Cyclic AMP metabolism in rat liver during 2-acetylaminofluorene carcinogenesis

Christofferson, T.; Brønstad, Gunnar; Walstad, Paul M.; I, Oye

doi:10.1016/0304-4165(74)90192-5

Cited by 20 publications

(6 citation statements)

References 56 publications

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“…(Table I). We have no explanation for this discrepancy, which was seen also for the adrenalin Christoffersen et al, 1974). It is a wellknown phenomenon that a large part of the adenylate-cyclase response towards hormones maybe lost ontissue homogenization (Achar et al, 1977), possibly owing to membrane derangement or non-optimal composition of the incubation mixture in broken-cell preparations.…”

mentioning

confidence: 72%

“…2. As (Christoffersen et al, 1974), the adrenalin response increased rapidly during the first weeks, reaching a maximum at about 8 weeks. It then declined, as has also been found during 3'-methyl-DAB carcinogenesis (Boyd et al, 1974(Boyd et al, , 1976, but in the final hepatoma the response to adrenalin was still greater than in normal liver tissue (Fig.…”

mentioning

confidence: 95%

“…It has previously been shown that during liver carcinogenesis the adrenalin responsiveness increases during the first weeks of carcinogen treatment (Christoffersen et al, 1972(Christoffersen et al, , 1974Boyd et al, 1974Boyd et al, , 1976). …”

mentioning

confidence: 99%

“…However, increased effects of adrenalin (Brown et al, 1970;Christoffersen et al, 1972;Boyd et al, 1974) and prostaglandin E1 (PGE1) (Chayoth et al, 1973) have also been described. Furthermore, during treatment of rats with chemical carcinogens, before tumour development, alterations in the response pattern of the adenylate cyclase have been observed, including increased responsiveness to adrenergic agents (Christoffersen et al, 1972(Christoffersen et al, , 1974Christoffersen, 1975;Boyd et al, 1974Boyd et al, , 1976 and to PGE1 (Chayoth et al, 1973).…”

mentioning

confidence: 99%

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Effect of prostaglandins and hormones on cyclic AMP formation in rat hepatomas and liver tissue

Brønstad¹,

Christoffersen²,

Johansen³

et al. 1978

Br J Cancer

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Summary.-The formation of cyclic AMP was studied in normal liver, subcutaneous hepatomas derived from MH1C1 cells, and premalignant liver and primary hepatomas induced by the carcinogens 2-acetylaminofluorene (AAF) and 4-dimethylamino-azobenzene (DAB). While only very slight effects of prostaglandins (PG) were seen in slices of normal liver, all the hepatomas responded strongly to PGE1 and PGE2. The hepatomas also had increased PGE,-sensitive adenylate-cyclase activity. PGFia and PGF2as did not increase the cAMP level significantly either in the liver or in the hepatomas. During AAF carcinogenesis the response to PGE1 increased slightly during the carcinogen feeding, and was greatly elevated only in the fully developed hepatomas. This is in contrast to the increase in adrenalin response seen during carcinogenesis, which starts much earlier, and reaches a peak value within 8-10 weeks. It is concluded that various hepatomas have elevated responsiveness to PGE1 and PGE2 as well as to adrenalin, but the course of change in the tissues' ability to respond to these agents during carcinogenesis is very different.

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confidence: 72%

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confidence: 95%

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confidence: 99%

mentioning

confidence: 99%

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Effect of prostaglandins and hormones on cyclic AMP formation in rat hepatomas and liver tissue

Brønstad¹,

Christoffersen²,

Johansen³

et al. 1978

Br J Cancer

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“…Release of " foetal reversion products ", such as carcinoembryonic antigen (CEA) and ofoetoprotein (Neville and Cooper, 1976) and ectopic hormone production (Rees and Ratcliffe, 1974) are common examples. Other phenomena which have been observed are changes in the number or type of hormone receptors at the cell surface (Schorr et al, 1971;Christoffersen et al, 1972;Christoffersen et al, 1974;Boyd, Louis and Martin, 1974;Christoffersen and Berg, 1975) and alterations in the metabolism of cyclic nucleotides (Clark, Reprint requests to Professor T. J. Martin. Morris and Weber, 1973;Minton, Wisenbaugh and Matthews, 1974;Ryan and Heidrick, 1974;DeRubertis, Chayoth and Field, 1976).…”

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confidence: 99%

Calcitonin-responsive adenylate cyclase in a calcitonin-producing human cancer cell line

Hunt¹,

Ellison²,

Underwood³

et al. 1977

Br J Cancer

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Summary.-A calcitonin-responsive adenylate cyclase has been found in a cell line of a poorly differentiated bronchial carcinoma (BEN cells The characteristics of the adenylate cyclase response to SCT did not change over the period between cell adhesion (after subculture) and confluence. However, preincubation of cells for 4 h with SCT (150 nM) abolished the subsequent adenylate cyclase response of particulate preparations to further hormone. The practical difficulties encountered in purifying and quantifying the large-mol.-wt. form of CT-M secreted by BEN cells has precluded direct investigation of the potential relationship between hormone secretion and the occurrence of the calcitonin receptor. This relationship is discussed in terms of its possible biological significance.

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In vitro measurement of carcinogen‐resistant liver cells during hepatocarcinogenesis

Laishes

Farber

1978

Intl Journal of Cancer

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Following the transfer of r a t liver cells from 2-acetylaminofluorene-induced, grey-white hyperplastic nodules t o a primary, monolayer cell culture system, the proportion of the nodule cells which were resistant t o the cytotoxic effects of aflatoxin B1 was determined normal and nodule hepatocytes were great following aflatoxin B1 treatment. Aflatoxin B1 treatment inhibited the spreading of normal hepatocytes, whereas the highly resistant nodule hepatocytes continued t o spread out on the plastic substratum. Supplementation of the culture medium with dexamethasone routinely increased the proportion of resistant normal cells exposed t o some concentrations of aflatoxin B1 but did not significantly increase the size of the resistant nodule cell population.

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Cyclic AMP metabolism in rat liver during 2-acetylaminofluorene carcinogenesis

Cited by 20 publications

References 56 publications

Effect of prostaglandins and hormones on cyclic AMP formation in rat hepatomas and liver tissue

Effect of prostaglandins and hormones on cyclic AMP formation in rat hepatomas and liver tissue

Calcitonin-responsive adenylate cyclase in a calcitonin-producing human cancer cell line

In vitro measurement of carcinogen‐resistant liver cells during hepatocarcinogenesis

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