Significance of P21 and C-mye expression in urinary bladder lesions

Immunohistochemical tissue expression of the anti- proliferative marker P21 and the oncogenic marker C-myc were estimated in 40 cases with non-neoplastic and neoplastic urinary bladder lesions with or without schistosomal infection to assess the significance of their expression as a diagnostic tool in patients with higher risk of developing cancer bladder. P21 expression was detected in 50% of simple cystitis cases and all cases with premalignant changes were positive for P21 immunoreactivity expressed into about 16% of urothelial cells. Eighty-five% of malignant cases expressed P21 in 48-55% of urothelial cells without significant variance between different histologic tumor types. Extent of P21 expression inversely correlated with bilharzial association, upgrading of malignancy and tumor invasiveness. C-myc was detected in 80% of simple chronic cystitis cases [75% cytoplasmic, 25% cytoplasmic and nuclear expression] and in all cystitis cases with premalignant changes [as cytoplasmic and nuclear expression]. Eighty-nine% of cancer cases were C-myc positive with predominance of nuclear expression to be seen in 16.74 and mixed with cytoplasmic expression in another 58.3% of positive cases. Malignancy upgrading and invasiveness raised C-myc positivity. It was concluded that P21 expression increases in an attempt to check cellular proliferation, while the increase in the oncogen C-myc goes ahead. Loss of P21 and increased C-myc expression in a malignant lesion is a predictor of malignancy progress to higher grade or stage

Study of kinetics of circulating schistosome antigens in tissues and sera of infected mice using anti-schistosoma mansoni soluble egg antigen monoclonal antibody

In the present study, the kinetics of uptake and deposition of Schistosoma mansoni antigens in liver, spleen, kidney and intestine of C57BL/6 mice infected with 100 Schistosoma mansoni cercariae as well as their levels in sera have been investigated during the course of infection [12 weeks]. The presence of antigen was demonstrated by indirect immunofluorescence using IgM anti-soluble egg antigen monoclonal antibody [anti-SEA MAb]. Immunofluorescence reactivity was evident in both renal and spleen tissues 3 weeks post-infection [p.i.], in Kupffer cells of liver 4 weeks p.i. and in intestinal mucosa [5 weeks p.i.]. Maximal immunofluorescence staining was reached during the patent phase [5-9 weeks p.i.]. During the chronic stage of infection [9-12 weeks pi.], diminution of immunofluorescent intensity was evident in liver tissue, while it remained constant in other studied organs. Circulating schistosome antigen [CSA] level in mice sera was determined using a sandwich ELISA with a MAb for both antigen capture and detecting antibody. CSA was demonstrated in mice sera [one week p.i.] reaching its peak at 6 weeks p.i. and remained at a detectable level until the end of the study [12th week p.i.]

Splenic cytokine mRNA expression in mice intravenously injected ith schistosoma mansoni 26-kDa glutathione S-transferase or soluble egg antigen before infection with schistosoma mansoni cercariae

This work was designed to assess the changes in hepatic granuloma formation associated with hyporesponsiveness to schistosomal egg antigen [SEA] or S.mansoni-26GST[Sm-26GST]. Multiple small doses of SEA [10 micro g x 4] or Sm-26GST [I micro g x 4] were injected intravenously [i.v.] into C57B1/6 mice 7 days prior to cercarial exposure. Mice were sacrificed 6 and 8 weeks post-infection, hepatic granuloma diameter was evaluated and mRNA expression of splenic cytokines IFN- alpha, IL-2, IL-4, IL-10 and IL-12 was estimated using the semiquantitative reverse transcription-polymerase chain reaction [RT-PCR]. Compared to infected controls, both SEA and Sm-26GST-treated groups showed significant decrease in hepatic granuloma diameter 8 wks post infection [p.i.] associated with lowered level of IFN- alpha and IL-4 mRNA; while the levels of both IL-10 and IL-12 were higher than that of infected controls. The present data show that Sm-26GST has an antipathology effect similar to SEA if it is used by i.v. route. The predominant cytokine involved in this hyporesponsiveness is IL- 10 and to a lesser extent IL- 12