RESUMO
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
Assuntos
Biomarcadores TumoraisRESUMO
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.]
Assuntos
Animais de Laboratório , Cinética , Proteínas do Ovo , Ensaio de Imunoadsorção Enzimática , Sorologia , Camundongos , Antígenos de Helmintos , Anticorpos MonoclonaisRESUMO
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