Mammary Tumor Regression. and Loss of Substrates by Tumors

Gullino, P M; Grantham, Flora H.; Losonczy, Ilona; Berghoffer, Bela

doi:10.1093/jnci/49.6.1675

Cited by 32 publications

(10 citation statements)

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“…A decreased RNA content per cell as expressed by the RNA:DNA ratio has been found in regressing rat mammary tumors (Hilf et al, 1969(Hilf et al, , 1971Gullino et al, 1972b, Nicholson et al, 1973, in agreement with our results in G R mouse tumors. This would seem to point to a decrease either in RNA synthesis or in RNA stability.…”

Section: Days a F T E R Days A F T E R Hormone De Prsupporting

confidence: 92%

Biochemical changes during regression and regrowth of hormone‐dependent gr mouse mammary tumors

Schülein¹,

Daehnfeldt²,

Briand³

1976

Intl Journal of Cancer

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Discontinuation of recommencement of estrone-progesterone treatment causes regression and regrowth, respectively, of transplantable hormone-dependent GR mouse mammary tumors. This tumor model was found convenient for the demonstration of hormonal responses in hormone-dependent mouse mammary tumor cells. Tumor regression was palpable 2 days after discontinuation of hormonal treatment and tumors reached half their size within 3-6 days. At this point, hormones were readministered and 2-4 days later the tumors had grown to their preregression size. In the growing and regressing tumor we have investigated: (1) the content of RNA, DNA and protein per g wet weight, (2) in vivo incorporation for 45 min of 32P-orthophosphate into RNA and DNA and the 35S-methionine incorporation into protine; (3) SDS polyacrylamide gel electrophoresis of soluble proteins after in vivo incorporation of 14C- and 3H-leucine. The RNA content per g wet weight was found to decrease during regression and to increase during regrowth. DNA and protein content showed no variation. RNA/DNA ratio thus varied in parallel to the RNA content. The precuursor incorporation into all three macromolecular species decreased during regression. The incorporation into DNA showed the most pronounced decrease. After readministration of hormones, regrowth was accompanied by a rapid increase in precursor incorporation into RNA, while the incorporation into DNA showed a lag of 1 to 2 days. SDS polyacrylamide gel electrophoresis was carried out with soluble proteins labelled in vivo with 14C- and 3H-leucine during regression and regrowth, respectively. No differences in 14C/3H ratios could be demonstrated for the major fractions detectable in the electropherogram.

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Section: Days a F T E R Days A F T E R Hormone De Prsupporting

confidence: 92%

Biochemical changes during regression and regrowth of hormone‐dependent gr mouse mammary tumors

Schülein¹,

Daehnfeldt²,

Briand³

1976

Intl Journal of Cancer

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“…The fibrous stroma of epithelial tumors is generally regarded as being recruited by the neoplastic epithelium to support tumor growth (15). Indeed, it has been demonstrated that in transplanted tumors collagen production is carried out by the host but regulated by the tumor epithelium (16). When a transplantable mouse mammary carcinoma cell line (CMT-315) was transplanted into nude mice, tenascin was detected by immunohistochemistry in the host-supplied stroma of the resulting tumor (Y.I.…”

Section: Discussionmentioning

confidence: 99%

Tenascin is a stromal marker for epithelial malignancy in the mammary gland.

