Advances in flow cytometry techniques and the availability of monoclonal antibodies

Advances in flow cytometry techniques and the availability of monoclonal antibodies that detect key functional molecules on lymphocytes have contributed greatly to a more precise diagnosis of the chronic lymphoproliferative disorders. splenic lymphoma with villous lymphocytes are cyclin D1 positive.23 This study showed a good correlation between cyclin D1 expression and RT-PCR for cyclins D1 D2 and D3 and fluorescence in situ hybridisation (FISH) for the detection of the t(11;14.)(q13;q32) translocation with 85% sensitivity and specificity. Although SLx-2119 cyclin D1 overexpression is found in most mantle cell lymphomas and rarely in other B cell diseases the specificity of cyclin D1 expression for mantle cell lymphoma whether detected by flow cytometry on cell suspensions or immunohistochemistry in tissue sections is below that for the FISH demonstration of the t(11;14) translocation.24 SLx-2119 Thus cells from a variety of non-haemopoietic neoplasms and multiple myeloma may overexpress cyclin D1 as a result of gene amplification and it has also been documented in cases of hairy cell leukaemia and more rarely in cells from other B cell disorders.25 26 Nevertheless the estimation of cyclin D1 by flow cytometry or by immunocytochemistry may be useful as a first diagnostic step in cases where mantle cell lymphoma is suspected-for example in CD5 positive B cell disorders with a phenotype not typical of CLL (score < 3) particularly when results are compounded with other laboratory features. As for immunohistochemistry when results are equivocal by flow cytometry other tests should be undertaken to exclude the diagnosis of mantle cell lymphoma. MONOCLONAL ANTIBODIES TO CD38 CD38 is a 45 kDa transmembrane molecule. The gene encoding CD38 has been assigned to chromosome 4. The monoclonal antibody that recognises this antigen was first documented in the early 1980s as a T cell differentiation antigen 27 but its function and its potential pathogenic and/or prognostic role in leukaemia did not become apparent until the past decade.28 documented a correlation between CD38 expression and cases with unmutated IgVH genes and suggested that CD38 might be a good discriminatory marker between cases with good and bad prognosis.29 In this study CLL cases with > 30% CD38 positive cells had a significantly shorter survival than those with < 30% CD38 positive cells and most of the former had unmutated IgVH.29 However the correlation between CD38 expression and mutational status of IgVH has been a matter of controversy.31 32 Although the report SLx-2119 by Damle suggested that CD38 expression correlated with cases SLx-2119 having an unmutated IgVH gene 29 more recent studies indicate that CD38 is an independent prognostic marker.33-36 The prognostic value of CD38 for shorter survival and for the need for treatment has been shown in advanced and early clinical stages of the SLx-2119 disease including Binet stage A CLL. Because of the simplicity of CD38 evaluation unlike Ig sequencing Compact disc38 is normally a marker that needs to be incorporated in to the regular panel for the analysis of CLL due to its prognostic worth. From the specialized viewpoint it’s important to measure the appearance of Compact disc38 in the leukaemic CLL lymphocytes because Compact disc38 could be portrayed in regular circulating Rabbit polyclonal to ACBD5. B and T cells. The very best approach is normally a triple system immunostaining using the next monoclonal antibodies: Compact disc38 Compact disc5 and Compact disc19.29 At the moment it appears reasonable to consider as positive an outcome where 30% or even more from the leukaemic cells stain with CD38 but further research are had a need to confirm the very best cutoff stage. MONOCLONAL ANTIBODIES TOWARDS THE P53 Proteins p53 is normally a 393 amino acidity protein encoded with the tumour suppressor gene p53 on the brief arm of chromosome 17 (17p13.1). The proteins works as a multifunctional transcription aspect and is involved with cell routine arrest differentiation DNA fix and genomic balance.37 38 Mutations and deletions from the p53 gene have already been proven to play a significant role in disease initiation and/or development in a number of individual cancers including lymphoid malignancies. p53 abnormalities have already been reported using a variable regularity in chronic lymphoproliferative disorders including CLL prolymphocytic leukaemia and B cell.