Epidemiology of benign breast lesions: lack of association with oral contraceptive use.
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Oral contraceptives and reduced risk of benign breast diseases.
In 1970 a questionnaire on oral-contraceptive use was mailed to 97,254 married women 25 to 49 years of age in Greater Boston. Sixty-nine per cent responded. During the subsequent 30 months, 1072 of the women were hospitalized for breast diseases. Hospitalization rates for fibrocystic disease were similar for non-users of oral contraceptives and users of one to 12 months' duration. However, users for 13 months to 24 months and 25 or more months had rates only 70 and 35 per cent, respectively, of those of non-users. Detailed analysis of these results, and their similarity to findings in previous studies, suggest that the association is causal--use of oral contraceptives appears to lower risk of fibrocystic breast disease. A similar association was seen for fibroadenoma. Rates of breast cancer were lower for users than for non-users, but this finding was neither related to duration of use nor statistically significant.
Adenofibroma↗
Particles containing RNA-instructed DNA polymerase and virus-related RNA in human breast cancers.
Human breast cancers contain an RNA related to that of mouse mammary tumor virus. In 79% of the breast malignancies examined, this type of RNA is a 70S-component encapsulated with RNA-instructed DNA polymerase in a particle possessing the density characteristics of RNA tumor viruses. Further, the DNA synthesized by the human RNA enzyme complex hybridizes specifically with the RNA of mouse mammary tumor virus. Thus, four features diagnostic of agents similar to mouse mammary tumor virus are also exhibited by a particle found with high frequency in human breast cancers. The accumulating evidence for the involvement of RNA tumor viruses in at least some human neoplasias is becoming increasingly compelling.
Adenocarcinoma↗
Genetic alteration of the c-myc protooncogene (MYC) in human primary breast carcinomas.
We have studied the genomic organization of the c-myc locus (MYC) from 121 human primary breast carcinomas. Two types of alterations were observed: (i) the c-myc protooncogene appeared to be amplified 2- to 15-fold in 38 (32%) of the carcinoma DNAs and (ii) a non-germ-line c-myc-related fragment of variable size was detected in 5 primary breast carcinoma DNAs. With three exceptions, all the tumors containing a genetic alteration of the c-myc locus were invasive ductal carcinomas. A significant correlation (P less than 0.02) was observed between patients more than 50 years old and the presence of a genetically altered c-myc. Enhanced levels of c-myc RNA were observed in 10 of 14 breast carcinomas examined. The c-myc gene was genetically altered in 6 of these 10 tumors. The frequency with which the c-myc gene is altered and its correlation with age suggest that it may play a role in the development of breast carcinomas.
Adenofibroma↗
Tenascin is a stromal marker for epithelial malignancy in the mammary gland.
Tenascin is an extracellular matrix glycoprotein that is not present in the normal mature rat mammary gland. The distribution of tenascin was examined by immunohistochemistry in mammary tumors from carcinogen-treated and untreated rats, in virus-induced mammary tumors from mice, and in a variety of mammary gland lesions from humans. Tenascin was detectable in the stroma of the malignant but not of the benign tumors from all species. An inhibition ELISA, testing homogenates of rat tumors, confirmed that tenascin was present in malignant but not in benign tumors. Thus, tenascin was consistently found to be a stromal marker for epithelial malignancy in the mammary gland. It is concluded that tenascin may be involved in the interactions between the epithelial and mesenchyme-derived (stromal) components of the mammary gland, which are known to influence epithelial carcinogenesis in this organ.
Adenocarcinoma↗
Studies on leukemia developing spontaneously in an inbred family of rats.
