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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Breast cancer is the result of a multistage carcinogenic process. Initiation, promotion, dependency and autonomy make up a sequence of experimentally distinguishable phases of this process. Progression--the transition from dependency on hormonal support to autonomy--is demonstrable clinically. High-affinity saturatable estrogen binding by breast cancer cytosols distinguishes endocrine-responsive mammary neoplasms from autonomous breast cancers. Approximately 70% of neoplasms containing estrogen-recepor protein at a level of 2.5 femtomoles per mg. protein or higher regress after endocrine ablation (ovariectomy in premenopausal women; adrenalectomy or hypophysectomy in postmenopausal women). Only about 5% of neoplasms lacking the receptor will respond to these maneuvers. Estrogen-receptor content also predicts clinically for estrogen and androgen responsiveness, and experimentally for prolactin dependency. Fifty per cent of primary breast cancers in women are receptor-positive. Normal breast tissue and benign breast lesions characteristically lack receptor protein. The receptor proteins appear to be induced in neoplastic cells during mammary carcinogenesis in endocrinologic settings where non-cancerous breast cells do not contain free receptor in large amounts and fail to manifest endocrinologic growth stimulation. Implications of these findings for endocrinologic management of disseminated mammary cancer, adjuvant therapy, and breast cancer prevention are discussed.
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PMID:Endocrinology in cancer of the breast. Status and prospects. 17 80

Prolactin has an effect on the cells of the genetic organs. Experiments were conducted on the molecular mechanisms of the action of prolactin on normal, non-differentiated epithelial cells. One of the 1st effects of the action of prolactin is a stimulation of RNK synthesis. The action of prolactin also increases the activity of proteins I and II. The role of prolactin in the appearance and growth of malignant tumors of the mammary glands was studied in rats and mice with provoked chemical cancer. A treatment of metastasis in the cancer of the mammary gland in patients with a reduction of the level of prolactin is disucssed. Prolactin plays a role of promoter in the development of carcinomas in the mammary glands of animals with chemical and viral carcinoma; it speeds up the malignant process. Further studies are still necessary for the understanding of its significance in the carcinogenesis of human mammary glands.
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PMID:[Role of prolactin in carcinogenesis and growth of mammary and breast neoplasms in animals and in man]. 79 16

The association between mammary carcinogenesis induced by 7,12-dimethylbenz(alpha)anthracene (DMBA) in the rat, the influence by manipulations of its hepatic metabolism and the secretion of prolactin has been investigated. Various test compounds: coumarin, 4-methylcoumarin, phenobarbital and CCl4 all elevated serum prolactin level, but only coumarin and 4-methylcoumarin reduced tumor incidence. These observations do not support the assumption that the suppression of DMBA-induced breast adenocarcinoma by coumarin and 4-methylcoumarin is mediated via prolactin.
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PMID:Is there any association between elevated serum prolactin level and mammary adenocarcinoma induced by 7,12-dimethylbenz(alpha)anthracene. 80 60

Mammary tumours were induced in 3 groups of male Long-Evans rats by a series of 6 fortnightly gastric intubations of 7,12-dimethylbenzanthracene. Two weeks before the initial carcinogen treatment one group of rats was grafted with 3 pituitary homografts underneath the kidney capsule of each recipient (hyperprolactinaemia). A second group, 2 weeks before the initial carcinogen treatment and for the duration of the study (35 weeks), were injected 4 X weekly with 2-Br-alpha-ergocryptine (CB-154) (hypoprolactinaemia). A third group of rats served as controls. A significant increase in the incidence of mammary tumours and a reduced latency period of tumour appearance in the hyperprolactinaemia group, when compared with the controls, were observed in this study. Mammary tumour incidence and latency period of tumour appearance in the hypoprolactinaemia group, however, did not differ significantly from controls. Thus, an increased secretion of pituitary prolactin in rats appears to be an important enhancing endocrinic condition in carcinogenesis of the male mammary gland.
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PMID:Enhancement by prolactin of carcinogen induced mammary cancerigenesis in the male rat. 81 53

The effects of prolactin, estradiol, and progesterone on 3-methyl-cholanthrene (MCA)-induced cervical carcinogenesis in the NMRI strain of mice are reported. Females were ovariectomized at 6-9 weeks of age. 1 week later cotton threads impregnated with a mixture of MCA and beeswax were inserted into the uterine cervix. In 1 group animals were injected with 5 mcg of ovine prolactin in a solvent. A 2nd group received 5 mcg of estradiol-17beta in the same solvent. A 3rd group received both prolactin and estradiol. The control group received only the solvent. Injections were started on the day of operation and given for 6 days. Some animals were killed on the day after the last injection, others 4 weeks later. In other groups progesterone was injected every 3rd day after the estradiol and progesterone injections. Animals which were killed 1 week after insertion of the MCA threads had stratified squamous epithelium with mild atypica in some areas. A few scattered epithelial ''buds'' were seen to penetrate the stroma. In estradiol-injected animals, 2 of 8 had similar ''buds'' and signs of direct stromal invasion of cells from the basal epithelial layer. In 9 animals receiving only prolactin, 2 showed ''buds'' and doubtful basal membrane invasion. In 6 of 9 animals injected with both prolactin and estradiol, larger ''buds'' were present and overt invasion was seen. In animals killed 4 weeks after operation, squamous cervical carcinomas were found significantly more frequently among animals injected with both estradiol and prolactin (p less than .001) than in other groups. Progesterone had no definite effect on the incidence of carcinoma.
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PMID:A synergistic effect of oestradiol and prolactin influencing the incidence of 3-methylcholanthrene induced cerivical carcinomas in mice. 97 Jan 26

