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At least 577 records · Page 32Linked to original sources
PubMed1985

Chemical induction of ovarian tumors in rats.

The production and pathogenesis of ovarian cancer was investigated in noninbred albino weanling female rats by surgical fixation into the left ovaries of sutures chemically impregnated with the chemical carcinogens formic acid 2-[4-(5-nitro-2-furyl)-2-thiazolyl]hydrazide (FNT), a nitrofuran antibiotic; N-methyl-N'-nitrosourea (MNU), a direct-acting alkylating agent; or 7,12-dimethylbenz[a]anthracene (DMBA). Rats living more than 30 days following surgery were subjected to complete necropsy of external, thoracic, and abdominal tissues when they died or were killed at 407 days, the study termination. Mean survival of rats in treated and control groups was comparable. All carcinogen-treated rats exposed to FNT, MNU, or DMBA developed one or more ovarian, uterine, or mammary neoplasms with a total of 31 tumors in 22 rats as compared with no tumors in 5 control rats. All carcinogen-treated rats (22) developed ovarian adenomas (18) or adenocarcinomas (4); 3 developed uterine fibroadenomas (1) or squamous cell carcinomas (2); and 6 developed mammary adenocarcinomas. No neoplasms were present in the right ovaries of carcinogen-treated rats. These data suggest that direct application of carcinogens to ovarian tissue is a satisfactory way to develop ovarian adenoma and adenocarcinoma.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1989

A case report of three synchronous stage I malignant neoplasms.

A patient with three synchronous, Stage I neoplasms of the ovary, kidney, and lung, who underwent resection of all lesions at the same operative procedure, is presented. The incidence of multiple primary malignancies and the prognosis for Stage I cancers of the ovary, kidney, and lung are reviewed.

Adenocarcinoma↗
PubMed1986

Actuarial analysis of the hazard for mammary carcinogenesis in different rat strains after X- and neutron irradiation.

Mammary carcinogenesis in three different rat strains has been studied after single and fractionated irradiations with X-rays and monoenergetic neutrons of three energies. The aims of the programme are the investigation of the nature of the dose-effect relationships, and the determination of the relative biological effectiveness (RBE) of neutrons. Histopathological examinations of tumours has been completed and dose-effect relations are reported separately for the induction of benign and malignant lesions. Appropriate corrections have been made for competing risks in the tumour rate analysis. The probability curves for survival without evidence of tumours have been described by Weibull distributions. This continuous parametric failure-time model is used to derive the relative excess hazard for exposure to X-rays and neutrons. The different rat strains show considerable differences in susceptibility for the induction of cancer by radiation. In general linear dose-response curves have been observed for mammary tumourigenesis in the three rat strains for both X-rays and fast neutrons. Within the statistical precision of the data a dependence of the RBE on neutron dose cannot be recognised. The highest RBE values, varying between 7 and 15 for different types of tumours in the three rat strains have been observed for 0.5 MeV neutrons. These RBE values are lower in general than those observed by other groups for beams of comparable energy.

Adenofibroma↗
PubMed1986

The gene transfer-misrepair hypothesis of radiation carcinogenesis tested for induction of mammary tumours in rats.

Mammary tumour induction was studied in female WAG/Rij rats following exposure with single doses of 0.3 and 1.2 Gy gamma radiation and with the same total doses delivered in fractions of 2.5 and 10 mGy respectively at intervals of 12 h. All rats were implanted with pellets containing 2 mg of estradiol-17 beta prior to the irradiation. The occurrence of mammary carcinomas and of fibroadenomas was recorded. The relative excess hazard for tumour induction was lower for the fractionated regimens than for the single dose exposures. The results are compatible with the predictions of the gene transfer-misrepair hypothesis for radiation carcinogenesis.

Adenofibroma↗
PubMed1985

Lifetime toxicity of chloroform and bromodichloromethane when administered over a lifetime in rats.

Chloroform (CHCl3) and bromodichloromethane (CHBrCl2) are the two most common haloorganic contaminants of chlorinated drinking water. A significantly increased incidence of hepatic neoplastic nodules was found in female rats when each of these compounds was administered in drinking water to Wistar rats throughout their life span. Hepatic adenofibrosis was also produced by chronic ingestion of these two halomethanes.

