Role of prolactin in rat mammary carcinogenesis: detection of carcinogenicity of low-dose carcinogens and of persisting dormant cancer cells.
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Adenocarcinoma↗
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RNA: DNA ratios in human tumors.
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Adenofibroma↗
Abnormal monocyte chemotaxis in patients with breast cancer: evidence for a tumor-mediated effect.
The chemotactic responsiveness of peripheral blood monocytes was measured in 194 individuals: 37 patients with breast cancer, 17 patients with a history of breast cancer but clinically free of disease after surgery, 42 patients with benign breast masses, and 98 normal controls. Monocyte chemotactic responsiveness (MCR) in vitro was not significantly different from normal [mean = 72.8 migrating monocytes/oil immersion field, +/- 9.3 (1 SD)] in 2 groups of patients: a) those with benign breast masses (mean = 72.6 +/- 15.1; P greater than 0.3) and b) those previously having breast cancer resected and remaining clinically free of disease (mean = 69.0 +/- 12.5; P greater than 0.4). However, MCR was significantly depressed in the group of patients with active breast cancer (mean = 57.2 +/- 20.7; P less than 0.0025). Resection of malignant breast masses resulted in a significant change in MCR (P less than 0.0025), whereas resection of benign lesions did not (P greater than 0.4). MCR was abnormal in all clinical stages of breast cancer, including breast cancer without evidence of metastasis to regional lymph nodes. These data supported the hypothesis that neoplasms adversely affect monocyte function and may thereby hinder immunologically mediated destruction of malignant cells.
Adenocarcinoma↗
Immunologic relationship between breast carcinoma and benign breast disease as detected by the leukocyte migration inhibition assay.
Patients with benign diseases of the breast reacted in a migration inhibition assay with extracts of breast cancer and benign breast lesions and a human breast cancer-derived cell line, MCF-7. The incidence of reactivity of the patients with benign breast diseases against these antigens was similar to that of breast cancer patients. In addition, patients with breast cancer reacted to some extracts of benign breast lesions. The reactivity occurred in patients with several different histopathologic types of breast lesions, but was not found in women with no detectable pathologic lesions.
Adenofibroma↗
Mammary carcinogenic effect of low-dose fission radiation in Wistar/Furth rats and its dependency on prolactin.
The mammary carcinogenic effect in rats of low-dose fission radiation and its dependency on prolactin were studied. A total of 141 female W/Fu rats were exposed to 4.8, 8.9, or 19.5 rads of fission radiation that had both fision neutrons of 2.0 million electron volts (MeV) and gamma ray components similar to those produced by the Hiroshima bomb. Only 1 of 48 rats (2.0%) developed mammary tumor (MT) after irradiation alone, whereas 20 of 48 rats (41.6%) developed MT's if prolactin was supplied shortly after irradiation by means of grafting of the prolactin-secreting pituitary tumor. Furthermore, MT's occurred in 11 of 45 rats (24.4%) treated with prolactin as late as 12 months after irradiation, which suggested the long-term survival of radiation-induced dormant MT cells. A correlation was found between the development of MT and the elevation of serum prolactin level; most MT's appeared shortly after the grafted mammotropic pituitary tumor became palpable. The growth of MT's appeared to be promoted by prolactin in collaboration with ovarian hormones; the growth of adenocarcinomas was dependent on prolactin and ovarian hormones, whereas the growth of fibroadenomas appeared to be less hormone-dependent. Much higher biologic effectiveness, especially in the low-dose range, was found with 2.0-MeV fission neutrons compared with 14.1-MeV fast neutrons or 180-kilovolt peak X-rays in rat mammary carcinogenesis.
Adenocarcinoma↗
Inhibitory effect of disulfiram on rat mammary tumor induction by N-2-fluorenylacetamide and on its metabolic conversion to N-hydroxy-N-2-fluorenylacetamide.
