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

The purpose of this investigation was to determine whether diets high in animal or vegetable fat affected mammary tumorigenesis when fed to rats only prior to and during the initiation phase of carcinogenesis. Weanling 21-day-old female Sprague-Dawley rats were divided into different dietary treatment groups and were allowed to feed and libitum on one of the following diets: 5% (normal fat) corn oil; 20% (high fat) corn oil; 20% palm oil; 20% beef tallow; or 20% lard. At 52 days of age, all rats were given p.o. 7.5 mg 7,12-dimethylbenz(a)anthracene (DMBA). One week following DMBA administration, all rats were switched to the 5% corn oil control diet and were maintained on this diet for the duration of the experiment. Rats fed a 20% lard diet during the treatment period showed a significant increase in mammary tumor incidence and number 19 weeks after DMBA administration, when compared to all other dietary treatment groups. Rats fed a 20% beef tallow diet during this same time period also demonstrated enhanced mammary tumor development, during the 10- to 19-week time period after DMBA. Mammary tumor development in rats fed 20% corn oil or palm oil diets during this treatment period was similar to that of normal fat controls. Estrogens are potent stimulators of mammary tumor growth and development in rats. Because mammary tumorigenesis was enhanced in rats fed high animal, but not vegetable fat diets, it was possible that estrogens present in animal fat might be responsible for this stimulation. Further studies demonstrated however, that increased mammary tumorigenesis in rats fed diets high in animal fat could not be explained on the basis of endocrine stimulation. Average day of vaginal opening for all groups fed 20% fat diets was similar and occurred earlier than in normal fat controls. In addition, 50- to 65-day-old rats in the different dietary treatment groups showed no differences in basal or surge levels of serum prolactin, luteinizing hormone, or estradiol. Rat diestrus uterine weight also showed no significant differences among dietary treatment groups. Thus diets containing high levels of animal fat caused little if any increased estrogenic activity in rats. In conclusion, high dietary intake of lard and beef tallow, but not vegetable fat, fed from weaning until only 1 week after DMBA administration, significantly enhances mammary tumorigenesis in rats. The mechanism(s) by which animal fat induces this stimulation is not clear, but it does not appear to result from endogenous or exogenous endocrine stimulation.
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PMID:Comparative effects of different animal and vegetable fats fed before and during carcinogen administration on mammary tumorigenesis, sexual maturation, and endocrine function in rats. 394 Jun 41

Estrogens prevent or diminish the sensitivity to dopamine of prolactin (PRL) secretion by cultured rat pituitary cells. Cultured tumor cells prepared from a transplantable rat PRL-secreting tumor were insensitive to dopamine and bromocriptine, while the anti-estrogen tamoxifen restored this sensitivity. Cultured normal human pituitary cells were shown to be more sensitive to dopamine, if they were preincubated with estradiol, while cultured human prolactinoma cells became insensitive to bromocriptine after they were exposed to estrogens. This sensitivity was restored, however, by tamoxifen. These results point to an important species difference between primates and rodents with regard to the normal regulation of PRL secretion.
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PMID:Interactions of steroids with prolactin secretion in vitro. 405 37

This editorial consists of summaries of the discussions on incidence, pathogenesis, prognosis and patient follow-up, and transcripts of the discussions on detection and treatment of endometrial carcinoma, from a symposium held in Carefree, Arizona. 75% of the cancers occur in postmenopausal women; average age is 52 years, but is decreasing. Endometrial carcinoma rose from 20.3 to 46.3% of all uterine cancers in Cleveland University Hospitals from 1941-1970. Older patients are often diabetic, overweight, nulliparous, with anovulatory or familial history; young women frequently resemble mild Stein-Levinthal syndrome. Clinically, 20% of patients are assymptomatic, others may have softer or larger uterus, larger ovaries, irregular postmenopausal bleeding, or lengthy onset of menopause. The Gravlee jet wash is indicated for high risk patients and those about to take estrogen. Endometrial carcinoma first affects epithelium, then endometrial stroma, then upper myometrium, lower myometrium, then other organs, perhaps via lymphatics, vagina, tubes, but ascites is uncommon. Generally, U.S. physicians use intrauterine radium followed by surgery, British use surgery first, and Swedish use radiation only. Cases must be treated individually, e.g. surgery only for minimal cancer, radium and surgery for more serious cases, and preoperative external radiation also for advanced disease. Although radiation lessens chance of implantation during surgical trauma, insertion of intrauterine radium enhances spread of tumor cells. Injectable progestins sometimes control metastatic disease, although they require 8 weeks to act. Progestins may help those with late recurrence, squamous metaplasia, or who are under 50 years of age. Estrogens are rarely effective. Prognois for terminal patients often includes subjective improvement, bowel obstruction, lung complications, hemorrhage. Radiation side effects and menopausal symptoms are often problems for cured patients. In young cured patients the endometrium should be suppressed with progestins or oral contraceptives.
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PMID:Endometrial cancer: rising incidence, detection and treatment. 469 33