Adenofibroma↗
PubMed1981

CT scanning of the breast using a conventional CT scanner.

Using a conventional body CT scanner, computed tomography of the breast was performed on 32 patients known to have or suspected of having breast masses. Xeromammograms were available for comparison in all cases. All mass lesions were histologically proved. Seven patients were examined prone, 25 supine. The prone position yielded pictures that resembled craniocaudal mammograms. Breast asymmetry, skin thickening, stranding from a mass to the chest wall, calcification, and axillary lymphadenopathy could be demonstrated by means of CT. The portion of the breast adjacent to the chest wall was more readily examined by means of CT than by conventional mammography. Internal mammary nodes could not be demonstrated.

Adenofibroma↗
PubMed1995

p53 mutation in epithelial ovarian carcinoma and borderline ovarian tumor.

We have investigated a series of 19 human ovarian carcinomas and 17 borderline ovarian tumors to determine the loss of heterozygosity on chromosome 17p and possible concurrent p53 mutations. Allelic losses were assessed using restriction fragment length polymorphism study, and p53 gene mutations were detected by single strand conformation polymorphism analysis and by direct sequencing. In addition, we stained the same tumor sections immunohistochemically to detect p53 protein in tissues. Among 19 ovarian malignant tumor samples tested, we identified 17p allelic deletions in 12 (63.2%) of 19 informative cases. The p53 gene mutation was observed in 7 of 19 (36.8%) malignant ovarian tumors, and it was predominantly observed in tumors with allelic loss on 17p (six of seven tumors, 85.7%). Although 9 cases of 17 borderline ovarian tumors showed shifted bands on single strand conformation polymorphism analysis, only one case was proved to have a point mutation in direct sequencing. We also obtained six cases (31.6%) of positive immunoreactivity from 19 ovarian cancers and 3 cases (17.6%) from 17 borderline ovarian tumors. We conclude that loss or inactivation of tumor suppressor gene function by chromosome 17p allelic deletions or p53 mutations are important genetic changes in ovarian cancer.

Adenofibroma↗
PubMed1992

Eccrine syringofibroadenomatosis: a clinical and histologic study and review of the literature.

A 56-year-old man had an 11-year history of a psoriasiform eruption of the palms, soles, and shins. An examination revealed well-demarcated patches and plaques of erythematous, fissured, and hyperkeratotic skin with focal erosions. There was no clinical evidence of ectodermal dysplasia. On histologic examination these lesions proved to be eccrine hamartomas that consisted of anastomosing cords and strands of cuboidal epithelial cells with well-formed ducts and a fibrovascular mucinous stroma. Eccrine ductal origin was indicated by histopathologic, histochemical, immunopathologic, and electron microscopic evaluation. These multiple palmoplantar eccrine hamartomas, unassociated with ectodermal dysplasia, represent a sporadic hamartomatous condition that is best designated as "eccrine syringofibroadenomatosis."

Adenofibroma↗
PubMed1984

Methylene chloride: a two-year inhalation toxicity and oncogenicity study in rats and hamsters.

A long-term study was conducted to determine the possible chronic toxicity and oncogenicity of methylene chloride. Rats and hamsters were exposed by inhalation to 0, 500, 1500, or 3500 ppm of methylene chloride for 6 hr per day, 5 days a week, for 2 years. No exposure-related cytogenetic effects were present in male or female rats exposed to 500, 1500, or 3500 ppm. Females rats exposed to 3500 ppm had an increased mortality rate while female hamsters exposed to 1500 or 3500 ppm had decreased mortality rates. Carboxyhemoglobin values were elevated in rats and hamsters exposed to 500, 1500, or 3500 ppm with the percentage increase in hamsters greater than in rats. Minimal histopathologic effects were present in the livers of rats exposed to 500, 1500, or 3500 ppm. Decreased amyloidosis was observed in the liver and other organs in hamsters exposed to 500, 1500 or 3500 ppm. While the number of female rats with a benign tumor was not increased, the total number of benign mammary tumors was increased in female rats in an exposure-related manner. This effect was also evident in male rats in the 1500- and 3500-ppm exposure groups. Finally, male rats exposed to 1500 or 3500 ppm had an increased number of sarcomas in the ventral neck region located in or around the salivary glands. Therefore, in this 2-year study, some effects were observed in male and female rats exposed to 500, 1500, or 3500 ppm of methylene chloride. In contrast, hamsters exposed to the same exposure concentrations had less extensive spontaneous geriatric changes, decreased mortality (females), and lacked evidence of definite target organ toxicity.

