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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hormonal influences on dimethylbenz(a)anthracene-induced tumor growth were investigated in detail by endocrine ablation and replacement of hormones. The majority of tumors regressed following ablation and most of them were reactivated by subsequent administrations of estrogen (0.1 to 5 mug) or prolactin (2 mg). Increasing numbers of tumors, however, were not stimulated by prolactin when administration was delayed, and a basal level of estradiol (0.01 mug) in addition to prolactin was required for reactivation of tumors. Nafoxidine hydrochloride, a competitor of estrogen at the receptor sites, arrested growth of a large portion of dimethylbenz(a)anthracene-induced tumors in intact animals but failed to retard growth of prolactin-stimulated tumors. On withdrawal of prolactin-nafoxidine, rapid regression of tumor occurred and readministration of prolactin failed to activate most of the tumors for as long as 28 days. Our results give good supporting evidence that estrogen plays a primary role in tumor growth. The interactions of prolactin and estrogen at tumor sites are necessary for regulatory events related to tumor growth.
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PMID:Estrogen-prolactin dependency in 7,12-dimethylbenz(a)anthracene-induced tumors. 16 87

Alteration of growth of dimethylbenz[a]anthracene-induced mammary tumors was caused by removal of estrogen (ovariectomy), or insulin (diabetes), or by inhibition of prolactin secretin (treatment with an ergoline derivative). The levels of cyclic AMP (cAMP) and cGMP were measured in carcinomas classified as growing, static, and regressing. The amount of cAMP, expressed as pmoles/mg tumor weight or pmoles/mg protein, was lowest in growing tumors, intermediate in static tumors, and highest in those regressing. No correlation was seen between tumor growth and cGMP levels. Cyclophosphamide-induced tumor stasis did not elevate cAMP levels. The data suggest a role of cAMP in arrest of hormone-induced tumor growth.
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PMID:Relationship of adenosine 3',5'-cyclic monophosphate and guanosine 3',5'-cyclic monophosphate to growth of dimethylbenz(a)anthracene-induced mammary tumors in rats. 17 3

The relation between the histological type and thepresence of estrogen receptor or response to oophorectomy in the mammary cancers induced by 7,12-dimethylbanz(a)anthracene in Sprague-Dawley rats is discussed. 23 tumors were evaluated for histological classification. 4 were poorly differentiated (Type A), 16 were well-differentiated (Type B), none was atrophic (Type C), and 3 were secretory (Type D). Of the 4 Type A tumors, 3 had the estrogen receptor. Of the 16 Type B tumors, 10 were with the receptor. 3 secretory Type D tumors showed binding. The response to oophorectomy in each group showed no coorelation to the histological type of the tumor. However, there was a good correlation b etween the presence of estrogen receptor and response to oophorectomy in that 12 of 14 tumors that contained the estrogen receptor responded well. None of the 9 tumors that did not show the binding capacity had a good response. The biochemical feature of estrogen receptor has not been shown to exert influence on structural difference of these tumor cells.
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PMID:Lack of correlation between the presence of estrogen receptor and histological type of mammary cancer induced by 7,12-dimethylbenz[alpha]anthracene. 17 60

Retention of estrogen receptor in regrowing tumors long after endocrine ablation in rat and human breast cancer is reported. Mammary cancer was induced in Sprague-Dawley rats by 7,12-dimethylbenz(a)anthracene (DMBA). More than 10 weeks after oophorectomy, tumors that were continuously growing or recurrent after regression were again submitted to estrogen receptor assay. 4 of the 8 tumors did not contain estrogen receptor before oophorectomy; 2 of these responded temporarily and the other 2 did not respond. The estrogen receptor was not found after oophorectomy in any of these 4. In the other 4 with presence of estrogen receptor all showed some response to oophorectomy. All the recurrent tumors in these 4 rats maintained their ability to bind titrated estradiol specifically. There were no definite change of Ks or (Ns) values. In the 4 patients with breast cancer, the metastatic or recurrent tumors disappeared once or regressed after a major endocrine ablation operation. After a relatively long period of regression, the malignancy had recurred. Assay of estrogen receptor and estimation of associated constant (Ks) and concentration of binding sites ((Ns)) continued the same as determined before the ablative therapy. It is assumed that these tumors initially contained cells of 2 types: sensitive and autonomous. The recurrent tumor is thought to be composed of autonomous cells while the sensitive cells have been eliminated by withdrawal of their supporting hormone. Results seem to be contradictory to the concept of autonomy in recurrent breast cancer after hormonal manipulation. The secondary recurrent cancer may sometim es be successfully checked by another hormonal manipulation or by some blocking agents that compete with the estrogen-receptor complex formation.
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PMID:Possible retention of the estrogen-binding capacity after endocrine ablation therapy in the rat and human breast cancer. 17 62

