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At least 685 records · Page 38Linked to original sources
PubMed1974

Serum oestradiol-17 beta in women with benign and malignant breast disease.

Serum concentrations of oestradiol-17β were measured daily throughout one menstrual cycle in 32 normal women, 31 women with benign disease of the breast and 10 with cancer of the breast. The concentrations were found to differ significantly from normal in women with cysts and to a lesser extent in those with cancer of the breast. In 25 normal post-menopausal and in 27 post-menopausal women with cancer repeated assays disclosed consistently low levels of oestradiol-17β.

Adenofibroma↗
PubMed1975

Inappropriate production of collagen and prolyl hydroxylase by human breast cancer cells in vivo.

Thirty-two scirrhous cancers of breast have been examined to determine the origin of the collagen stroma in these tumours. Employing two immunohistochemical techniques it has been shown that the malignant epithelial cells in 30 of these tumours contain not only collagen but also prolyl hydroxylase, a key enzyme in collagen biosynthesis. Neither this enzyme nor collagen was detectable in the spindle cells in the stroma of these tumours. Neither the epithelium in normal breast, that in fibrocystic disease and in fibroadenomata, nor the malignant epithelium in two medullary cancers of breast contained either collagen or prolyl hydroxylase. These results strongly suggest that the malignant epithelium of scirrhous breast cancers produces its own collagen stroma and that the scirrhous reaction in these tumours is not a host response to tumour invasion. The production of collagen and prolyl hydroxylase by breast cancer cells (of the scirrhous type) therefore represents another example of inappropriate protein production by a human tumour.

Adenofibroma↗
PubMed1975

Urinary aetiocholanolone in patients with early breast cancer from South East Scotland and South Wales.

Urinary aetiocholanolone levels have been measured in 417 women aged between 20 and 70 years. The women were drawn from South East Scotland and South Wales and consisted of patients with either benign or malignant disease of the breast and control patients suffering from no detectable breast disorder. The pattern of aetiocholanolone excretion with respect to age and menopausal status has been defined in each group of patients. No significant differences in urinary levels have been detected between patients with breast disease, whether benign or malignant, and control patients. More detailed examination of the 201 women with early cancer of the breast has also shown that there is no consistent correlation between pre-operative aetiocholanolone levels and factors of prognostic significance detectable at the time of primary treatment-tumour size, grade, round cell infiltration, histological involvement of nodes by tumour and the clinical palpability of lymph nodes. It would seem, therefore, that the prognostic value of pre-operative aetiocholanolone measurements is somewhat limited in patients with early breast cancer. It is noted, however, that low levels of aetiocholanolone are associated with post-menopausal patients, a group in which the prognosis is generally poorer than that in pre-menopausal women.

Adenofibroma↗
PubMed1977

Spectral and metabolic characteristics of mitochondrial fractions from rotenone-induced tumours.

Mitochondrial fractions isolated from tumours induced with the respiratory inhibitor rotenone lack respiratory control, oxidative phosphorylation, are partially or totally insensitive to cyanide and have a near-normal content of respiratory carriers. These characteristics are more similar to those of mitochondria from atrophic mammary gland than to those of mitochondria from spontaneous mammary adenomas. Thus, the characteristic structural and biochemical mitochondrial alteration of rotenone-induced tumours would represent a lack of mitochondrial differentiation as the tumour develops from the atrophic mammary gland. Slices of rotenone-induced tumours are insensitive to oligomycin and dinitrophenol, thus indicating that glycolysis would be their sole source of metabolic energy.

Adenofibroma↗
PubMed1978

NMR in cancer, XIII: application of the NMR malignancy index to human mammary tumours.

One hundred and nineteen specimens of human mammary tissue taken from 112 individuals, were inspected by pulsed proton magnetic-resonance techniques (at 22.5 MH2). The purpose of the study was to evaluate the diagnostic capabilities of the nuclear magnetic resonance (NMR) technique with regard to the recognition of malignancy. The combination of two NMR parameters (spin lattice (T1) and spin-spin(T2) relaxation times) into a malignancy index produced better than 95% discrimination between the 2 populations of tissue on a case-by-case basis. The mean and standard deviations obtained were 2.002 +/- 0.351 for normal tissue, and 3.137 +/- 0.667 for malignant specimens. The probability that this difference is not significant is considerably less than 0.01. In addition, specimens of fibrocystic disease and fibrous mastopathy had indices of 2.263 +/- 0.503 and 2.151 +/- 0.505 respectively. Both groups yielded P values less than 0.01 when compared to the malignant specimens.

