, amounts of fibrous tissue (and therefore malignant cells), invasion of blood vessels and lymphatics or presence of plasma cells. Multivariate analysis indicates that disease-free survival is longest with an intermediate production of tumour total PG-LM. Of the 82 patients now dead, the cause was attributed to metastatic disease in 69 cases. No relationship of PG-LM to the length of survival was seen with univariate or multivariate analysis. However, when just the post-menopausal patients who died within the first 3 postoperative years were analysed, there was a highly significant inverse correlation between the tumour total PG-LM and the time to death. The reason(s) for these different findings on overall survival compared with just the patients who died are not understood, but the results may indicate that one or more other variables must co-exist with a high tumour PG-LM to hasten death.Many tumours can produce more prostaglandins (PGs) than the normal tissues in which they arise (Bennett, 1979(Bennett, , 1982(Bennett, , 1988. Similarly, more prostglandin-like material (PG-LM), assayed on rat gastric fundus which is most sensitive to PGE2, was extracted from homogenates of human mammary carcinomas than from benign tumours or macroscopically normal breast tissue (Bennet et al., 1977). Various PGs and related substances extracted from breast carcinomas were identified by Stamford et al. (1983) using gas chromatography-mass spectrometry; the products were arachidonate, 12-hydroxy-eicosatetraenoate (12-HETE), thromboxane B2, 15-keto-l 3,14-dihydro-TXB2, 6-keto-PGFJ,, 6,15-diketo-PGF1,,, 615-diketo-1 3,14-dihydro-PGF1,,, PGD2, PGE2 and PGF21,. Quantitative gas chromatography-mass spectrometry showed substantial amounts of 6-keto-PGF, . and some PGD2, PGE2 and PGF20,, with much higher yields of arachidonate (Stamford et al., 1986). It might be expected that these potent substances contribute to breast cancer, but the problem is complex because PGs have numerou...

“…Susceptibility to tumour growth (measured in terms of tumour-colony-forming efficiency, CFE) in the lung and other organs, however, is markedly increased in grown rats by the induction of states of topical or systemic stress (van den Brenk et al, 1976a). Thus, local X-irradiation of the lungs (van den Brenk et al, 1973b;Milas and Withers, 1970) injection of rats with adrenergic drugs, inflammatory agents (cellulose sulphate, Compound 48/ 80) or chemical convulsants, and physical restraint of rats (van den Brenk et al, 1974) markedly increased tumour OFE.…”

mentioning

confidence: 99%

Effect of toxic thioureas on resistance of rats to growth in the lungs of intravenously and intratracheally seeded tumour cells

Brenk¹,

Kelly²,

Holland³

1978

Self Cite

Summary.-Clonogenic growth (colony-forming efficiency, CFE) of i.v. injected allogeneic W256 tumour cells in the lungs was markedly enhanced by treatment of rats with x-naphthyl thiourea (ANTU) injected i.p. from 2 h before to 2 h after the tumour cells. ANTU specifically increases pulmonary vascular permeability in adult rats and causes acute pulmonary oedema and pleural effusion. Inhibition of drug toxicity to the lungs by tachyphylaxis, specific antimetabolites or iodides did not abolish the effect of ANTU on CFE. CFE was not increased when cells were seeded by i.v. injection in lungs affected by advanced pulmonary oedema at 6 to 24 h after treatment with the drug. ANTU did not enhance growth of intratracheally injected cells.Although ANTU has no cytotoxic or immunosuppressive action, treatment of tumour-immunized rats with ANTU caused apparent "breakdown" of tumour immunity in 50% of rats, by causing growth of tumour colonies in the lungs.Possible mechanisms for the ANTU-induced decrease in innate resistance to growth of tumour in the lungs are discussed.