Phospholipids and their acyl group composition in mammary adenocarcinomas and mammary tissue of the same tumor-bearing animals were investigated. Breast adenocarcinoma induced by dimethybenz(a)anthracene exhibited a phospholipid pattern which was different from that of the mammary tissue. Tumor phospholipids had higher proportions of diacyl-GPI, diacyl-GPE, and alkenylacyl-GPE and a lower proportion of diacyl-GPC than the controls. The acyl groups of most phospholipids in tumors showed a marked increase in the proportion of 18:1 and a decrease in the proportion of 18:2. The fatty acid composition of plasmalogen and triglyceride, however, remained unchanged. In spite of the decrease in the proportion of 18:2, there was no apparent difference in the proportion of 20:4 in most of the phosphoglycerides; however, a significant decrease in this fatty acid was noted in diacyl-GPI. Results of this study demonstrated that the membrane phospholipids of mammary adenocarcinoma were altered in respect to acyl group composition. Changes in physical properties of the cell membrane, in turn, could lead to abnormal manifestation of membrane regulated events in tumor cells.
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PMID:Acyl group composition of membrane phospholipids in mammary tissues and carcinoma induced by dimethylbenz(a)anthracene. 18 77

Prolactin reverses the inhibitory effects of pharmacological doses of androgen on 7,12-dimethylbenz(a)anthracene-induced mammary tumor growth (Quadri, S.K., Kledzik, G.S., and Meites, J.J. Natl. Cancer Inst., 52: 875-878,1974). To determine whether this effect is due to an alteration in the ability of the tumor cell to bind prolactin, we have quantitated prolactin receptors in androgen-responsive and nonresponsive tumors. Prolactin receptors were measured with 125I-labeled ovine prolactin in a subcellular fraction which reproducibly contained 60 to 80% of the total receptor present in tumor homogenates. Prolactin binding was reversible, reached a steady state in 9 hr, and was completed by excess unlabeled prolactin. Prolactin bound to its receptor with a Kd of approximately 1 X 10(-10) M. Growing tumors were biopsied, and rats bearing regrown tumors were given injections of 4 mg testosterone propionate twice a week. Prolactin receptors were reduced in most of the tumors, which regressed after testosterone treatment by an average of 63% compared to the pretreatment biopsy specimens. Nonresponsive tumors and vehicle-injected controls showed no signifcant alterations in receptor content. This reduction of prolactin receptors is probably insufficient to account for androgen-induced mammary tumor regression.
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PMID:Prolactin receptors and androgen-induced regression of 7,12-dimethylbenz(a)anthracene-induced mammary carcinoma. 18 48

We induced pancreatic adenocarcinomas in Long-Evans rats by placing crystals, 2-3 mg, of 7,12-dimethylbenz[a]anthracene (DMBA) in a 2- to 3-mm incision in the "head" of the pancreas approximately 1 cm from the duodenum. The incisions were closed with one or two silk sutures. The animals were killed 4-10 months after DMBA implantation, and nodules were removed and routinely prepared for light and/or electron microscopic study. Histologic organization varied from normal, through areas of tubule-like structures, to sheets of pleomorphic tumor cells. Electron microscopic study of tumor cells revealed large electron-lucent nuclei that frequently had irregular outlines and prominent nucleoli. The predominant feature of the cytoplasm was abundant rough endoplasmic reticulum. Zymogen granules were rare. Adjacent cells sometimes were jointed by an apical junctional complex to form a lumen into which projected irregular microvilli. A basal lamina sometimes occurred at the bases of the tumor cells. The fine structural similarity of these tumor cells to acinar cells was noted.
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PMID:Fine structure of pancreatic adenocarcinoma induced in rats by 7,12-dimethylbenz(a)anthracene. 18 82

