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M F Press

Publications and source records attributed to M F Press.

70 records · Page 4Linked to original sources
PubMed1985

Lead-induced permeability changes in immature vessels of the developing cerebellar microcirculation.

The ultrastructure and microcirculatory permeability changes of lead encephalopathy were studied in an animal model using horseradish peroxidase as an intravascular tracer. The fine structure of capillary sprouts in the developing cerebellar microcirculation of lead-poisoned rats were described. Immature vessels, characterized by the presence of endothelial sprouts, were found to have focal areas of endothelial injury with degenerating endothelial cells. These disruptions of the microcirculatory endothelium had tracer extending from the vessel lumen to the surrounding neuropil. The degenerating endothelial cells were found as early as 24-28 h after the first administration of lead acetate by gastric lavage (2-3-day-old rats). The early injury to endothelial cells of immature vessels in the developing microcirculation is suggested as an important component of the vascular permeability changes which characterize lead encephalopathy. Older animals (5-10 days old) had microaneurysmal vascular dilatations which had a complex internal structure formed by endothelial cells. These microaneurysmally dilated vessels may represent an endothelial response to preceding endothelial injury of immature vessels.

Animals↗
PubMed1985

Endometrial "sarcomas" complicating ovarian thecoma, polycystic ovarian disease and estrogen therapy.

Unopposed endogenous and exogenous estrogenic stimulation has been considered by most investigators to have a role in the pathogenesis of carcinoma of the endometrium. Although a few cases of "sarcomas" of the endometrium that had developed in an estrogenic setting have been reported, a clear-cut association between estrogenic stimulation and these forms of endometrial cancer has not been established. We report six cases of endometrial sarcomas complicating ovarian thecomas, polycystic ovarian disease, or prolonged estrogen therapy. Three ovarian thecomas, which are considered to be estrogenic tumors, were associated with endometrial malignant mullerian mixed tumor, mullerian adenosarcoma, and low-grade stromal sarcoma in postmenopausal women. Polycystic ovarian disease, a condition characterized by unopposed estrinism due to the peripheral conversion of excessive androstenedione to estrone, was found in a 27-year-old infertile woman with an endometrial malignant mullerian mixed tumor. A pure osteogenic sarcoma of endometrial stromal origin developed in a 28-year-old woman with gonadal dysgenesis (Turner's syndrome) who had received estrogens for 18 years. The sixth woman, with an empty sella turcica after radiation therapy of a pituitary adenoma, had an endometrial mullerian adenosarcoma at the age of 40 years after 16 years of estrogen therapy. None of these patients had had pelvic radiation therapy. The evidence from this series of cases and from six additional cases identified in the literature suggests that the risk of endometrial sarcomas may be increased by estrogen therapy or endogenous disorders that lead to unopposed estrogenic stimulation of the uterus.

Adult↗
PubMed1985

Immunoelectron microscopic localization of estrogen receptor with monoclonal estrophilin antibodies.

The recent production of a series of monoclonal estrophilin (estrogen receptor) antibodies recognizing estrogen receptor derived from a wide variety of animals and target tissues permits the development of immunoelectron microscopic techniques for identifying estrogen receptor. We have determined suitable conditions for the ultrastructural localization of estrogen receptor in tissue sections. Localization of receptor was observed in the euchromatin, but not in the marginated heterochromatin or nucleoli of epithelial and stromal nuclei of human endometrium. Competition studies indicate that only estrogen receptor specifically inhibits nuclear staining. The absence of any specific cytoplasmic localization at the electron-microscopic level is consistent with earlier light-microscopic observations and suggests that the majority of the cellular pool of estrophilin exists in the nucleus of hormone-responsive cells.

Antibodies, Monoclonal↗
PubMed1985

Immunocytochemical identification of estrogen receptor in ovarian carcinomas. Localization with monoclonal estrophilin antibodies compared with biochemical assays.

