Clinical molecular pathology最新文献

{"title":"Induction of intercellular adhesion molecule 1 and class II histocompatibility antigens in colorectal tumour cells expressing activated ras oncogene.","authors":"V Stoneman,&nbsp;A Morris","doi":"10.1136/mp.48.6.m326","DOIUrl":"https://doi.org/10.1136/mp.48.6.m326","url":null,"abstract":"<p><p>Aims-To determine whether there is a correlation between activation of the ras oncogene and the induction of MHC class II antigens and intercellular adhesion molecule 1 (ICAM-1) by interferon-gamma (IFN-gamma).Methods-Expression of class II antigens, ICAM-1 and intracellular ras oncoprotein (p21) in established colorectal cell lines and short term cultures of primary colorectal tumour cells was determined by flow cytometry and mutation in the ras gene by sequencing of amplified segments of the gene.Results-The cell lines showed a variation in their modulation of MHC class II antigens and ICAM-1, ranging from no induction to a 98-fold increase in class II antigen expression in the HT29 cell line. Previous work indicated that most tumours could not be induced to express class II antigens. Four of the five least inducible lines either contained mutant ras or highly expressed the oncoprotein. The four highly inducible cell lines all contained non-mutant ras. Of the 21 tumours studied in primary culture, 10 were inducible, one of which contained mutant ras. Of the remaining non-inducible tumours, four were mutant.Conclusions-Correlations between ras activation and failure to respond to IFN-gamma could not be shown to be significant. Therefore, ras activation, and concomitant subversion of intracellular signalling pathways, is probably not the major determinant in failure to activate class II antigens and ICAM-1.</p>","PeriodicalId":87395,"journal":{"name":"Clinical molecular pathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.48.6.m326","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26020570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating IgG autoanti-IgE antibodies in atopic patients block the binding of IgE to its low affinity receptor (CD23).","authors":"S J Smith,&nbsp;N S Jones,&nbsp;F Shakib","doi":"10.1136/mp.48.6.m342","DOIUrl":"https://doi.org/10.1136/mp.48.6.m342","url":null,"abstract":"<p><p>Aims-To investigate the ability of circulating IgG autoanti-IgE antibodies from atopic rhinitis patients to block the binding of IgE to its low affinity receptor (FcepsilonRII), also termed CD23.Methods-This involved the use of a well validated flow cytometric method to detect inhibition of FITC labelled IgE binding to human B cells expressing CD23 (RPMI 8866 cell line).Results-Taking inhibition values greater than 20% as being significant, 15 out of 20 IgG anti-IgE containing sera inhibited the binding of IgE-FITC to the RPMI 8866 cells. The inhibitory effect was recoverable in the IgG fraction of serum, but was not related to the titre of either IgG1 anti-IgE or IgG4 anti-IgE, thus suggesting that it might be related to epitope specificity. No such inhibition was demonstrable with rheumatoid sera containing autoanti-IgG (that is, rheumatoid factor), but lacking autoanti-IgE.Conclusions-The capacity of anti-IgE to block the binding of IgE to CD23 has important implications, particularly in terms of upregulation of IgE synthesis and the consequent perpetuation of the inflammatory response.</p>","PeriodicalId":87395,"journal":{"name":"Clinical molecular pathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.48.6.m342","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26018982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enumeration of semen leucocytes by fluorescence in situ hybridisation technique.","authors":"R A Conte,&nbsp;S Luke,&nbsp;R S Verma","doi":"10.1136/mp.48.6.m319","DOIUrl":"https://doi.org/10.1136/mp.48.6.m319","url":null,"abstract":"<p><p>Aim-To determine whether the fluorescent in situ hybridisation technique (FISH) using a total human DNA genomic probe can be used to enumerate semen leucocytes.Methods-Semen samples from five donors were subjected to a mild KC1 solution. These samples were then biotin labelled under FISH conditions using a total human DNA genomic probe and the leucocyte counts were determined. To check the accuracy of the technique a monoclonal antibody against the common leucocyte antigen CD45 [KC56(T-200)] served as a control. An isotypic control for [KC56(T-200)], the immunoglobulin [MsIgG1], served as a secondary control.Results-Semen leucocytes stained by the FISH technique were easily detected because of their distinct bright yellow colour, while the sperm cells were red. The leucocyte count ranged from 0.5 to 4.9 x 10(6) per ml of semen. KC56(T-200) and its isotypic control MsIgG1, which served as control for the FISH technique, accurately identified 94% and 97% of the semen leucocytes of a control donor, respectively.Conclusions-The FISH technique using a total human DNA probe can accurately and effectively enumerate the overall leucocyte population in semen.