ISSN:0022-3417    

DOI:10.1002/path.1711660302

出版商:John Wiley&Sons, Ltd.    

年代:1992

数据来源: WILEY

ISSN:0022-3417    

DOI:10.1002/path.1711660303

出版商:John Wiley&Sons, Ltd.    

年代:1992

数据来源: WILEY

摘要:

AbstractAberrant expression of c‐mychas been implicated in the development of colorectal carcinomas. We have used monoclonal antibodies 6E10 and 9E10, raised against mid‐sequence and C‐terminal peptides of the c‐mycprotein, to study the distribution ofmycprotein in normal and diseased bowel at the light microscope and ultrastructural levels. Normal mucosa showed staining only of some nuclei in the proliferative zones of crypts. In adenomas, staining varied from predominantly nuclear to pancellular to focal or pancytoplasmic. Moderately well differentiated areas of carcinomas gave strong focal cytoplasmic staining, while in poorly differentiated tumours staining was pancytoplasmic. Electron microscopy with these antibodies detectedmycprotein associated with dense chromatin and, where cytoplasmic staining occurred, with polyribosomes. Tumours showed a reduced staining of nuclear pores compared with normal tissue. Comparison of staining patterns with 6E10 and 9E10 in normal tissue, adenomas, and tumours suggests that tumour progression is associated with an accumulation of cytoplasmic c‐mycprotein, perhaps resulting from alterations to the C‐terminus which reduce the efficiency of nuclear targeting of the protein and thus disrupt the regulation of the

ISSN:0022-3417    

DOI:10.1002/path.1711660304

出版商:John Wiley&Sons, Ltd.    

年代:1992

数据来源: WILEY

摘要:

AbstractP53 is a tumour suppressor gene, located in the short arm of chromosome 17, which encodes for a nuclear protein involved in the control of cellular growth, regulating the entry of the cell into the S‐phase. P53 mutations have been identified in a progressively increasing number of human malignancies. Nuclear p53 protein is usually present in non‐tumour cells in minute concentrations, due to its short half‐life. In contrast, tumours with p53 mRNA mutations show a higher nuclear protein concentration, detectable by immunohistological techniques, due to stabilization by complexing with other proteins such as heat‐shock protein or wild‐type p53 protein.Leveis of nuclear p53 protein detected by immunohistochemistry with the monoclonal antibody PAb 1801 were measured with the aid of an image analysis system in 83 non‐Hodgkin's lymphomas (NHLs) and 13 cases of Hodgkin's disease, as well as in 14 cases of normal thymus, reactive tonsils, and lymphadenitis. High levels of p53 protein (>5 per cent of the cells) were present only in high‐grade lymphomas (in the proportion 13/55), with a peak incidence in Burkitt's lymphoma (5/8 cases). Lower levels (<5 per cent) of p53 protein were detected in low‐grade B‐ and T‐cell lymphomas, as well as in most of the cases of Hodgkin's disease, where p53 protein was selectively present in Hodgkin and Reed‐Sternberg cells. In 5/14 reactive tonsils or lymph nodes, occasional p53‐positive cells were identified.These results suggest a relationship between levels of p53 protein and the aggressiveness of NHL. The sporadic presence of p53‐positive cells in human reactive tissues suggests that its expression could depend not only on mutation, but also on stabilization of the protein through complexing with other nuclear proteins. It is not known if this mechanism is also responsible for the p53 nuclear accumulatio

ISSN:0022-3417    

DOI:10.1002/path.1711660305

出版商:John Wiley&Sons, Ltd.    

年代:1992

数据来源: WILEY

摘要:

AbstractThe murine monoclonal antibody, LH39 was characterized in this study and appeared to bind to a novel basement membrane epitope. This antigen was expressed in the epithelial basement membrane of human tissue derived from all three germ cell layers and in basement membranes surrounding small blood vessels within the stroma of all organs examined. LH39 antigen could be first detected in fetal skin at the dermo‐epidermal junction at 7 weeks estimated gestational age but was not present in the dermal vasculature until 16 weeks. When tested against tissue from a range of lower mammalian species, LH39 antigen appeared to be primate‐specific. The epithelial basement membrane zone in organotypical cultures, where there isde novosynthesis of basement membrane components, contained abundant LH39 antigen in contrast to other basement membrane components, type IV collagen, laminin, and type VII collagen. Ultrastructural localization of LH39 epitope, using immunogold electron microscopy on unfixed freshly frozen tissue, was to the lamina lucida. No cross‐reactivity could be detected between LH39 and laminin, fibronectin, and collagens I, III, IV, and V using the ELISA assay.In vitrostudies with a range of proteolytic enzymes suggested that the antigen was non‐collagenous in nature. LH39 precipitated a polypeptide with a molecular weight of 185 kD from extracts of metabolically labelled cultured keratinocytes, and polypeptides of 185 and 200 kD from the culture medium. The tissue distribution of LH39 antigen suggested that it may be an epitope within anchoring filaments. Potential applications of this antibody include the study of benign and malignant human vascular disorders, diseases and tumours associated with angiogenesis, epithelial neoplasms, and conditions of tissue regeneration and repair, such as wound

ISSN:0022-3417    

DOI:10.1002/path.1711660306

出版商:John Wiley&Sons, Ltd.    

