Pathological and immunohistochemical study of gastrointestinal lymphomas with detection of chromosomal translocation t [11;18] by fluorescence in situ hybridization

Twenty seven cases of primary gastrointestinal non-Hodgkin's lymphoma [GI-NHL] selected from a total of 57 archived specimens with the same diagnosis during the period from January 2000 to December 2006. Of the 57 studied specimens [28/57] 49.1% had gastric lymphoma, while 29/57 [50.9%] had intestinal localization. Cases were classified histopathologically as 21 diffuse large B cell lymphoma. 15 Mucosa Associated Lymphoid Tissue [MALT], 7 diffuse large cell lymphoma with concomitant areas of MALT, 10 Burkitt's lymphoma, 2 Mantle lymphoma, 1 immunoproliferative small intestinal disease [IPSID] and 1 lymphoplasmacytic lymphoma Immunohistochemical staining using 2 monoclonal antibodies; CD20 [L-26] as B-cell marker and CD45 RO [UCHL-1] as T-cell marker whenever needed. FISH technique was used to detect chromosomal translocation t [11; 18]. FISH was done using the locus specific identifier [LSI] dual colour, dual fusion AP12/MALTI probe on 27 cases. Six of the cases [22.2%] were scored positive for translocation t [11;18] [q21;q21]. 5/6 of the positive cases were located in the stomach and only 1/6 had small intestinal location. All the six positive cases were subclassified as MALT lymphoma. The results recommended that translocation t [11;18] [q21;q21] appears to have a role in GI MALT lymphoma, but further investigations in a larger number of series are warranted to clarify this hypothesis. FISH technique can be expected to become an important simple tool for diagnosis and management of MALT lymphoma

Transforming growth factor- beta 1 in patients with angiographically proven coronary heart disease

Transforming growth factor- beta 1 [TGF- beta 1] is a multifunctional cytokine that exhibits vasculoprotective properties. Production and plasma levels of TGF- beta 1 are influenced by polymorphisms in the TGF- beta 1 gene. A T-C transition at nucleotide 29 of the TGF- beta 1 gene results in a Leu-Pro substitution at amino acid 10 of the signal peptide. We investigated whether the T29-C polymorphism of TGF- beta 1 is associated with myocardial infarction among a sample of Egyptian coronary artery diseased males. The study population consisted of 90 patients with angiographically proven myocardial infarction and 30 control individuals without signs or symptoms of myocardial infarction. Polymorphism-related genotypes were determined with allele-specific PCR [polymerase chain reaction]. In this study; we found no differences between patients with MI and healthy subjects regarding the genotype and allele frequencies of codon 10 TGF- beta 1 polymorphism. Thus, our results indicate that this polymorphism does not appear to predispose to the development of MI. There was an agreement between genotypes observed and those predicted by the Hardy-Weinberg equilibrium in the control group [Codon 10, x[2] goodness of fit was not significant = 0.777, p; 0.87]. Negative association findings in this study did not exclude that TGF- beta 1 is a susceptibility locus for myocardial infarction, but further study on a larger scale is needed

Study of the role of CD40 / CD40-L interaction in the pathogenesis of rheumatoid arthritis [RA]

CD40/CD40 ligand [CD4O/CD4O-L] interaction has pleiotropic effects in a variety of cells and biological processes including immune response. Within the immune system, these molecules represent a critical link between its humoral and cellular arms. Numerous autoimmune diseases are associated with CD40/CD40-L interaction. CD40 is a cell surface receptor that belongs to the tumor necrosis factor-receptor [TNF-R] family, and that was first identified and functionally characterized on B- lymphocytes. CD40 ligand [CD40-L] or [CD154], a member of the TNF superfamily, is a cell membrane molecule expressed on activated CD4+ T-lymphocytes. Therefore, it is now thought that CD40/CD40-L interactions play a more important role in autoimmune disease regulation. The aim of the present work was to measure the level of surface expression of CD40-L and CD40 on PB lymphocytes of rheumatoid arthritis [RA] patients and to correlate it with clinical and laboratory data and with disease activity. To achieve this goal, 30 patients with RA [Group I] who were further subdivided into group IA [15 patients with active RA] and group IB [15 patients with inactive RA], in addition to 20 healthy control volunteers [group II] were studied. All studied groups were subjected to routine laboratory investigations including, complete blood count [CBC], ESR, C-reactive protein [CRP], rheumatoid factor [RF] measured by latex test and by Rose-Waaler test. Surface CD40-L and CD40 expression on lymphocytes was measured by flowcytometry on peripheral blood [PB] of all studied groups. Statistical analysis of the results of the present study showed that surface expression of CD40-L on PB T-lymphocytes was significantly higher in RA compared to the control group. Among RA patients surface expression of CD40-L was significantly higher in active RA patients compared to inactive patients. As regards CD40 expression on PB, no statistical significance was observed among the studied groups. Therefore increased expression of CD40-L on PB T-lymphocytes could be regarded as a marker of disease activity in RA patients and to drive the activation of autoreactive beta-lymphocytes in the disease. These findings are particularly useful for clarifying the pathogenic process in RA patients and for developing a therapeutic approach that blocks pathogenic cytokine and antibody production