The effect of an antioxidant, disulfiram (DSF), on the carcinogenicities of N-2-fluorenylacetamide (2-FAA) and N-hydroxy-N-2-fluorenylacetamide (N-OH-2-FAA) was examined. DSF given in a diet at a concentration of 0.9% for 1 week before and throughout the carcinogen treatment (0.1 mmol/kg 3 times a week for 4 weeks) reduced the incidence of mammary tumors induced with 2-FAA by 50% and extended the mean latency period of malignant tumors from 5 to 10 months. By contrast, DSF had no effect on mammary carcinogenesis by N-OH-2-FAA. Consistent with these results was the demonstration of the inhibitory effect of DSF on the first step of metabolic activation of 2-FAA, i.e., N-hydroxylation. N-hydroxylation of 2-FAA was significantly inhibited in hepatic microsomes of untreated and 2-FAA-treated male and female rats by DSF given orally. A similar inhibition was shown in vitro after preincubation of hepatic microsomes with DSF. Measurements of cytochrome P450 after pretreatment of rats or microsomes with the inhibition showed no appreciable changes in the hemoprotein content. It was concluded, therefore, that the inhibitory effect of DSF on N-hydroxylation of 2-FAA is accomplished through mechanism(s) other than depression of the cytochrome P450 level. Because both 2-FAA and DSF bind to cytochrome P450 producing a type I spectrum, DSF may interfere with the binding of 2-FAA and thus alter its metabolism.
2-Acetylaminofluorene↗
Inhibition of chemically induced mammary carcinogenesis in rats by short-term exposure to butylated hydroxytoluene (BHT): interrelationships among BHT concentration, carcinogen dose, and diet.
Dietary butylated hydroxytoluene (BHT) fed 14 days before and 14 days after carcinogen administration resulted in a dose-dependent inhibition of 7, 12-dimethylbenz[a]anthracene (DMBA)-induced mammary tumor incidence in outbred Sprague-Dawley rats. In addition, the inhibitory effects of BHT were strongly influenced by the dose of initiating carcinogen and the type of diet in which BHT was administered. In animals fed the NIH-07 diet and receiving a low dose of DMBA (5 mg/rat), the inhibitory effect of BHT was manifested at all four BHT concentrations (6,000 leads to 300 ppm). Maximal inhibition was approximately 50% in animals given 5 mg DMBA and receiving 6,000 ppm BHT. However, in the group administered a high dose of DMBA (15 mg/rat), the inhibitory effect of BHT was expressed only at 6,000 ppm, the highest concentration given. Lower concentrations (300 and 1,000 ppm) of BHT had no detectable effect on tumor incidence. In animals fed the defined, semipurified AIN-76A diet during the 4-week treatment period and initiated with 5 mg DMBA, BHT at 6,000 ppm inhibited tumor development. However, at 15 mg DMBA animals fed the AIN-76A diet differed markedly from those fed the NIH-07 diet. In the former group, BHT at 6,000 ppm was unable to elicit any inhibitory response; in the latter group, BHT inhibited tumor development by 40%. Dietary BHT also inhibited DMBA-induced adrenocortical hyperplastic nodules in a dose-dependent fashion. These results indicate that short-term exposure to dietary BHT can inhibit experimental mammary tumor development at environmentally relevant concentrations.
9,10-Dimethyl-1,2-benzanthracene↗
Adenovirus type 9-induced tumorigenesis in the rat mammary gland related to sex hormonal state.
Adenovirus type 9 was inoculated sc into newborn Wistar/Furth rats, divided into four groups: (1) six male rats, not treated further; (2) 11 male rats, castrated at 4 weeks of age; (3) 12 male rats, castrated at 4 weeks of age and subsequently treated repeatedly with estrogen; and (4) 12 female rats, not treated further. All of the rats in group 3 developed mammary hyperplasia and tumors (fibroadenomas and lipomas), in some cases with malignant histologic structure. Rats in group 4 developed similar mammary tumors, but with later appearance and significantly slower growth. A fifth group of rats, not virus inoculated but castrated and estrogen treated as in group 3, did not develop any demonstrable mammary lesions. The results show that the effects of the virus on the mammary gland are dependent upon an estrogenic background, which by itself cannot cause tumor development in males. It is suggested that viral DNA is incorporated into the cellular DNA in such a way that it influences the synthesis and/or activity of steroid receptors, triggering tumor development.
Adenofibroma↗
Benign breast tumor and estrogenic hormones: a population-based retrospective study.
Histories of the usage of oral contraceptives and other estrogens were obtained from 320 women 20-49 years of age who had pathologically confirmed diagnoses of benign breast disease made at Washington County Hospital in Hagerstown, Maryland, during the period 1968 through 1972. Similar histories were obtained from 320 controls matched for race, sex, age, residence in county, and willingness to participate in a health survey. No association could be found between oral contraceptive usage and benign breast tumor. The use of other estrogens, notably diethylstilbestrol, was significantly related to the presence of benign breast disease.
Adenofibroma↗
Epidemiologic characteristics of benign breast disease.