年代:1992

数据来源: WILEY

摘要:

AbstractIt has been previously proposed that there is a primary microvascular abnormality in patients with systemic sclerosis. In this study using conventional light and electron microscopy, immunohistochemistry, and labelled adenosine uptake techniques, changes in the dermal microvasculature have been related to the various clinical stages of skin disease in systemic sclerosis.The earliest pathological changes are seen in clinically normal skin. They constitute changes in endothelial cell function and their consequences. Perivascular oedema is an early feature. With progression in the clinical disease, there is, at first, an inflammatory cell infiltrate into the dermis, particularly the papillary and mid‐dermis, and platelet aggregation within vessels. Further clinical progression is associated with increasing dermal fibrosis, loss of adnexae, and vascular effacement.It is postulated that the recruitment of different types of mononuclear cells into the dermis is causally linked with the preceding endothelial cell dysfunction and the subsequent induction of fibroblast proliferation and collagen synthesi

ISSN:0022-3417    

DOI:10.1002/path.1711660307

出版商:John Wiley&Sons, Ltd.    

年代:1992

数据来源: WILEY

摘要:

AbstractThe objective of this study was to test the hypothesis that excessive severity of ischaemic heart disease in diabetics is due, in part, to capillary inadequacy. Sections from autopsied hearts of diabetic patients with and without myocardial infarction as well as from those of patients with infarcts and no diabetes were used for morphometric studies of intramural microvessels in areas without infarction. Normoglycaemic patients with normal hearts were also examined. Two to five transverse sections from each of 44 hearts (stained with methenamine silver) were examined for capillary numerical density, capillary to myofibre ratios, and myofibre diameters. Averages for each case and totals for each group were calculated and compared. Normoglycaemic patients with infarcts had increased morphometric values. Diabetics with infarcts had significantly lower capillary densities than the other groups. In conclusion, it is suggested that in diabetes there is an inadequate ischaemia‐induced, reactive angiogenesis. This may contribute towards increased myocardial vulnerability in further ischaemic injury and perhaps to diabetic cardiomyopath

ISSN:0022-3417    

DOI:10.1002/path.1711660308

出版商:John Wiley&Sons, Ltd.    

年代:1992

数据来源: WILEY

摘要:

AbstractThe pseudomembrane formed in association with late aseptic prosthesis failure contains a mixed giant cell and histiocytic infiltrate with variable numbers of lymphocytes. Immunolabelling with a panel of antibodies on paraffin sections was undertaken to define the nature of the lymphoid infiltrate in 19 cases. In all cases, the predominant lymphoid cell was a memory (CD45RO +, CD45RA‐) T‐cell. B‐cells were rare. Tissue from patients with rheumatoid arthritis (RA) contained greater numbers of T‐cells when compared with patients with osteoarthritis (OA), suggesting that the intensity of the lymphoid infiltrates reflects the underlying joint disease rather than necessarily being part of a hypersensitivity response to wear

ISSN:0022-3417    

DOI:10.1002/path.1711660309

出版商:John Wiley&Sons, Ltd.    

年代:1992

数据来源: WILEY

摘要:

AbstractThe antigenic phenotype of cartilage and synovial cells from six cases of primary synovial chondromatosis (PSC) was determined. This was compared with profiles similarly obtained for adult and fetal cartilage cells. The Ki‐67 (proliferation‐associated) antigen was present on 40–50 per cent of chondrocytes in the proliferative zone of fetal epiphyseal cartilage but absent in chondrocytes of adult articular cartilage and PSC cartilage nodules. The absence of Ki‐67 antigen suggests that there were no proliferating cells in the synovium or cartilage in these cases of PSC. In PSC alone, some chondrocytes in the cartilage nodules and mononuclear subintimal cells around the nodules also reacted for CD68, suggesting that growth of the cartilage nodules may occur by a metaplastic process. All synoviocytes in PSC were positive for leucocyte common antigen, HLA‐DR, and CD68, a pattern typical of reactive rather than normal

ISSN:0022-3417    

DOI:10.1002/path.1711660310

出版商:John Wiley&Sons, Ltd.    

年代:1992

数据来源: WILEY

摘要:

AbstractLoss of cell–substratum adhesion is an important factor during tumour progression. We have previously described reduced focal contact components and poorly organized cytoskeletal actin in renal cell carcinomas. In this study, we have used the potent tumour promoter TPA on cultured human renal epithelium to mimic neoplastic transformation. The morphological changes induced by TPA were examined by phase contrast and fluorescence microscopy. TPA treatment caused rounding up of cells and loss of adhesion to either fibronectin or laminin substrata. Cytoskeletal actin was redistributed from orientated stress fibre bundles to a perinuclear circumferential arrangement. This was accompanied by a progressive reduction in the number of vinculin‐containing contacts with accumulation of vinculin in punctate spots in the perinuclear region. These altered membrane‐cytoskeletal interactions induced by TPA are entirely reversible and mimic epigenetic changes which occur during tumour progre

ISSN:0022-3417    

DOI:10.1002/path.1711660311

出版商:John Wiley&Sons, Ltd.    

年代:1992

数据来源: WILEY