This study is a continuation of our recently reported observations on leukemia and lymphomas developing spontaneously in a subline of Sprague-Dawley rats bred by brother-to-sister mating in our laboratory. The previous preliminary report described our observations made in the course of the initial 12 generations of our leukemic subline. The current study reviews the data collected during 8 additional generations and results of experimental and morphologic studies. There was no problem in transmitting the spontaneously developing leukemia by inoculation of suspensions of leukemic cells into newborn or very young suckling Sprague-Dawley rats. Attempts to transmit the disease by inoculation of cell-free, filtered leukemic extracts gave thus far positive results only in one experiment in which two of six inoculated rats developed leukemia and a third one developed an angiosarcoma on the neck. In six additional experiments, of a total of 37 rats inoculated with leukemic filtrates, none developed leukemia and 9 females developed mammary fibroadenomas. Reviews of microscopic slides of blood and of sections of lymphoid tumors, livers, spleens, kidneys, and fragments of bone marrow of the leukemic animals are discussed as well as electron microscopic studies.
Adenofibroma↗
Fibroadenoma of the female breast. Some epidemiologic surprises.
In a study of 70 cases of fibroadenoma of the female breast, two ages of peak incidence were recorded, one of them in the late 20s to early 30s and a second in the late 40s to early 50s. At the time of diagnosis, the lesions usually were less than 3.0 cm in diameter. Almost two thirds of the tumors were situated in the lateral quadrants of the breast. Incidence of fibroadenoma was significantly higher among parous females tham among nulliparas. Review of family histories showed a remarkably high incidence of breast disease of all types in the mothers and sisters of the patients studied. An inordinately high proportion of patients under 40 years of age were nonwhite. Recurrences and multiple lesions were much more frequent in patients over 40. "Recurrences" are undoubtedly serial presentations of multicentric lesions.
Adenofibroma↗
Office management of the breast mass.
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Adenofibroma↗
Thrombin-antithrombin III and D-dimer plasma levels in patients with benign or malignant ovarian tumours.
In 50 patients with benign ovarian tumours, 39 malignant ovarian carcinoma patients and 39 age-matched healthy women, plasma levels of thrombin-antithrombin III complex and D-dimer were determined as well as CA 125. The coagulation activation marker thrombin-antithrombin III complex and D-dimer levels were elevated in the malignant group compared to the benign and control groups. The results suggest that coagulation and fibrinolysis must play a prominent role in ovarian cancer. Moreover, D-dimer and thrombin-antithrombin III were equally useful as CA 125 for the discrimination of patients with benign or malignant ovarian tumours as evidenced by receiver operating and likelihood ratio calculations.
Adenocarcinoma↗
The relationship between dietary fat, adipose tissue composition, and neoplasms of the breast.
Dietary fat has been implicated in the development of carcinoma of the breast. Because of the difficulties in obtaining accurate dietary histories, we analyzed subcutaneous adipose fatty acids to compare the quality of fat intake in three groups of patients undergoing investigations for breast masses. These included carcinoma (n = 37, avg. age 54 yrs.), fibroadenoma (n = 27, age 31 yrs.), and other types (n = 21, age 50 yrs.). Subjects in the carcinoma group were heavier, although they were not obese. A one-way analysis of variance of nine adipose fatty acids and their derived ratios [polysaturates:saturates (P:S)] did not show any systematic differences in the three groups. The quality of dietary fat does not appear to be associated with the development of neoplasia of the breast in this population, which consumes a diet of a high P:S ratio.
Adenofibroma↗
Effects of high-fat diet on incidence of spontaneous tumors in Wistar rats.
In a 2.5-year carcinogenicity study, two groups, both including male and female Wistar rats, were fed two different diets with 4% and 16% fat. In addition to 4% soybean oil, the high-fat diet contained 12% mono- and diglycerides, of which 85% was stearic acid and 13% palmitic acid. There was no difference in food consumption, body weight, weight gain, and longevity between the two groups. A statistically significant increase in the incidence of tumors in the high-fat group was seen in fibroadenoma of the mammae (female, p = 0.05). No statistically significant difference was seen when the incidence of benign mammary tumors (adenomas and fibroadenomas) was combined, just as the overall incidence of mammary tumors (adenomas, fibroadenomas, and adenocarcinomas) was not significantly different between the groups. A statistically significant decrease in the incidence of tumors in the high-fat group was seen in adenoma of the parathyroid gland (male, p = 0.04) and medullary carcinoma of the adrenal gland (male, p = 0.04). Combining the incidence of benign and malignant tumors of the adrenal medulla led to a further increase in the level of significance (p = 0.02). The present study showed that a high-fat diet influenced the tumor incidence in certain organs of rats. However, the overall differences in tumor incidence between rats fed the low- and the high-fat diet are considered marginal. Therefore we were not able to confirm or deny the hypothesis that a high-fat diet promotes the development of cancer. It should be noted that, in our study, fat accounted for about 30% of the total energy in the high-fat diet. This is much below the amount of fat normally found in the western diet but corresponds well to the level recommended for human intake. In addition, the rats fed the high-fat diet did not gain more weight, even though no difference was recorded in food consumption (g/kg body wt) between the groups.