Mackie¹,

Chiquet‐Ehrismann²,

Pearson³

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

230

119

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Tenascin is an extracellular matrix glycoprotein that is not present in the normal mature rat mammary gland. The distribution of tenascin was examined by immunohistochemistry in mammary tumors from carcinogen-treated and untreated rats, in virus-induced mammary tumors from mice, and in a variety of mammary gland lesions from humans. Tenascin was detectable in the stroma of the malignant but not of the benign tumors from all species. An inhibition ELISA, testing homogenates of rat tumors, confirmed that tenascin was present in malignant but not in benign tumors. Thus, tenascin was consistently found to be a stromal marker for epithelial malignancy in the mammary gland. It is concluded that tenascin may be involved in the interactions between the epithelial and mesenchyme-derived (stromal) components of the mammary gland, which are known to influence epithelial carcinogenesis in this organ.Epithelial-mesenchymal interactions are important for the normal embryonic and postnatal development of many organs including the mammary gland (1). In addition, interactions between the epithelial and mesenchyme-derived (stromal) components are known to influence epithelial carcinogenesis in the mammary gland (2). Grobstein's studies suggested that induction of epithelial development is mediated by the extracellular matrix laid down by the organspecific mesenchyme (3). Thus, mesenchymal extracellular matrix molecules that show variations in their tissue distributions during development and neoplasia are potential mediators of mesenchymal-epithelial interactions. The extracellular matrix glycoprotein tenascin, which was previously described as myotendinous antigen (4), and may be identical to J1 (5), cytotactin (6), and glioma-associated extracellular matrix antigen (7), appears to be such a molecule. Tenascin is present in the early fetal rat mammary gland only in the dense mesenchyme closely surrounding the epithelial rudiment (8). It is not detectable in the mature rat mammary gland but is present in the stroma of rat mammary adenocarcinomas induced by the carcinogen N-methyl-Nnitrosourea (MNU; ref. 8). In the present study, the distribution of tenascin was examined in a wide variety of mammary tumors from laboratory animals to determine whether the presence of tenascin could be correlated with any particular type of neoplastic change in the mammary gland. Because of the potential clinical importance of an antigen that is not present in the normal gland but appears in mammary tumors, various human mammary lesions were also investigated. MATERIALS AND METHODSPreparation of Antiserum. Antiserum was raised in rabbits to tenascin purified from conditioned medium of chicken embryo fibroblast cultures, as described (8). The antiserum was found to cross-react with rat, mouse, and human tenascin.Tissues and Immunohistochemistry. Outbred Sprague-Dawley rats were treated with MNU for the induction of mammary tumors as described (8). Spontaneous mammary tumors were obtained from 7 of 213 untreated rats. Rat tumors and some tumor...

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“…This pattern is observed in the oviduct and crop sac of birds, and in the mammary gland, uterus, prostate, and other accessory sex organs of mammals (5)(6)(7)(8). The regression of mammary tumors is also initiated by hormonal withdrawal (9). In other cases, tissue destruction is induced by hormones, e.g., the thyroxine-induced degeneration of the tail during amphibian metamorphosis (10); or programmed by hormones, as in the ecdysone-mediated degeneration of insect muscles (11).…”

mentioning

confidence: 92%

Rapid Inactivation of Ovalbumin Messenger Ribonucleic Acid after Acute Withdrawal of Estrogen

Palmiter¹,

Carey²

1974

Proc. Natl. Acad. Sci. U.S.A.

147

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Synthesis of ovalbumin mRNA is induced and maintained in the avian oviduct by estrogen. When estrogen is rapidly removed from circulation, there is a general involution of the oviduct and an unusually rapid decay of ovalbumin mRNA activity. The kinetics of ovalbumin mRNA decay were not first order; instead, the rate of degradation increased about 10-fold over a 20-hr period after removal of estrogen. These results are in contrast with first-order decay kinetics observed for ovalbumin mRNA in estrogen-stimulated chicks (tl/, = about 24 hr) and in cell-free extracts. The degradative response triggered by hormonal withdrawal becomes more rapid between 1 and 4 days of estrogen-stimulated growth. We conclude that in the process of inducing egg-white protein synthesis, estrogen produces a cellular environment in which the egg-white protein mRNAs are relatively stable; removal of estrogen initiates cellular catabolism in a manner that is not understood.

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Mammary Tumor Regression. and Loss of Substrates by Tumors

Cited by 32 publications

References 0 publications

Biochemical changes during regression and regrowth of hormone‐dependent gr mouse mammary tumors

Biochemical changes during regression and regrowth of hormone‐dependent gr mouse mammary tumors

Tenascin is a stromal marker for epithelial malignancy in the mammary gland.

Rapid Inactivation of Ovalbumin Messenger Ribonucleic Acid after Acute Withdrawal of Estrogen

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