Estrogen receptor (estrophilin) has been identified in ovarian carcinomas by a variety of physicochemical methods. Since these methods require disruption of the tissue, they do not provide any anatomic information about the cellular distribution and location of receptor. The authors have used monoclonal estrophilin antibodies and an indirect immunoperoxidase technique to study the immunocytochemical localization of estrogen receptor in 43 tissue samples of ovarian carcinoma from 27 patients. The immunocytochemical findings were compared with the results of conventional estrogen receptor assays of cytosolic and nuclear extracts prepared from adjacent pieces of ovarian carcinoma. Exclusively nuclear localization of estrogen receptor was observed with the immunocytochemical technique in all of the 25 tumor samples which had a cytosolic estrogen receptor content, determined by either the dextran-coated charcoal or hydroxylapatite techniques, greater than 700 fmoles/gm wet weight of tissue. Only 3 of 16 tumor samples with cytosolic estrophilin concentrations of less than 700 fmoles/gm wet weight displayed nuclear staining for estrogen receptor; two of these three were metastases from receptor-rich primaries. Specific cytoplasmic staining for estrogen receptor was not observed. These results indicate that many ovarian carcinomas have estrogen receptor, predominantly localized in the nucleus, which is similar to tissues of the female genital tract (vagina, cervix, endometrium, fallopian tube) and breast carcinoma.

Adenocarcinoma↗
PubMed1984

An immunocytochemical method for demonstrating estrogen receptor in human uterus using monoclonal antibodies to human estrophilin.

We have used monoclonal antiestrophilin antibodies to develop an improved immunocytochemical method for localizing estrogen receptors in tissue sections with an indirect immunoperoxidase technique. Rat monoclonal antibodies were raised against human estrogen receptor (estrophilin) protein derived from the cytosol of MCF-7 human breast cancer cells. These monoclonal antibodies have been shown to have extensive cross-reactivity with estrogen receptors from various primate and nonprimate tissues. We have used frozen sections of human proliferative phase endometrium and an indirect immunoperoxidase technique to establish conditions for demonstrating estrogen receptor antigenic determinants in frozen tissue sections. The method involves (a) brief fixation with formaldehyde-containing fixatives either prior to freezing or immediately after cutting cryostat sections, (b) bleaching the tissue of endogenous peroxidase activity, (c) application of primary antibody or control immunoglobulin, (d) application of an adsorbed bridging antibody (goat antirat IgG), and (e) application of rat peroxidase-antiperoxidase followed by diaminobenzidine. Specific nuclear staining for estrogen receptor antigenic determinants was observed in the vast majority of epithelial and stromal cells. No specific cytoplasmic staining was identified in cryostat sections of any of the 17 cases studied for this report.

Adult↗
PubMed1984

Immunohistochemical assessment of estrogen receptor distribution in the human endometrium throughout the menstrual cycle.

Monoclonal antiestrophilin antibodies (H226Sp gamma and H222Sp gamma) were used with an indirect immunoperoxidase technique to localize estrogen receptor in frozen sections of normal human endometrium. Estrogen receptor was detected in the nuclei of the vast majority of epithelial and stromal cells from all early, middle, and late proliferative phase endometria. However, middle and late secretory phase endometria showed a dramatic reduction in the amount of estrogen receptor localized. Specific staining for estrogen receptor in the functionalis of middle and late secretory phase endometria was weak and limited to nuclei of scattered epithelial and stromal cells. In contrast, strong staining for receptor was observed in epithelial cell nuclei of some glands in the basalis. The early secretory phase appeared to be a period of transition from the strong and ubiquitous staining for receptor characteristic of proliferative phase endometria to the weak, focal pattern of estrogen receptor localization characteristic of the functionalis from middle and late secretory endometria. Postmenopausal endometria showed consistently strong nuclear localization of estrogen receptor in epithelial and stromal cells. Myometrial smooth muscle cell nuclei also contained estrogen receptor. However, the endothelial cells of uterine vessels showed no localization of receptor. Specific staining for estrogen receptor was always limited to nuclei; no specific cytoplasmic staining was observed.

Adult↗
PubMed1983

Epithelial peroxidase and endometrial granulocytes in the normal cyclic human endometrium.