Adenofibroma↗
Radiation carcinogenesis in experimental animals and its implications for radiation protection.
Cancer induction is generally considered to be the most important somatic effect of low doses of ionizing radiation. It is therefore of great concern to assess the quantitative cancer risk of exposure to radiations of different quality and to obtain information on the dose-response relationships for carcinogenesis. Tissues in the human with a high sensitivity for cancer induction include the bone marrow, the lung, the thyroid and the breast in women. If the revised dosimetry estimates for the Japanese survivors of the atomic bomb explosions are correct, there is no useful data base left to derive r.b.e. values for human carcinogenesis. As a consequence, it will be necessary to rely on results obtained in biological systems, including experimental animals, for these estimates. With respect to radiation protection, the following aspects of experimental studies on radiation carcinogenesis are of relevance: Assessment of the nature of dose-response relationships. Determination of the relative biological effectiveness of radiations of different quality. Effects of fractionation or protraction of the dose on tumour development. For the analysis of tumour data in animals, specific approaches have to be applied which correct for competing risks. These methods include actuarial estimates, non-parametric models and analytical models. The dose-response curves for radiation-induced cancers in different tissues vary in shape. This is exemplified by studies on myeloid leukaemia in mice and mammary neoplasms in different rat strains. The results on radiation carcinogenesis in animal models clearly indicate that the highest r.b.e. values are observed for neutrons with energies between 0.5 and 1 MeV. On the basis of such results it might be concluded that the maximum quality factor of 10 for neutrons should be increased. Based on current evidence, an increase by a factor of 2 to 3 seems more realistic than a tenfold rise. The diversity of dose-response relationships point to different mechanisms involved in the induction of different tumours in various species and even in different strains of the same species.
Adenocarcinoma↗
Paramagnetic changes during development of DMBA-induced mammary tumours in Sprague-Dawley rats.
Paramagnetic changes occurring during development of mammary tumours in Sprague--Dawley rats induced by the chemical DMBA were studied using electron spin resonance. A two-fold increase in free-radical signal intensity was observed at the time of appearance of the tumour. The free radical concentration remained elevated to this level throughout the experiment. This change is different from the gradual decrease reported for frozen ESR samples in other experimental tumour systems and from the pattern reported for lyophilised samples. A gradual increase in the concentration of Mn2+ was also observed. A high frequency (35 GHz) ESR spectrometer was used which enabled us to study the small amount of tissue available from small tumours and normal breast tissue. Quantitative histological analysis of the samples after ESR study indicated that the ESR signal in the normal tissues could not be attributed to any particular cell type, including glandular cells. The increase observed in the tumour appeared to be due to an increased concentration of paramagnetic species in the tumour cells. Most of the tumours were adenocarcinomas but several benign adenomas were also observed. The ESR signals in the benign tumours were indistinguishable from those of the malignant tumours.
9,10-Dimethyl-1,2-benzanthracene↗
X-ray characterisation of normal and neoplastic breast tissues.
