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

Electron microscopy revealed the presence of intracisternal virus-like particles in a mixed pituitary adenoma consisting of growth hormone cells and prolactin cells. The tumor was removed by surgery from a 48 year old man with a multiple endocrine adenomatosis type I syndrome. The significance of virus-like particles in the pathogenesis of pituitary adenomas remains to be elucidated.
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PMID:Intracisternal virus-like particles in a human pituitary adenoma. 13 Jul 39

The estrogen-binding capacity of mammary tumors induced by 7,12-dimethylbenz(a)anthracene was measured in lesions from animals after the ovariectomy, deprival of insulin (diabetes), or treatment with lergotrile mesylate to inhibit prolactin secretion. The average estrogen-binding capacity was 30 fmoles/mg cytosol protein in growing or static carcinomas from intact (control) animals. A significant reduction in estrogen-binding capacity was observed in regressing but not static mammary tumors from ovariectomized animals. In regressing and static tumors from diabetic rats, estrogen-binding capacity was significantly lower than in lesions from intact animals; this effect was not seen in growing tumors from diabetic rats. Tumors that were growing or static in lergotrile-treated animals showed reduced capacity to bind labeled estradiol. The effects of duration of hormone treatment or time of tissue storage on estrogen-binding capacity were examined and did not appear to be correlated with the decreased binding in tumors from treated animals. The results suggest that hormones capable of producing altered neoplastic growth may influence the level of estrogen receptors.
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PMID:Influence of hormonal alteration of host on estrogen-binding capacity in 7,12-dimethylbenz(a)anthracene-induced mammary tumors. 13 55

Primary liver cancer occasionally presents with feminization. The mechanism is unknown. We studied a young man with primary liver cancer associated with feminization that disappeared after removal of the tumor. Before operation, the serum estrone level was markedly (1113 pg per milliliter) and estradiol and estriol levels were slightly elevated. Human placental lactogen was also increased (0.52 microng per milliliter). Luteinizing hormone, follicle-stimulating hormone and prolactin levels were normal, and testosterone reduced. Beta subunits of human chorionic gonadotropin were not detected in the serum. In vitro assay of tumor tissue showed estrogenic activity and high levels of these subunits. With a reversed isotope dilution technic with crystallization to constant specific activity, we showed the tumor tissue to convert dehydroepiandrosterone sulfate and dehydroepiandrosterone to estrone and estradiol. Production of beta subunits of chorionic gonadotropin and raised serum levels of placental lactogen provided further evidence that the tumor was functioning as trophoblastic tissue.
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PMID:Mechanism of feminization in primary liver cancer. 13 68

In women, dietary modification and life style affect the risk of breast cancer and may alter the hormonal status, while in experimental animals diet can alter the incidence of induced mammary tumors. In this study, a high fat diet increased the incidence of DMBA-induced tumors in rats while this increase in incidence was lowered and the effect of a high fat diet obliterated by an anti-prolactin during CB154. Premenopausal Japanese women had a higher estradiol level than their Caucasian counterpart. In Japanese but not Caucasian breast cancer patients, the estradiol decreased. When nurses were transferred from the Western to a vegetarian diet, the menstrual cycle was shortened, while their prolactin and testosterone decreased. Data indicate that dietary factors influence tumor incidence and hormone profile in rat mammary cancer and the hormonal status in women.
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PMID:Diet and endocrine-related cancer. 14 2

A prolonged suppression of the adrenal cortex was produced by giving dexamethasone to 6 postmenopausal women with generalized mammary carcinoma. Plasma cortisol levels decreased rapidly while plasma dehydroepiandrosterone and androstenedione persisted. Plasma testosterone did not fall, except in ovariectomized patients. Plasma estrogens gradually decreased. This slow disappearance of estrogen indicated that persisting adrenal androgens continued to be precursors of estrogen synthesis in peripheral tissues, and possibly within the tumor tissue also. Plasma dihydrotestosterone estimations were similar to those of plasma estrogens. Plasma gonadotropins remained the same. Prolactin increased gradually. Since the growth of mammary carcinoma in postmenopausal women may be partially under endocrine control and the hormones involved are the sex hormones, and possibly prolactin, the persistence of sex hormones and rise of plasma prolactin may be why dexamethasone produces only a minimal response.
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PMID:Steroid sex hormones and prolactin in postmenopausal women with generalized mammary carcinoma during prolonged dexamethasone treatment. 14 Sep 15