</p>","PeriodicalId":87395,"journal":{"name":"Clinical molecular pathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.48.6.m319","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26020568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apoptosis in Immunology","authors":"A. Morris","doi":"10.1136/mp.48.6.M351-a","DOIUrl":"https://doi.org/10.1136/mp.48.6.M351-a","url":null,"abstract":"Apoptosis is now recognised as the mechanism by which unwanted cells are tidily eliminated with no messy consequences such as inflammation. This is nowhere more important than in the immune system which is typified by the overproduction of all sorts of cells-particularly self-reactive lymphocytes-which would be a severe embarrassment to the organism if not removed. Autoimmunity and cancer are the consequences of not having enough apoptosis. Apoptotic mechanisms also play a role in killing of target cells by immune effector cells, as for example cytotoxic T cells. A volume dealing with apoptosis and immunity is therefore opportune. This book is a compilation of invited papers by eminent authors who have written ably on the nature of apoptosis in immunology. More accurately, apoptosis in lymphocytes as there is in fact little about the many interesting non-lymphocytic cells of the immune system, or other related haematopoietic cells. There is, in addition, some chapters on apoptosis in AIDS and so we see that this book is somewhat of a pot pourri of topics, all interesting, but neither providing nor presumably aiming to provide a comprehensive coverage. I do not see, for example, substantial sections on apoptosis in cytotoxic cell killing nor is material gathered together on apoptosis induced via the Fas/tumour necrosis factor receptor mediated pathways, although there are many scattered references to these. The value of such a book as this is rather that you might hope to find some interesting information that would otherwise have eluded you, and in this I for one was not disappointed. For example, I found there is evidence for proteases and the ubiquitin pathway in apoptosis, and I learned that p53 is not necessary for apoptosis induced by antiCD4 in peripheral T cells. There is of course much solid worth here and some good writing. I particularly valued the chapter by Boise et al with its succinct description of Bcl-2like proteins; that by Harrison et al, introducing the concept of the undead cell; and the good account given by Kabelitz et al of This book has 11 chapters, which might be apoptosis induced via the TCR. viewed as representing three main sections. On the whole, all the main points about Firstly, the principles of PCR; chapter 1 deals the stimuli and pathways of apoptosis, at least with how the method works and gives an in lymphoid cells, are covered in this book, overview of its applications, with chapter 2 and certainly for an immunologist it is a useful describing quantitative PCR. The second source book. However, this book has the 'section', encompassing applications in faults of its sort, repetition, as each author microbiology, is covered by chapters 3 to 6. introduces the topic afresh, and yet paraThe remaining chapters deal with apdoxically the lack of background material to plications of PCR in the fields of inherited put into context the specialist contributions. diseases and cancer. Clearly, it is aimed at a scientist who ","PeriodicalId":87395,"journal":{"name":"Clinical molecular pathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.48.6.M351-a","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64426783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Detection of c-Ki-ras mutations in bile samples from patients with pancreatic and biliary cancers.","authors":"S O'mahony,&nbsp;M Longfellow,&nbsp;M J McMahon,&nbsp;A T Axon,&nbsp;P Quirke","doi":"10.1136/mp.48.6.m316","DOIUrl":"https://doi.org/10.1136/mp.48.6.m316","url":null,"abstract":"<p><p>Aim-To determine whether c-Ki-ras mutations can be detected in bile from patients with biliary strictures caused by pancreatic cancer and other biliary tumours, with a view to developing bile c-Ki-ras mutations as a non-invasive diagnostic marker of pancreatic cancer.Methods-Bile was collected from 89 subjects (47 controls (including patients with bile duct stones or benign stricture), 20 patients with pancreatic cancer, 11 with cholangiocarcinoma, five with ampullary cancer, and six with metastatic biliary obstruction) referred for endoscopic retrograde cholangiopancreatography. DNA was extracted from bile and c-Ki-ras codon 12 mutations were detected using PCR and a restriction enzyme digestion method.Results-c-Ki-ras mutations were detected in 10 (50%) of 20 patients with pancreatic cancer, in one (9%) of 11 with cholangiocarcinoma, and in two (33%) of six patients with metastatic biliary obstruction (primary tumours: colon and prostate). C-Ki-ras mutations were not detected in the controls and patients with ampullary cancer.Conclusions-The sensitivity of this test is too low at 50% to recommend its use clinically, but with refinement has potential as a diagnostic marker for pancreatic cancer.