Adenofibroma↗
PubMed1982

Concentration of endogenous oestradiol as related to oestradiol receptor sites in breast tumor cytosol.

Biopsies or mastectomy specimens from 69 malignant and 17 non-malignant human breast tumours have been examined with respect to cytoplasmic oestradiol receptors and endogenous oestradiol concentration. Of the malignant tumours, 45 (65%) had significant oestradiol receptor concentrations (136.7 fmol/mg protein +/- 38.3 S.E.M.). Oestradiol values in the cytosol were not correlated to receptor levels. Cytosol oestradiol concentrations in the receptor-negative tumours were normally distributed about a mean value of 7.4 fmol/mg protein +/- 0.9 (S.E.M.). Oestradiol levels were similar to the median concentration of receptor found in tumours from younger women, and consequently may influence receptor measurements in such tumours. In receptor-positive cytosols a much wider range (less than 1 to 69.7 fmol/mg protein) and a non-symmetrical distribution of oestradiol values were found which closely corresponded to the range of occupied receptor concentrations previously measured in tumour cytosol. When tumours having undetectable oestradiol values were excluded, receptor-positive cytosols had significantly higher oestradiol concentrations than those found in receptor-negative tumours (P less than 0.01). No significant difference in cytosol oestradiol concentration was found in receptor-positive and negative pre- and postmenopausal women. This would indicate that factors other than plasma levels influence tissue availability of oestradiol.

Adenofibroma↗
PubMed1984

Presence and characterization of prolactin receptors in human benign breast tumours.

Prolactin receptors have been determined in 64 benign breast tumours. A specific binding of 0.5% or more (with a range of 0.5-3.3%) was found in 34.4% of the cases and was considered prolactin-receptor-positive. The binding was found to be specific only for lactogenic hormones. By Scatchard analysis the dissociation constant was 2.55 X 10(-10) mol/l and the binding capacity was 4.6 fmol/mg protein.

Adenofibroma↗
PubMed1984

Blood flow and reactivity to noradrenaline in induced and autotransplanted DMBA rat mammary neoplasia.

Blood flow during the 'resting condition' and during noradrenaline infusion was compared by means of a microsphere tracer technique in induced DMBA-tumours along the mammary ridge and in autotransplanted tumours, as well as in abdominal skin, skeletal muscle, liver and kidneys. During 'resting conditions' the blood flow of tumours transplanted into skeletal muscle of the hindlimb, liver and kidney was similar to that of the non-transplanted tumours present along the mammary ridges. A pronounced decrease of blood flow upon moderate noradrenaline infusion was characteristic of autotransplanted as well as non-transplanted tumours, which contrasted to the insignificant reaction of skeletal muscle. The striking similarities in blood flow and reactivity of non-transplanted DMBA tumours and autotransplanted ones, and the dissimilarities of the transplanted tumours and the hosting tissues, favour the idea that these tumours regulate their blood supply irrespective of host tissue.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1984

Differences in DMBA-induced mammary neoplastic responses in two lines of Sprague-Dawley rats.