Two types of mammary dysplasias occurring in 7,12-dimethylbenz[a]anthracene (DMBA)-treated BALB/cCrgl mice were transplanted into the cleared mammary fat pads of syngeneic mice for an assessment of their growth behavior and tumor potentials. Keratinized nodules, numerous in DMBA-treated, pituitary isograft-bearing BALB/cCrgl mice, produced primarily ductal outgrowth in control mice and very few tumors (7%) 56 weeks after transplantation. Such dysplasias transplanted into mice bearing pituitary isografts exhibited lobuloalveolar development and produced a higher incidence of tumors (32%). Hyperplastic alveolar nodules (HAN), though relatively rare in DMBA-treated BALB/cCrgl mice, produced lobuloalveolar outgrowth in control mice and had a 100% tumor incidence. Four HAN outgrowth lines were developed by serial transplantation of samples of the nodule outgrowths. The tumor potentials of these nodule lines in intact controls and ovariectomized mice was determined over several transplant generations. The tumor potentials of two of the three nodule lines were decreased in the absence of ovarian hormones. However, the growth of 23 mammary tumors derived from these nodule lines and of nine derived from in situ primary tumors was unaffected by the absence of the ovary. These results, along with those published previously, suggest that mammary tumors in chemical carcinogen-treated mice arise from several precursor populations. These preneoplastic populations comprise both alveolar and ductal hyperplasias.
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PMID:Mammary tumorigenesis in chemical carcinogen-treated mice. VI. Tumor-producing capabilities of mammary dysplasias in BALB/cCrgl mice. 18 96

The effect of prolactin in supporting the growth of 7, 12-dimethylbenz(a)anthracene-induced mammary tumor in adult female Sprague-Dawley rats was investigated when estrogen receptors were blocked by the nonsteroidal antiestrogen, Tamoxifen, ICI 46,474. Following an oophorectomy-induced remission, perphenazine, which stimulates endogenous prolactin release, was able to restore tumor growth whether or not Tamoxifen was added. A second course of perphenazine treatment, instituted after the tumors were allowed to shrink, was again effective in stimulating tumor growth. After a regression in tumor size induced by oophorectomy and daily administration of Tamoxifen, perphenazine was able to restore original tumor size despite continued treatment with Tamoxifen. In intact rats, after regression was obtained by daily administration of Tamoxifen and the prolactin inhibitor, lergotrile mesylate, perphenazine induced tumor growth when the latter was discontinued, even though Tamoxifen was continued for 50 days. Estrogen receptors measured at the time of maximum stimulation by perphenazine were undetectable. On the other hand, estradiol did not stimulate tumor growth when serum prolactin was depressed to undetectable levels by lergotrile. These results indicate that prolactin supports the growth of 7, 12-dimethylbenz(a)anthracene-induced rat mammary tumor and that estrogen receptors are not required under these conditions.
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PMID:Predominant role of prolactin in stimulating the growth of 7, 12-dimethylbenz(a)anthracene-induced rat mammary tumor. 19 Nov 82

In this investigation, prolactin receptor sites were localized by autoradiography in 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumors from rats. Tumors were removed when they reached the size of 2 X 4 cm and sliced to a thickness of .5 mm. Sections cut from the slices were incubated for 3 hours in medium 199 (1% bovine serum albumin, 5 mM CaC12, 5mM HEPES buffer) at pH 7.4 and 400,000 counts/minute of iodine-125-ovine prolactin in the presence or absence of 1 mcg of unlabeled prolactin. After further preparation and storage for 4 months in a light-tight box slides were developed, fixed and stained and then photographed. All tumors were labeled by iodine-125-ovine prolactin. Prolactin receptors were associated with only half the total cells. Specific prolactin binding was confined to tumor cells and nonspecific binding was present in alveolar spaces and connective tissue. In some tumors prolactin recepotrs were found in all tummor cells, whereas in other tumors half of the cells did not contain any receptors, or very few. Reproductions of autoradiographs illustrate findings. Results suggest that variations in receptor content of the tumors may be caused by 2 distinct populations of cells. 1 type contains many receptors and the other very fewreceptor sites, or none at all.
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PMID:Autoradiographic localization of prolactin receptors in 7,12-dimethylbnez[a]anthracene-induced rat mammary carcinoma. 19 27


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