To see if the risk factors associated with fibroadenoma and cystic disease were similar to those reported for breast cancer, a retrospective study of benign breast tumor in a general population was conducted in Washington County, Maryland. The study population consisted of 320 white women 20 to 49 years of age who had had benign breast disease and 320 age-matched controls. More cystic disease cases than controls had the following characteristics, which had been reported to have been associated with breast cancer in other studies: higher socioeconomic status; fewer pregnancies; and a lack of association with lactation patterns. Nulliparity, late natural menopause and a maternal history of breast cancer were also more common among cystic cases than controls, although these differences could have occurred by chance. Cystic disease cases and controls did not differ with respect to other factors associated with breast cancer, such as early age at menarche, late age at first pregnancy, and negative history of artificial menopause. In contrast to cystic breast disease, fibroadenoma was not associated with most of the risk factors of breast cancer.
Adenofibroma↗
Oral contraceptives and breast disease. An epidemiological study.
A case-control study of the relationship between use of oral contraceptives and cancer of the breast, cancer of the corpus uteri, cancer of the ovary, and benign breast diseases was undertaken among women in the age group 20--44 years who had been admitted to several large hospitals in Connecticut. No significant association was seen between use of oral contraceptives and breast cancer. It was found that the longer a woman had used sequential oral contraceptives, the lower her relative risk of benign breast disease. Use of combination oral contraceptives, however, did not appear to influence the risk of benign breast diseases. The numbers of cases with cancer of the ovary and of the corpus uteri in this age group were too small for any conclusions to be reached.
Adenofibroma↗
Incidence rates and risk factors of benign breast neoplasms.
A case-control study of benign breast disease was conducted in Greater Boston in 1968-1969. Cases were nearly all women living in the reference population who were initially diagnosed as having fibrocystic disease, fibroadenoma or a "mixed" lesion during the study period. Controls were a random sample of the entire reference population. A mail questionnaire was completed for 678 cases and for 1807 controls. For fibrocystic disease the age-standardized incidence rate was 89.4 per 100,000 woman-years; for fibroadenoma it was 32.8. Fibrocystic disease rises in incidence to age 45 and then declines sharply. The incidence rate of fibroadenoma peaks during the 20's, while that of mixed tumors has a mode at 30 to 34. Among young women, the highest rates occur in married nulliparae, but this is not so at higher ages. Neither for fibroadenoma nor fibrocystic disease was there a consistent relationship of risk with parity or with age at first birth. Fibrocystic disease risk was strongly and directly related to age at natural menopause, directly but not strongly related to an index of socioeconomic status, and was increased among women who gave a history of arthritis. Both fibrocystic disease and fibroadenoma were much less frequent in more obese women. Neither fibrocystic disease nor fibroadenoma has an epidemiologic pattern which corresponds closely to that of breast cancer. Therefore, it seems reasonable to suggest that the apparent increased risk of breast cancer among women with benign breast disease is concentrated within a subset of these women.
Adenofibroma↗
Fibroadenoma and the use of exogenous hormones. A case-control study.
The association between fibroadenoma and the use of exogenous hormones in women aged 18-74 years was examined in a case-control study conducted in Connecticut during 1979-1981. The study population included 251 women with biopsy-confirmed fibroadenoma and 1,081 control women drawn from inpatient and outpatient general surgical services of five Connecticut hospitals. Among women under age 45 years, oral contraceptive use was negatively associated with the occurrence of fibroadenoma (age-adjusted odds ratio (OR) = 0.57, 95% confidence interval (CI) = 0.42-0.79). The odds ratio for women over age 45 years who had ever used oral contraceptives was 1.65 (95% CI = 0.58-4.68). Women over age 45 years who had ever used replacement estrogens had an elevated odds ratio for fibroadenoma (OR = 2.83, 95% CI = 1.21-6.60). The data suggest either that the effects of exogenous hormones may differ by age, or that the changing composition of exogenous hormones has brought about different associations depending upon the cohort of women.
Adenofibroma↗
A prospective study of the development of breast cancer in 16,692 women with benign breast disease.