Adenocarcinoma↗
PubMed1979

Effect of human, bovine and ovine prolactin on DNA synthesis by organ cultures of benign human breast tumours.

Ten benign breast tumours from 9 female patients (8 with fibrocystic disease and 1 with fibroadenoma) and 1 male patient (with gynaecomastia) were processed into slices and individually cultured for 2 days in serum-free Medium 199. [3H]-TdR was added to the culture medium to assess DNA synthesis. The addition of human prolactin to the culture medium (500 ng/ml) significantly (0.05 greater than P greater than 0.01) increased DNA synthesis; all 9 biopsy specimens from the 9 female patients responded positively to this hormone. Ovine prolactin (500 ng/ml) and bovine prolactin (500 ng/ml) increased the mean incorporation of [3H]-TdR into extracted DNA and increased the mean number of [3H]-TdR-labelled cells, but this increase did not reach the 5% level of probability. The sole case of male breast dysplasia analysed in this study did not respond to either human, ovine or bovine prolactin. These results provide evidence that human prolactin and, to a lesser degree, ovine and bovine prolactin are direct mitogenic stimulants to the epithelium in human (female) benign breast tumours.

Adenofibroma↗
PubMed1982

Cell turnover in the "resting" human breast: influence of parity, contraceptive pill, age and laterality.

Morphological identification of cell multiplication (mitosis) and cell deletion (apoptosis) within the lobules of the "resting" human breast is used to assess the response of the breast parenchyma to the menstrual cycle. The responses are shown to have a biorhythm in phase with the menstrual cycle, with a 3-day separation of the mitotic and apoptotic peaks. The study fails to demonstrate significant differences in the responses between groups defined according to parity, contraceptive-pill use or presence of fibroadenoma. However, significant differences are found in the apoptotic response according to age and laterality. The results highlight the complexity of modulating influences on breast parenchymal turnover in the "resting" state, and prompt the investigation of other factors as well as steroid hormones and prolactin in the promotion of mitosis. The factors promoting apoptosis in the breast are still not clear.

Adenofibroma↗
PubMed1985

Prostaglandin F2 alpha in benign and malignant breast tumours.

Prostaglandin F2 alpha (PGF2 alpha) was determined by radioimmunoassay in 57 breast carcinomata, 16 fibroadenomata, and 33 sclero-cystic-disease (SCD) specimens. In 41 cases of carcinoma and 10 cases of fibroadenoma, histologically non-malignant tissue was also obtained from the same breast. PGF2 alpha levels were significantly elevated in breast cancer when compared with the normal tissues and benign diseases (P less than 0.005 for each group). High PGF2 alpha levels were positively correlated with differentiation, positive oestrogen and progestagen receptor status, and low mitotic index. Tumours with good prognosis (less than 20 mm, negative lymph nodes, some degree of differentiation) showed significantly higher PGF2 alpha levels than tumours with a bad prognosis (greater than 20 mm, positive nodes and undifferentiated). A tendency for elevated PGF2 alpha levels was observed with negative lymphatic permeation, postmenopausal status, low grade of nuclear and cellular polymorphism and high degree of elastosis and fibrosis. No correlation was observed between PGF2 alpha levels and host-cell reaction. Plasma levels of 15-keto-13, 14-dihydro-PGF2 alpha were not elevated in cancer patients when compared with the SCD-group. The present study demonstrates that PGF2 alpha levels are high in tumours with good prognosis. However, since other authors have suggested that a high PGE2 production is a bad prognostic index, it is possible that conversion of PGE2 to PGF2 alpha by 9-keto-reductase explains this relationship. Nevertheless, the presented results question the unrestricted use of prostaglandin-synthesis-inhibitors in the treatment of breast cancer.

Adenofibroma↗
PubMed1986

gamma-Glutamyltranspeptidase activity in human breast lesions: an unfavourable prognostic sign.

The activity of gamma-glutamyltranspeptidase (gamma GT) (EC 2.3.2.2) was examined by histoenzymatic labelling on frozen sections derived from normal breast tissue, benign lesions and carcinomas. In biopsies from normal tissue and benign lesions, labelling was very intense in lumina and in the apical pole of the cells lining the lumina whilst in the cytoplasm it was slightly positive. In 34 out of 70 carcinomas, gamma GT activity was either undetectable or slightly positive while in the remaining 36 there was intense activity. Statistical examination of the results revealed no obvious correlation of gamma GT activity with histological grade of the tumour, progesterone receptor content or classification of patients by pre- or postmenopausal status. A good correlation between gamma GT activity and the following unfavourable prognostic signs: lymph node metastases and absence of oestradiol receptors. Patients with gamma GT-negative tumours may have a more favourable prognosis than those with gamma GT-positive tumours.