Normal and neoplastic breast tissues have been characterised in terms of x-ray attenuation. Samples of normal fat and fibrous tissue were obtained from reduction mammoplasty and autopsy, and infiltrating duct carcinoma specimens from mastectomy and lumpectomy. A high-purity germanium spectroscopy system and a beam of 120 kV constant potential x-rays were used to determine the linear attenuation coefficient from 18 to 110 keV. Densities were determined from buoyancy measurements and were used to obtain mass attenuation coefficients. Infiltrating duct carcinomas and fat are well distinguished by x-ray attenuation. For photon energies used for film-screen mammography, infiltrating duct carcinomas are more attenuating than fibrous tissue. Above 31 keV, the ranges of attenuation of the two tissue types overlap. The attenuation coefficients of tissues have been concisely represented by equivalent thicknesses of lucite and aluminium. Analysis based on the average attenuation properties of tissues indicates that dual-energy mammography, using an ideal imaging system, would require 0.06 cGy to provide images in which 1 cm infiltrating duct carcinomas are displayed with a signal to noise ratio of 5 against a background over which the fat/fibrous contrast has been suppressed. This dose is similar to that currently used in conventional film-screen mammography.
Adenofibroma↗
Measurement of small-angle photon scattering for some breast tissues and tissue substitute materials.
For photon energies encountered in diagnostic radiology the shape of the scattering distributions for low-atomic-number media exhibits peaks in intensity close to the forward direction that are not predicted by conventional theoretical models. The positions and shapes of the peaks depend upon the interatomic and intermolecular configurations of the scatterers. The phenomenon is of particular interest because of its relevance to the understanding and modelling of x-ray imaging processes and the possibility that the peaking may be characteristic of tissue type. In the present study, peaks in the forward scattering distributions have been demonstrated for 19 samples of breast tissue and three tissue substitute materials using a position-sensitive photon detector and a 60 kVp x-ray source. Prominent features were observed for all samples investigated. Large differences were found in the shapes of the distributions between adipose and fibroglandular tissues and only small differences were found between carcinomas and fibroglandular tissues.
Adenofibroma↗
Differential reactivity of a novel monoclonal antibody (DF3) with human malignant versus benign breast tumors.
We have defined a human breast tumor associated antigen using a murine monoclonal antibody (MAb DF3) prepared against a membrane-enriched fraction of a human breast carcinoma. This antigen has a MW of 290 kD and is detectable on the cell surface of human breast carcinoma cells using a live cell radioimmunoassay and fluorescence flow cytometry. More important, immunoperoxidase staining with MAb DF3 clearly distinguishes malignant and benign breast lesions. A cytoplasmic staining pattern has been observed with 40 of 51 (78%) breast carcinomas, but only one of 13 fibroadenoma or fibrocystic disease specimens. In contrast, reactivity of benign breast lesions with MAb DF3 primarily occurs along apical borders on ductules. These results demonstrate that the DF3 antigen is present on apical borders of more differentiated secretory mammary epithelial cells and in the cytosol of less differentiated cells.
Adenofibroma↗
Folate conjugase activity in the plasma and tumors of breast-cancer patients.
The activity of folate conjugase (pteroylpolyglutamate hydrolase, EC 3.4.22.12) was measured in plasma from normal subjects and patients with breast cancer using pteroylglutamyl-gamma-glutamyl-gamma-(U14C) glutamate as the substrate. Conjugase assays also were performed on samples of breast-tumor tissue, normal breast, and fibroadenoma. When assayed at pH 4.5 and 7.4, mean plasma conjugase activity was significantly (p less than 0.05) elevated in a group of patients with anatomically proven metastatic disease (n = 21) when compared with control subjects (n = 12) and a group of patients (n = 13) with no clinical evidence of disease after mastectomies. Mean plasma conjugase activity assayed at pH 4.5 also was significantly higher in the metastatic disease group when compared with breast cancer patients before mastectomy (n = 9) and fibroadenoma patients before biopsy (n = 3). The specific activity of tissue conjugase assayed at pH 4.5 was significantly higher (p less than or equal to 0.05) in infiltrating ductal carcinoma than in normal adjacent breast tissue according to the Wilcoxon test for paired samples (n = 10).
Adenofibroma↗
Florid breast fibroadenomas in patients taking hormonal oral contraceptives.
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Adenofibroma↗