It has been reported that female Sprague-Dawley rats obtained from a U.S. source and studied in the U.S. gave a larger and more rapid mammary neoplastic response to radiation than did female Sprague-Dawley rats obtained from a Dutch source and studied in The Netherlands. To learn if the different mammary neoplastic responses of the two 'lines' of Sprague-Dawley rats are due to inherent differences between the lines of rats or due to differences in experimental conditions, two groups of rats from the American source and one group from the Dutch source were studied for their response to a chemical carcinogen, dimethylbenzanthracene (DMBA), at the same laboratory. When 10 mg of DMBA per 100 g body wt was given by stomach tube to 28 rats from the Dutch source, 367 days later approximately 25% of these rats had developed mammary carcinomas and approximately 18% had developed mammary fibroadenomas. When the same dose of DMBA was given to rats from the U.S. source, 300 days later 90 and 100% had developed mammary carcinomas and 83 and 95% had developed mammary fibroadenomas. Similar trends were found for the number of neoplasms per rat and the mean time of appearance of the neoplasms. It was concluded that there are inherent differences between Sprague-Dawley rats obtained in the U.S. and Sprague-Dawley rats obtained in The Netherlands in regard to their mammary neoplastic responses to DMBA, as well as in their responses to radiation. Genetic differences between the two lines were confirmed by establishing dissimilarities in the expression of erythrocyte antigens coded for by RT1 (major histocompatibility complex).

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1989

Analysis of glycoproteins released from benign and malignant human breast: changes in size and fucosylation with malignancy.

Radiolabelled glycoproteins released into media from benign and malignant human breast tissue after 48 h organ culture have been analysed using SDS polyacrylamide gel electrophoresis and fluorography. Major differences were identified between benign and malignant tissues: (i) a considerably higher incidence of glycoproteins in the molecular weight range 210-280 kDa detected from carcinomas than benign samples, with incidence being greater in poorly differentiated tumours; (ii) fucosylation of these glycoproteins released from carcinomas but not benign breast; (iii) heterogeneity, particularly of fucosylation, between the carcinomas but consistency amongst benign breast. A glycoprotein of MW 230 kDa was of particular interest since it was not detected from any benign samples but was present in 11 of 17 carcinomas, when it was almost always fucosylated. This could prove to be a useful tumour marker.

Adenofibroma↗
PubMed1989

Daunorubicin-induced mammary tumors in the rat.

Eleven of 24 female Sprague-Dawley rats given a single i.v. injection of daunorubicin (10 mg/kg) developed mammary tumors within 8 months after the injection. Four of 12 rats given an intramammary injection of daunorubicin (4 or 8 micrograms) developed five mammary tumors in the injected area within 6.5 months of injection. Tissue distribution studies using tritiated daunorubicin revealed that the liver, kidney, lung, heart, and intestine had higher daunorubicin concentrations than mammary tissue during the first 24 h after i.v. injection. However, depletion of the drug from the internal organs was more rapid than from mammary tissue. Differences in ability to metabolize daunorubicin were compared in homogenates of isolated mammary epithelial cells and hepatocytes by high-performance liquid chromatography: after 90 min, hepatocytes metabolized about 70% of daunorubicin, whereas mammary epithelial cells did not metabolize the drug. Tritiated daunorubicin injected directly into rat mammary gland showed no metabolism in 24 h, and the drug did not get into the circulation. These results suggest that retention of daunorubicin because of the inability of mammary tissue to metabolize the drug is a cause of drug-induced mammary tumors in female Sprague-Dawley rats.

Adenocarcinoma↗
PubMed1991

Quantitative cytochemistry of glucose-6-phosphate dehydrogenase in benign and malignant breast tumours.

Glucose-6-phosphate dehydrogenase (G6PD) activity was quantified cytochemically in mammary epithelial cells within frozen tissue sections from 38 patients with breast cancer and 44 with benign breast disease. G6PD activities were measured under atmospheres of both N2 and O2. The mean (S.E.) G6PD value 2.5 (0.23) IE U/min measured in N2 in mammary epithelial cells from the group of malignancies was significantly greater than that of 1.6 (0.37) IE U/min in the benign group (P less than 0.001), but there was considerable overlap between individual values. G6PD measured in O2 was detectable in 84% of malignancies compared to only 14% of benign biopsies and the group mean of 1.3 (0.18) IE U/min in the former was significantly greater than that of 0.35 (0.20) IE U/min in the latter (P less than 0.001). Significant correlations between G6PD activities measured in N2 and O2 were observed in both groups. The techniques present a sensitive method of identifying increases in G6PD activity in mammary epithelial cells and provide an assay that in a majority of cases permits the separation of malignant from benign tissues.

Adenofibroma↗