The author makes a general review of the influence of hormones on carcinogenesis of the breast. He explains the efforts wich have been made these last years in order to formulate a pronostic which could predict the efficacy of a treatment. He finally discuss the possible part hormones could play and among them principally oestrogens and prolactin in the breast cancer.
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PMID:[Role of hormones in the genesis of breast cancer]. 119 38

The role of prolactin in carcinogenesis in experimental animals and in humans presented.
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PMID:[The role of prolactin in neoplastic disease]. 129 54

We found previously that mouse mammary epithelial cells cultured in the presence of the mammogenic hormones progesterone and prolactin and treated with the carcinogen N-methyl-N-nitrosourea produced a high frequency of hyperplastic alveolar nodules and carcinomas with squamous metaplasia upon transplantation to syngeneic mice. The majority of these mammary transformants had an activated c-Ki-ras proto-oncogene with a specific point mutation in codon 12 (G35 to A35). To determine whether these in vitro findings parallel mammary carcinogenesis in vivo, virgin female mice were pituitary isografted to increase their circulating levels of progesterone and prolactin. The pituitary isograft results in an increase in proliferation, leading to lobulo-alveolar development and differentiation of the mammary epithelial cells. Five weeks after pituitary isografting, the mice were treated with a single injection of N-methyl-N-nitrosourea (50 micrograms/g body weight). Greater than 90% of the N-methyl-N-nitrosourea-treated mice developed mammary carcinomas between 3 and 7 months after treatment. The majority (75%) of the carcinomas had histopathology identical to that of tumors induced in vitro in the presence of progesterone and prolactin. A number of the mammary cancers (17%) induced in pituitary-isografted mice also had the identical point mutation in the c-Ki-ras proto-oncogene found in the in vitro studies. These results suggest that the hormonal milieu around the time of carcinogen exposure affects not only the incidence and phenotype of the mammary transformants but also the molecular events associated with mammary carcinogenesis.
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PMID:Incidence of c-Ki-ras activation in N-methyl-N-nitrosourea-induced mammary carcinomas in pituitary-isografted mice. 139 97

Mapping the chronome's multi-frequency (about-daily, -weekly, and -yearly) neuroendocrine and immune rhythms can help determine when potential chronobiologic response modifiers (CBRMs) should be applied. Aimed at shielding in time by manipulating rhythms, CBRMs may be pertinent to all stages of carcinogenesis, from prevention to treatment, by forestalling the neuroendocrine, immunologic or cell cycle-related recurrent susceptibility peaks from getting aligned, favoring cancerous growth. Pituitary/hypothalamic isografts in the virus-free Bagg albino mouse and designs described as heterophasic allow the systematic investigation of the effect of internal shifts among neuroendocrines. Rhythm manipulation by CBRMs can then aim at lowering (breast or prostate) cancer risk by reproducing identified favorable low risk chronome configurations such as a circannual amplitude in blood that is small for TSH and large for prolactin in women and vice versa for men.
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PMID:Chronobiologic response modifiers and breast cancer development: classical background and chronobiologic tasks remaining. 152 Aug 41

Although several retinoids have been evaluated for prevention of mammary carcinogenesis in rats and mice, retinyl acetate (RA) and N-(4-hydroxyphenyl)retinamide (4-HPR) proved most effective. In rats, dietary administration of the retinoids reduced the incidence and number, and increased the latency of N-methyl-N-nitrosourea (MNU)-induced mammary cancers. 4-HPR reduced the number of hyperplastic alveolar nodules (HAN) in MTV- mice and the number of tumors in MTV+ mice. Other studies indicate that the synergistic effect of retinoid administration and hormonal deprivation is more efficacious in prevention of MNU-induced mammary cancer than either modality alone. Furthermore, retinoids alone and the combination of retinoid and tamoxifen inhibit the appearance of mammary cancers following the surgical removal of the first cancer as well as inhibit the growth of established cancers. Again, the combined modality was the most effective. Retinoids also exert an antiproliferative effect upon the mammary epithelium in vivo, which is represented morphologically by a bare duct system with little branching, end buds, and few, if any, alveoli. In organ culture, retinoids inhibit mammary end bud differentiation and proliferation induced by insulin and prolactin or carcinogens.
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PMID:Retinoids as chemopreventive agents for breast cancer. 155 Nov 41


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