Hormone-dependent (HD) mammary tumors can be induced in mice and rats either by endocrine manipulations or by treatment with carcinogens. The tumors metastasize at a low frequency which may be due to immunogenic properties and does not exclude that the tumors are malignant. Hormone deprival may lead to tumor regression. However, regrowth of hormone-independent (HI) tumor cells probably always occur. Estrogens, progesterone, and prolactin are the most important hormones involved in mammary tumor growth, but androgen- and insulin-dependent mammary tumors have also been described. The most important biochemical difference between HD and HI mammary tumors is perhaps the higher hormone receptor content in HD tumors, but high iodide uptake may prove to be the most specific biochemical characteristic of HD tumors. The relevance of rodent mammary tumor models to human breast cancer is discussed.
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PMID:Hormone-dependent mammary tumors in mice and rats as a model for human breast cancer (review). 630 70

A case of acute intestinal vascular necrosis in a 19-year-old user of oral contraceptives (OCs) is described, and hypotheses explaining the digestive complications of synthetic estrogens are reviewed. The patient had originally presented with a violent gastric pain that subsequently spread to the entire abdomen. An abrupt worsening of her condition involved cardiovascular collapse associated with a peritoneal syndrome, vomiting and dehydration, and hyperleukocytosis. Emergency opening of the peritoneum was followed by evacuation of a large quantity of fetid gas and alimentary debris, and observation of a completely necrosed stomach. A careful lavage of the entire intestinal cavity led to temporary improvement, but it became clear during an attempt at gastrectomy that further treatment would be unavailing and the patient died shortly thereafter. Estrogens were believed to be responsible for the digestive necrosis because it occurred in a young woman who had used an estrogen-rich OC for 3 years and who smoked; a hapatic biopsy confirmed the diagnosis. No traces of other risk factors such as hypertension, hyperlipidemia, diabetes, neoplasia, or obesity were observed. Recent publications indicate that OCs are responsible for a certain number of digestive problems, which may include acceleration of intestinal transit, severe diarrhea, rectorrhagia, ischemic or ulcerative colitis, intestinal infarct which is usually localized, and hepatocellular problems ranging from moderate hepatic insufficiency to malignant tumor and Budd-Chiari syndrome. OCs do not modify hemodynamic regimes, but they may cause elevation of fibrinogen and thrombin, diminution of antithrombin III acitivty, increased platelet adhesivity, and decreased fibrinolysis leading to hypercoagulability. These modifications in hemostasis occur in all OC users and are not statistically correlated with occurence of thrombotic accidents. OCs are probably responsible for parietal vascular lesions; experimental injection of synthetic estrogens is associated with both arterial and venous lesions. The most characteristic anomaly is at the level of the intima, with proliferation of smooth muscle cells and increased conjunctive tissue fibers associated with proliferation of the media or the endothelium. The absence of lipid deposits, the simultaneous appearance of arterial and venous lesions, and other evidence argues against and atheromatous origin of parietal lesions. A significant correlation has been found between high levels of anti-synthetic ethinyl estradiol antibodies and the presence of vascular lesions. It is hypothesized that these circulating immune complexes penetrate the vascular walls of OC users and produce lesions, which may depend on factors such as smoking.
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PMID:[Digestive complications of oral contraceptives: a case of extensive digestive necrosis in a young woman]. 647 54