</p>","PeriodicalId":87395,"journal":{"name":"Clinical molecular pathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.48.6.m316","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26020567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PCR Applications in Pathology. Principles and Practice","authors":"D. Burnett","doi":"10.1136/mp.48.6.M351-b","DOIUrl":"https://doi.org/10.1136/mp.48.6.M351-b","url":null,"abstract":"","PeriodicalId":87395,"journal":{"name":"Clinical molecular pathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1995-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.48.6.M351-b","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64426788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological indices in the assessment of breast cancer.","authors":"A S Leong,&nbsp;A K Lee","doi":"10.1136/mp.48.5.m221","DOIUrl":"https://doi.org/10.1136/mp.48.5.m221","url":null,"abstract":"","PeriodicalId":87395,"journal":{"name":"Clinical molecular pathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1995-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.48.5.m221","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26020843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AgNOR measurements as indices of proliferation, ploidy and prognosis.","authors":"J C Underwood","doi":"10.1136/mp.48.5.m239","DOIUrl":"https://doi.org/10.1136/mp.48.5.m239","url":null,"abstract":"","PeriodicalId":87395,"journal":{"name":"Clinical molecular pathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1995-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.48.5.m239","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26022020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of a thrombin receptor with factor Xa receptor and tissue factor in human pancreatic carcinoma cells.","authors":"A K Kakkar,&nbsp;N R Lemoine,&nbsp;S R Stone,&nbsp;D Altieri,&nbsp;R C Williamson","doi":"10.1136/mp.48.5.m288","DOIUrl":"https://doi.org/10.1136/mp.48.5.m288","url":null,"abstract":"<p><p>Venous thromboembolism is a common feature of pancreatic cancer. The underlying mechanism is unclear, but is likely to involve thrombin generation on the cell surface. Human pancreatic carcinoma cell lines (n=8) have been studied immmunohistochemically for the expression of tissue factor, factor Xa receptor, and thrombin receptor. Each antigen had a distinct pattern of immunoreactivity in cell membrane and cytoplasm. Tissue factor was predominantly localised to the membrane, whereas thrombin and factor Xa receptor were largely cytoplasmic in distribution. The results support the hypothesis of a coagulation cascade that starts with tissue factor, leads to thrombin generation, and might confer a biological advantage on tumour cells.</p>","PeriodicalId":87395,"journal":{"name":"Clinical molecular pathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1995-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.48.5.m288","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26020561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interphase ribosomal RNA cistron staining in chronic myeloid leukaemia.","authors":"N N Mamaev,&nbsp;G N Salogub,&nbsp;A V Koloskov","doi":"10.1136/mp.48.5.m260","DOIUrl":"https://doi.org/10.1136/mp.48.5.m260","url":null,"abstract":"<p><p>Aim-To evaluate the haemopoietic function of bone marrow blood forming cells in human chronic myeloid leukaemia (CML) by means of silver staining of nucleolar organiser region (AgNOR).Methods-Nucleoli were investigated in bone marrow blast cells and in erythroid, granulocytic, and megakaryocytic cells from 10 haematologically healthy subjects and from 26 patients with chronic myeloid leukemia (17 in benign phase, nine with blast crisis). The investigation was done before treatment, by means of a one step silver staining method. In every case 50 to 100 blasts, promyelocytes, myelocytes, immature (pronormoblastic and basophilic normoblastic) and mature (polychromatic normoblastic) erythroid elements, and megakaryocytes were evaluated for the mean numbers of nucleoli and for the average number of AgNORs per nucleus. Student's t test was used to compare the patient and control groups. Other statistical analyses were carried out by means of the computer assisted \"HEMA\" system.Results-Compared with controls, activation of NORs was noticed only in CML blasts, while there was a decrease in NORs in the erythroid elements, promyelocytes, and megakaryocytes. The AgNOR score of polychromatic normoblasts and megakaryocytes started to decrease in the benign stage of CML, whereas a similar decrease in pronormoblasts, basophilic normoblasts, and promyelocytes was detected only in patients with CML blast crisis.Conclusions-The loss of AgNOR sites in cell series in CML may be related to intrinsic defects in their proliferation.</p>","PeriodicalId":87395,"journal":{"name":"Clinical molecular pathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1995-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.48.5.m260","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26020844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}