Adenofibroma↗
PubMed1987

Presence and possible significance of immunohistochemically demonstrable prolactin in breast apocrine metaplasia.

Paraffin wax embedded formalin-fixed benign breast disease tissue taken from 17 patients (15 with microcystic disease and 2 with fibroadenoma) was studied for the presence of tissue bound prolactin using a rabbit antiserum against human prolactin applied in conjunction with a highly sensitive modified version of the dinitrophenyl (DNP)-hapten sandwich staining (DHSS) procedure. Sections taken from 14 of the 15 cases showing apocrine cystic changes exhibited strong prolactin staining restricted to the cytoplasm of metaplastic apocrine cells lining the cysts. Normal lobules and ducts and blunt duct proliferations were all negative, as were also the two cases of fibroadenoma. In contrast 6 out of 8 cases of breast cancer examined showed heterogenously distributed cytoplasmic staining in the cancer cells. Maximal prolactin staining in the apocrine cells was observed at antiserum dilutions as high as 1:60,000. This compared favourably with a 1:120,000 dilution that gave maximal levels of staining in the prolactotrophs present in serial sections taken from formalin fixed paraffin wax embedded post mortem human anterior pituitaries. In both types of tissues the specific staining was abolished by pre-absorption of the antiserum with human prolactin (10 micrograms ml-1). No staining was observed when the anti-prolactin serum was either omitted or substituted with DNP-labelled normal rabbit serum. Apocrine metaplasia in cystic disease of the breast has recently been found to be associated with an increased breast cancer risk. The strong and selective presence of immunohistochemically demonstrable prolactin in the metaplastic cells may be of significance in view of the hormone's known growth stimulating effect on the breast epithelium.

Adenofibroma↗
PubMed1990

Different methylation of oestrogen receptor DNA in human breast carcinomas with and without oestrogen receptor.

The methylation of the human oestrogen receptor (ER) gene was analysed by restriction enzymes in normal and neoplastic human breast tissues and cell lines. CCGG sequences in regions inside the gene, which are methylated both in normal breast and in tissues that are not the target of the oestrogen, are hypomethylated in 30% of tumours, both ER+ and ER- carcinomas. Moreover, 5' sequences of the gene, which are hypomethylated in normal breast and not in tissues not the target of oestrogen, are methylated to a lower degree in ER+ carcinomas, whereas they are methylated to a greater degree in ER- carcinomas. However, the same region is equally hypomethylated in both ER+ and ER- cancer cell lines. Our results indicate that in breast carcinomas ER DNA methylation is deranged, and in cancer cell lines is different from that observed in primary tumours. Furthermore, the abnormal methylation in the 5' end seems to be related to abnormal expression, namely diffuse hypomethylation in carcinomas with high ER content and hypermethylation in carcinomas without ER. These findings support our previous hypothesis that DNA methylation could be involved in the control of ER gene expression and demonstrate that abnormal ER gene methylation is a typical feature of breast cancers.

Adenofibroma↗
PubMed1992

Differential expression of translation-associated genes in benign and malignant human breast tumours.

The human gene sequences encoding the translation-associated functions of alpha-subunit of elongation factor 1 (EF-1 alpha) and the ubiquitin carboxyl extension protein (HUBCEP80) have been isolated by differential cDNA screening, and found to have significantly higher levels of expression in fibroadenomas (benign) compared with carcinomas (malignant) of the breast. These data parallel our previous findings that the acidic ribosomal phosphoprotein P2 also has higher expression levels in the benign breast tumours (Sharp et al., 1990). In situ hybridisation has shown these genes to be expressed predominantly in the epithelium of breast tumours.

Adenofibroma↗
PubMed1995

Elevated levels of members of the STAT family of transcription factors in breast carcinoma nuclear extracts.

The transcription factor, milk protein binding factor (MPBF/Stat5), is a member of the STAT family of signalling molecules which mediates prolactin signal transduction in lactating mammary gland by binding to GAS (gamma-interferon activation site) DNA elements. We have determined the levels of STAT factors in nuclear extracts from a variety of human breast tissues including carcinoma and normal 'resting' breast by electrophoretic mobility-shift assay. The results show that the level of STAT binding activity is low in normal 'resting' breast and benign lesions while carcinoma samples have significantly higher (P < 0.01) amounts of STAT binding activity. Supershift analysis suggests that Stat1 and possibly other members of the STAT family of signalling factors, including Stat3, are activated in breast cancer tissues.

Adenofibroma↗
PubMed1995

Chromosome 11 allele imbalance and clinicopathological correlates in ovarian tumours.