Human MCF7 breast tumor cells grew as estrogen-dependent tumors in nude mice. In contrast, they were not estrogen-dependent for proliferation in serumless culture media. Charcoal-dextran stripped female human serum supplemented media (5% to 40%) inhibited their proliferation in a dose dependent pattern. Estrogens reversed this inhibition. Concentrations of 2% of this serum allowed for maximal yield regardless of the presence of estrogens. Charcoal-dextran stripped fetal bovine serum was also inhibitory but less potent than the human serum. Non-estrogenic steroids, insulin, epidermal growth factor and transferrin failed to overcome the inhibitory effect of human serum. These results suggest that 1) human and bovine sera contain an inhibitor of the proliferation of estrogen-sensitive cells, and 2) estrogens promote cell proliferation by neutralizing this serum-borne inhibitor.
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PMID:Mechanism of estrogen action on cellular proliferation: evidence for indirect and negative control on cloned breast tumor cells. 647 50

Estrogen receptors (ER) and progesterone receptors (PR) play an important role in the growth and development of the reproductive tract. Estrogen and progesterone influence tissues sensitivity by regulating levels of their own receptors and receptors for other hormones, with estrogen increasing levels of ER and PR and progesterone decreasing levels of ER and PR. Serum levels of estrogen and progesterone and their effect on receptor levels within the endometrium, fallopian tube, and ovary correlate with proliferative and secretory changes observed in uterine tissue throughout the menstrual cycle. Estrogens cause rapid growth of endometrium, while estrogen and progesterone in combination moderate endometrial growth and promote glandular differentiation and secretion. Serum levels also affect receptor levels in the uterus, with estrogen enhancing uterine growth by increasing tissue levels of ER and PR and progesterone antagonizing estrogen action by decreasing receptor levels. In the postmenopausal uterus, ER content and synthesis are continually stimulated by estrogen and unopposed by progesterone. The ability of the uterus to respond to estrogen is related to the quantity of cytoplasmic ER per cell. Although the ontogenic relationship between ER, PR, cellular growth, and differentiation remains unclear, alpha-fetoprotein may play a protective role in the fetus and neonate and may be related to the onset of puberty. The role of receptors during pregnancy also needs further study, but it has been suggested that increased PR in the amnion near term removes progesterone from its protective role in the myometrium, thereby triggering labor. Insufficient production of androgen receptors in certain genotypic males results in the development of phenotypic females and may be the basis for the testicular feminization syndrome. The application of receptor technology has not yet been established in gynecologic oncology; however, in breast cancer, the success of hormonal treatments is related to the presence of ER in tumor tissue and antiestrogens are assumed to suppress tumor growth through an effect on ER. A patient's endocrine status is thought to determine the antagonist's biologic activity.
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PMID:The role of sex steroid receptors in obstetrics and gynecology. 686 53

Various experimental and clinical studies have been made to evaluate possible relationships between estrogen and endometrial cancer. Estrogens do not induce endometrial carcinoma in most species of laboratory animals. In contrast to the limited species effect of estrogen, known carcinogens such as 2-naphthylamine, nitrosamines or aflatoxin B1 produce tumor incidence in a variety of species. Some case-control studies provide the hypothesis that estrogens in menopausal or postmenopausal women may be associated with increased risk of endometrial carcinoma. These studies provide only for association, and the theory of direct relationship must be confirmed or denied by more direct measurements. Other data on estrogens do not show a relationship between estrogens and endometrial cancer. Cases of endometrial cancer have been observed in women using sequential oral contraceptives, particularly dimethisterone with ethinylestradiol, but a cause-and-effect relationship has not been established. Progestins may arrest the progress or cause regression of endometrial carcinoma, but the indications are that the progestin is not protective against the carcinoma in the dosage employed. No data indicates that combination oral contraceptives cause endometrial cancer. The progestin in combination oral contraceptives may offer some protection against endometrial neoplastic changes.
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PMID:Relationship of estrogens and oral contraceptives to endometrial cancer in animals and women. 698 99