Studies in animal models have clearly shown a relationship between the administration of estrogens and the appearance of peroxidase activity in growth-responsive estrogen target tissues (endometrium, cervix, vagina, breast, and DMBA rat mammary tumor). We have studied the ultrastructural localization of endogenous peroxidase activity in the normal cyclic human endometrium. Endogenous peroxidase activity was not identified in proliferative phase endometria, with the exception of one very late proliferative phase endometrium. Most secretory phase endometria showed at least some ultrastructurally identified peroxidase activity in glandular epithelial cells. The number of epithelial cells showing peroxidase activity varied from less than 10% to 85%. The peroxidase activity was present throughout the endoplasmic reticulum of these epithelial cells, extending from the perinuclear cistern to the most peripheral portions of the endoplasmic reticulum adjacent to the apical lumen. Biochemical assays of peroxidase activity in these endometria were compared with the ultrastructurally identified epithelial peroxidase and the endometrial granulocyte count. Uterine granulocyte peroxidase appeared to make a substantial contribution to the total peroxidase activity assayed by biochemical methods. Standard biochemical techniques alone, therefore were not considered to be adequate to evaluate epithelial peroxidase activity.

Adult↗
PubMed1981

Estrogen receptor and peroxidase activity in epithelial ovarian carcinomas.

The endocrine biology of cancers originating from the ovarian epithelium was examined with respect to three sequential indicators for estrogen action: available estrogen receptor in the cytosol, total extractable estrogen receptor from the nucleus, and endogenous tissue peroxidase--a putative postnuclear marker for estrogen-induced growth in uteri of laboratory animals and in some mammary tumor models. Cancers of human ovarian epithelium were distinguished from other ovarian tumors by a higher incidence of detectable (greater than 50 fmol/g tissue wet wt) estrogen receptor in the cytosol (P less than 0.001). Approximately one-half (14/29) of the ovarian adenocarcinoma specimens had greater than 500 fmol available estrogen receptor/g tissue wet weight in their cytosols when assayed by a 2-hour incubation with 17 beta-[2,4,6,7-3H(N)]estradiol followed by treatment with dextran-coated charcoal. With a single exception, ovarian adenomas and nondiseased specimens of premenopausal and postmenopausal ovaries (n = 24) contained less than 500 fmol available estrogen receptor/g tissue wet weight in their cytosols. With respect to extractable estrogen receptor in the nucleus, 11/14 primary and 3/9 metastatic ovarian adenocarcinomas had greater than 50 fmol/g wet weight, as assayed by exchange at 30 degrees C for 5 hours after adsorption of the extracted receptor to hydroxylapatite. Endogenous peroxidase activity, measured in vitro by guaiacol oxidation, occurred in substantially higher amounts in the primary ovarian adenocarcinomas than in benign tumors and control ovaries and could be demonstrated within ovarian adenocarcinoma cells by electron microscopy.

Adenocarcinoma↗
PubMed1977

Lead encephalopathy in neonatal Long-Evans rats: morphologic studies.

Lead encephalopathy was produced in neonatal Long-Evans rats by administering daily doses of lead acetate (600 milligrams of lead acetate/kilogram of body weight) through an esophageal catheter. Experimental rat pups showed behavioral changes, failed to gain weight at the same rate as controls, developed a paraplegia and died by 15 days of age. Lead analysis showed very high blood and tissue lead levels. Sequential histopathologic changes were studied in the cerebellum with observations also made in the choroid plexus, cerebral cortex and corpus striatum. Emphasis was placed on the cerebellum because this region of the brain was most severely altered. Petechial hemorrhages were evident in the cerebellum at three days and two days later the hemorrhagic lesions were almost confluent. The molecular and Purkinje cell layers were most extensively damaged by the hemorrhage. At eight, nine and ten days hemorrhages were fewer and massive amounts of edema fluid accumulated in the internal granular layer. Vascular anomalies of developing lead poisoned rats were examined with electron microscopy and with Golgi preparations. The evidence indicates that growing capillaries are the primary structure of the central nervous system (CNS) damaged by lead intoxication. The endothelial bud (or angioblast) appears to be a structure sensitive to lead poisoning and the encephalopathy probably results from the death of many of these buds.