Allele imbalance on chromosome 11 loci in ovarian cancer is a frequent event, suggesting the presence of tumour-suppressor genes for ovarian carcinogenesis on this chromosome. Ten highly polymorphic (CA) repeat microsatellites were used to determine allele imbalance in 60 primary ovarian tumours, including 47 epithelial ovarian cancers (EOCs). Forty EOCs (85%) showed allele imbalance at one or more loci, and in 39 of these (83%) the data suggested subchromosomal deletions: eight of 11p only; six of 11q only; and 25 of both 11p and 11q. Three consensus regions of deletion were indicated at 11p15.5-p15.3, 11q12-q22 and 11q23.3-q24.1. Allele imbalance at the 11q subtelomeric region (D11S912) correlated significantly with adverse survival, while imbalance at 11q14.3 and retention of heterozygosity at 11q22 (close to the site of the progesterone receptor gene) were associated with favourable clinicopathological features. The findings allow development of a preliminary model for the molecular evolution of epithelial ovarian cancer.

Adenocarcinoma↗
PubMed1996

Comparative analysis of the expression patterns of metalloproteinases and their inhibitors in breast neoplasia, sporadic colorectal neoplasia, pulmonary carcinomas and malignant non-Hodgkin's lymphomas in humans.

Matrix metalloproteinases (MMPs) and their inhibitors (tissue inhibitors of metalloproteinases, TIMPs) play essential roles in the remodelling of the extracellular matrix (ECM). Results of in vivo and in vitro studies suggest that the balance between MMPs and TIMPs is altered in neoplasia, contributing to the invasive and metastatic properties of malignant tumours. In this study we have analysed the expression of five MMP genes and TIMP-1 and TIMP-2 in 37 benign and malignant lesions of human breast using Northern blot analysis. MMP-9 (92 kDa gelatinase) and MMP-11 (stromelysin 3) were most consistently expressed by carcinomas. Based on detection of either MMP-9 or MMP-11 mRNAs, we were able to distinguish between malignant and benign disease with a predictive accuracy of 90% with 94% sensitivity and 85% specificity. Subsequently, these results were compared with results for carcinomas of colon and lung and malignant non-Hodgkin's lymphomas (NHL). Elevated MMP-9 and TIMP-1 expression was observed in all four systems. MMP-11 characterised all carcinomas as well as carcinomas in situ but was not detectable in NHL. Our data therefore argue that there are remarkably similar patterns of specific functions involved in ECM remodelling that correlate with malignancy in different human tumours of different histogenesis. However, MMP-11 expression is a characteristic of tumours of epithelial origin that is not found in lymphoid neoplasia. Thus it suggests that MMP-11 may play a regulatory role in the invasion and metastasis of carcinomas.

Adenofibroma↗
PubMed1999

The expression of CCAAT/enhancer binding protein (C/EBP) in the human ovary in vivo: specific increase in C/EBPbeta during epithelial tumour progression.

The CCAAT/enhancer binding protein (C/EBP) family of transcription factors is involved in metabolism and differentiation of cells, especially in rodent liver cells and adipocytes. Their roles in vivo and in particular during pathophysiological conditions in humans are largely unknown. We have investigated the presence of C/EBPalpha, -beta, -delta and -zeta in normal ovaries and in epithelial ovarian tumours of different stages. Immunohistochemical experiments demonstrated that C/EBPalpha and C/EBPbeta were preferentially expressed in epithelial/tumour cells irrespective of stage or grade of the tumour. C/EBPbeta was located in the nuclei of the cells, in contrast to C/EBPalpha, which was present only in the cytoplasm of these cells. The nuclear localization of C/EBPbeta indicates an active role of this transcription factor in tumour cells, whereas the cytoplasmic distribution suggests a more passive function of C/EBPalpha. C/EBPdelta and -zeta demonstrated a more diverse distribution with predominant localization to epithelial cells, but stromal distribution was also noted. The intracellular distribution was confined to both the nucleus and the cytoplasm for C/EBPdelta and -zeta. Western blotting demonstrated that C/EBPalpha, -beta, -delta and -zeta were present in a majority of the samples. The amount of C/EBPbeta increased markedly with malignancy, i.e. with degree of dedifferentiation, while the other members of the C/EBP family displayed a more constant expression level. These results demonstrate an association between the expression of members of the C/EBP family and the formation of epithelial ovarian tumours, with C/EBPbeta as a potential marker for these tumours. As C/EBPbeta is known to be expressed during proliferation of cells in vitro, it may participate in the proliferative process of ovarian epithelial tumour cells in vivo and play a central role in tumour progression.

Adenocarcinoma↗