The authors studied the relation between benign breast disease and subsequent breast cancer in 16,692 women with biopsy-diagnosed benign breast disease who had participated in the Breast Cancer Detection Demonstration Project throughout the United States. Women were classified into one of five benign breast disease categories: atypical hyperplasia, proliferative disease without atypia, nonproliferative disease, fibroadenoma, and other benign breast disease. A total of 485 incident cases of breast cancer were identified in the women from August 1973 to February 1986 after a median follow-up period of 8.3 years from the diagnosis of benign breast disease. Age-adjusted incidence rates were calculated for benign breast disease types stratified by family history and calcification status. Relative risk (RR) estimates of breast cancer for women in the five benign breast disease categories, compared with the screened women who did not develop recognizable breast disease (normal subjects), were computed using the proportional hazards model. Results indicated that risk was associated with the degree of epithelial atypia. Over all age groups, women with nonproliferative disease, proliferative disease without atypia, and atypical hyperplasia displayed progressively increasing risks of 1.5, 1.9, and 3.0, respectively, compared with normal subjects, with 95% confidence intervals (CI) exceeding unity. Particularly high risk was seen among women under age 46 years with atypical hyperplasia (RR = 5.7, 95% CI 3.0-10.6). Women with fibroadenoma as the only indication of their benign breast disease had a relative risk of 1.7, with a lower 95% confidence limit of 1.0. No increased risk was seen for women with other benign breast disease. Positive family history (RR = 1.8) and calcification (RR = 1.2) significantly increased a woman's risk proportionately over the risk associated with each benign breast disease subtype. The authors conclude that the risk of developing breast cancer varies by category of benign breast disease and is directly related to the degree of epithelial atypia.
Adenofibroma↗
Risk factors for fibroadenoma: a case-control study in Australia.
Risk factors for fibroadenoma were examined in a case-control study involving 117 fibroadenoma cases ascertained by a major private pathology laboratory in Adelaide, Australia, between January 1983 and October 1985. For each case a population control was randomly selected from the electoral roll in Adelaide and matched to the corresponding case by sex, age, and socioeconomic grading of area of residence. Another 189 women whose first biopsy for benign breast disease was examined in the same laboratory during the same time period as those of the cases, but did not show evidence of epithelial proliferation, were also included in the study as a biopsy control group. Risk of fibroadenoma was associated inversely with the Quetelet index, but there was no evidence of an association with age at menarche or menopausal status. The risk of fibroadenoma decreased with an increasing number of full-term pregnancies and was increased in association with use of oral contraceptives at an early age (under 20 years); however, these two associations were observed only when cases were compared with the population controls. Alcohol consumption and dietary fat intake were found not to be associated with altered risk of fibroadenoma, while in multivariate analyses, duration of cigarette smoking and daily vitamin C intake were both shown to have inverse associations with risk of fibroadenoma. Although fibroadenoma does share some risk factors with breast cancer, there is insufficient evidence to suggest that it represents a precursor state.
Adenofibroma↗
Classification of benign breast disorders. The ANDI classification based on physiological processes within the normal breast.
Terminology in benign breast conditions has been confused by multiplicity of terms which do not relate accurately to clinical or histological patterns. Further confusion arises because terminology is not based on sound concepts of pathogenesis. The ANDI classification has been put forward as a nomenclature based on pathogenesis to replace the division of benign breast disorders into 'normal' and 'disease'. It recognizes that a spectrum exists for most conditions which extends from normal, through mild abnormality--'aberrations'--to disease. This classification allows precise definition of an individual patient problem in terms of pathogenesis, histology and clinical implications. It has proved helpful in deciding rational clinical management and in teaching the significance of benign breast disorders.
Adenofibroma↗
Cystic disease and fibroadenoma of the breast: natural history and relation to breast cancer risk.
Approximately 25% of all 'discrete' breast lesions are fibroadenomas or breast cysts and they more commonly cause a breast lump than breast cancer. Despite their frequency, their natural history and relationship to subsequent breast cancer have not been clearly defined, although it would appear that palpable breast cysts, but not fibroadenomas, are associated with some increased risk of breast cancer. The diagnosis of these two entities is now possible by fine needle aspiration and excision of these lesions is only indicated in certain circumstances.
Adenofibroma↗
Diagnosis by team work: an approach to conservatism.
In the Nottingham Breast Clinic 5000 new cases are seen annually; 3000 are sent because the general practitioner believes that he/she has found a lump. It is the diagnosis and management of this common problem that is considered in this chapter. The traditional management of the palpable breast lump included excision to establish accurate diagnosis; indeed up until 20 years ago even simple cysts were excised. Now most surgeons accept that a woman with no residual palpable abnormality after aspiration of blood-free fluid from a cyst requires no further treatment. Most solid breast lumps are benign on histological examination; their routine removal a mistake in judgement. The challenge in the management of a palpable lesion is to correctly diagnose all the cancers without having to remove those which are benign, unless the patient wishes.
Adenofibroma↗