After reviewing the pathophysiology of the menopause, attention is directed to a review of the benefits of estrogen progestogen replacement therapy (vasomotor symptoms, urogenital atrophy, psychosomatic complaints, osteoporosis, cardiovascular disease, lipid metabolism); the risks of estrogen progestogen replacement therapy (endometrial cancer, endometrial hyperlasia, breast cancer, coagulation factors, gallbladder disease); and evaluation for estrogen therapy (nonoral estrogen administration). This author regards the menopause to be a hormonal deficiency state, and, like all endocrinopathies, should be managed as vigorously as need be, and without a necessary limitation of time. A wide variety of physical changes and symptoms have been associated with the climacteric. Some patients may only experience cessation of menses; others experience severe reactions that are occasionally disabling. Several factors may influence development of symptoms during the postmenopausal years, and the most important factor is probably the degree of estrogen depletion and the rate at which estrogen levels decrease. Additional factors may be an inherited or acquired propensity to withstand or succumb to the aging process and the psychologic impact of aging and the woman's ability to accept or deny the emotional changes of the menopause. The proven and almost universally accepted benefits of estrogen replacement therapy include relief of vasomotor symptoms, prevention of atrophic vaginitis, and prevention of osteoporosis. Estrogens may also help alleviate some of the psychogenic manifestations that menopause aggravates. Decreasing the risk of cardiovascular disease, particularly in oophorectomized young women may be another benefit by estrogen increased HDL cholesterol. 10 days of cyclic progestogen reduces the risk of endometrial cancer by preventing or treating estrogen induced endometrial hyperplasia. The risk of breast cancer has not been shown to be increased with estrogen therapy, and progestogens may provide additional protection for this tumor. The prognosis for breast carcinoma developing in hormone users is improved, most likely because of an earlier detection. Estrogens prevent demineralization of bone, and the addition of progestogen apparently promotes new bone formation. An increased risk of gallbladder disease may be associated with estrogen therapy, but this risk is minimal and has not been observed in all studies. There is no evidence that either estrogens or progestogens, in the small doses needed for menopause, increase the risk of thromboembolic disease. Newer routes of estrogen administration may further reduce the risks and increase the benefits.
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PMID:The menopause: benefits and risks of estrogen-progestogen replacement therapy. 704 Jan 16

Attention in this discussion of the management of the adolescent girl exposed "in utero" to diethylstilbestrol (DES) is directed to the following: history; scope of the problem; pathogenesis/embryology; management; future fertility; squamous cell carcinoma; and male factors. In the late 1940s and early 1950s, estrogen deficiency was thought to play a role in the high fetal death rate among pregnant diabetic women. DES was 1st used in diabetics and soon thereafter in patients who were threatening to miscarry, who had previous stillbirths, and previous spontaneous abortions. Estrogens were used by some physicians through the late 1960s. In 1970 Herbst and Scully reported 7 carcinomas of the vagina in young women. On careful review, it was found that the mothers of these young women with clear-cell cancer had been treated with DES at various stages of their pregnancies. Subsequent investigation led to the discovery of the condition of vaginal adenosis in many young women exposed "in utero" to DES. It is estimated that 80-90% of patients exposed to intrauterine DES will show gross and microscopic evidence of vaginal and cervical adenosis. It is now felt by most authorities that adenosis coexists with the clear-cell cancer rather than preceding the tumor. A clear-cell tumor registry has been established and, to date, over 400 cases have been registered. The age-range of DES-exposed clear-cell carcinoma is between 7 and 31 years of age. The care of a girl exposed to DES begins when the physician is informed that the patient's mother either received the medication or there was any possibility of such medication. If bleeding occurs before the menarche, the patient should be hospitalized and examined under anesthesia. In the women of menstrual age, management has been somewhat controversial. The use of the colposcope has allowed careful initial examination of the cervix and vagina as well as providing an excellent means of follow-up. The colposcope has been very helpful in delineating the changes caused by DES. There are numerous gross findings that represent adenosis. These include the cervical changes of the "cockscomb" or anterior cervical ridge or "hood," a cervix within a cervix, and a hermicervix. With the colposcope, the areas of adenosis are seen as grape-like projections which, on biopsy, represent columnar epithelium. Areas of metaplastic squamous tissue are easily identified. On occasion dysplasia can occur in areas of adenosis. Of equal importance is the digital examination of the vagina. At this time it is felt that adenosis requires no other treatment than observations. The treatment of clear-cell carcinoma of the vagina or cervix is best determined by a gynecologic oncologist. 80% of DES patients have had live births.
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PMID:Management of the adolescent girl exposed in utero to DES. 733 1


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