Age Factors↗
PubMedDate not supplied

Association of p53 mutations and a codon 72 single nucleotide polymorphism with lower overall survival and responsiveness to adjuvant radiotherapy in endometrioid endometrial carcinomas.

p53 Genetic alterations are associated with advanced stage and aggressive tumors in a variety of human malignancies. The aim of this study was to examine p53 for genetic alterations and to evaluate the association of these alterations with clinical outcome and response to adjuvant radiotherapy in endometrioid endometrial carcinomas. p53 mutations in exons 2-11 were assessed in 59 endometrioid carcinomas by polymerase chain reaction-single-strand conformational polymorphism and sequence analysis. Twelve mutations (20.3%) and nine polymorphisms were identified. Seven of the nine polymorphisms were codon 72 single nucleotide polymorphisms (SNP) with an Arg/Pro allelotype. Women harboring either a mutation or an Arg/Pro allelotype at codon 72 had a lower overall survival rate than women whose tumors lacked alterations in the p53 gene (P= 0.0029). Women were stratified based on p53 genetic alterations (p53 mutation or p53 codon 72 SNP) and whether or not they received adjuvant radiation therapy. Women with p53 genetic alterations who did not receive adjuvant radiotherapy had the lowest survival rate (P= 0.0005). Treated women with p53 genetic alterations and untreated women with no p53 alteration had similar rates of survival. Among women with p53 alterations, adjuvant radiotherapy substantially increased survival (P= 0.035). In multivariate analyses, the group of women with p53 genetic alterations who did not receive adjuvant radiation therapy had a 5.9-fold increased risk of death (95% confidence interval: 1.5-22.7) compared to women whose tumors lacked p53 alterations and did not receive adjuvant radiation therapy.

Adult↗
PubMedDate not supplied

Genomic semi-automated cycle sequencing as a sensitive screening technique for p53 mutations in frozen tumor samples.

Single-strand conformational polymorphism (SSCP) is the most widely used method for p53 gene mutation screening. Nucleotide sequence analysis is considered more sensitive for detection of mutations. We established a genomic semi-automated cycle sequencing protocol suitable for p53 gene mutation screening. The technique was applied to 44 SSCP-negative frozen ovarian cancer samples: Eleven mutations (11/44, 25%) were found, 6 point missense mutations, 3 silent point mutations, 1 nonsense mutation and 1 single-base deletion. Heterozygous mutations were readily detectable. Genomic semi-automated cycle sequencing is a sensitive, time-effective screening method requiring only small amounts of tumor tissue.

Amino Acid Substitution↗
PubMedDate not supplied

Prognostic significance of estrogen receptor expression in ovarian cancer. Immunoreactive Score (IRS) vs. Composition Adjusted Receptor Level (CARL).

An Immunoreactive Score (IRS) was compared to the Composition Adjusted Receptor Level (CARL) evaluating prognostic significance of estrogen receptor (ER) expression in 61 ovarian cancers after > or = 8 years. CARL of ER allowed for calculating individual risk curves in stage III and IV, Grade 2 and 3, serous ovarian carcinoma after surgical debulking to < or = 2 cm residual and platinum based chemotherapy. In overall analysis and in subsets defined by tumor stage, grade or a combination thereof significant prognostic distinction became possible using a cutoff IRS of 4 vs. 0 or vs. scores < or = 3. This study substantiates ER as a prognostic variable in human ovarian cancer and for the first time establishes the value of an IRS.

Female↗
PubMedDate not supplied

Chicken ovalbumin upstream promoter--transcription factor (COUP-TF) expression in human endometrial cancer cell lines.

COUP-TF is an orphan member of the steroid receptor superfamily. COUP-TF down-regulates hormonal induction by other steroid receptors involved in cell proliferation and differentiation. Previous study has suggested a role in gynecological adenocarcinoma. In the present study we evaluated COUP-TF expression in endometrial cancer. Fourteen permanent endometrial cancer cell lines were established front the primary site of 14 endometrial cancer patients. Immunocytochemistry for COUP-TF-like activity was performed using an affinity selected polyclonal rabbit-derived antibody in an immunoperoxidase staining technique. The staining intensity and cell surface area were quantified by image analysis. By immunostain 2 cell lines were COUP-TF (+), 6 (+ +) and 6 (+ + +). Quantitative differences in staining intensity and cell surface area were not significant in these groups. All cell lines tested were immunocytochemically negative for estrogen and progesterone receptors. COUP-TF is a new factor involved in endometrial cancer cell differentiation and growth, especially in estrogen receptor negative tumors.

Animals↗