A pituitary adenoma with suprasellar extension that had caused hyperthyroidism due to secretion of excess thyrotropin (TSH), as well as mild hyperprolactinemia, was studied with differential staining, immunocytochemistry and electron microscopy. Most cells of the tumor strained lightly with aldehyde thionin, which demonstrates the granules of normal thyrotrops, and immunocytochemically with antiserum to the hormone-specific beta chain of TSH. A minority of the cells was immunoreactive for prolactin. Electron microscopy revealed light cells interspersed with highly pleomorphic dark cells. Both were sometimes multinucleated, and contained variable numbers of small secretion granules, multiple Golgi complexes, and abundant endoplasmic reticulum.
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PMID:Pituitary adenoma producing thyrotropin and prolactin. An immunocytochemical and electron microscopic study. 14 21

Ultrastrucutral examination of 184 pituitary adenomas demonstrated the presence of extracellular accumulations of electron dense material in 3 out of 64 cases with acromegaly. Fibrillary structures were seen in larger deposits of such material. This material was only observed in biopsies fixed directly with osmium tetroxide; initial fixation with glutaraldehyde did not retain the material and left empty spaces. Positive immuno-histochemical reaction with specific antibodies demonstrated that the extracellular material contained growth hormone (GH). The presence of this extracellular material could not be related to the age or sex of the patient nor to the duration of symptoms, size of the tumor, presence of diabetes mellitus, or concomitant secretion of prolactin. The pericapillary fibrous sheath was heavily thickened in the patient with the longest duration of symptoms, intermediate in thickness in the second and normal in the third.
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PMID:Extracellular growth hormone deposits in pituitary adenoma. 14 77

Among 74 histochemically and ultrastructurally studied pituitary adenomas, 12 apparently chromophobe tumors were characterized by the presence of numerous argyrophil cells. All these argyrophil adenomas failed to reveal presence of GH, prolactin or ACTH cells. Two tumors were found to consist of well granulated cells reacting intensely with anti-TSH antibodies and resembling TSH cells of the normal pituitary. The remaining argyrophil adenomas did not show TSH immunostaining and, with one exception, failed to react with an anti-HCG serum staining gonadotroph cells of human pituitary. They were composed of small, closely apposed cells with small compact or vesicular granules. These tumor cells seem to correspond to some small argyrophil cells found in non-neoplastic pituitary, which differ from TSH cells and from all other types of functionally identified adenohypophyseal cells.
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PMID:Argyrophil pituitary tumors showing TSH cells or small granule cells. 15 28

The presence of ER in DMBA-tumors was demonstrated by the use of dextran-charcoal assay, sephadex chromatography, sucrose gradient sedimentation, and organ culture techniques. It was found that tumors have binding sites ranging from 10-13 to 10-15 moles/mg protein, and a dissociation constant of ER 10-9 to 10-10 M. In experiments with tumor explants, prolactin-insulin significantly stimulated ER binding capacity, as compared with control without prolactin. This stimulation was tissue-specific and inhibited by progesterone. Insulin had a synergistic effect on prolactin stimulation of ER. Our results presents a plausible explanation for tumor responses to these hormones in vivo. This interaction of prolactin, estrogen, and progesterone may be a common phenomenon for all estrogen-responsive tissues.
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PMID:On the mechanism of hormone action in 7,12 dimethylbenz(a)anthracene-induced mammary tumor. I. Prolactin and progesterone effects on estrogen receptor in vitro. 16 37

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


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