Format

Send to

Choose Destination
See comment in PubMed Commons below
Clin Cancer Res. 2005 Feb 15;11(4):1467-73.

Outcome in Hodgkin's lymphoma can be predicted from the presence of accompanying cytotoxic and regulatory T cells.

Author information

1
Department of Pathology, Hospital Verge de la Cinta, C/Esplanetes n degree 14, 43500-Tortosa, Spain. talvaro.htvc.ics@gencat.net

Abstract

PURPOSE:

Recent studies of Hodgkin's lymphoma (HL) have suggested that the presence of regulatory T cells in the reactive background may explain the inhibition of the antitumoral host immune response observed in these patients. This study aimed to assess the relevance of regulatory T cells and CTLs present in the background of HL samples in the prognosis of a series of classic HL (cHL) patients.

EXPERIMENTAL DESIGN:

Expression of granzyme B and TIA-1 (markers for CTL) and FOXP3 (a marker for regulatory T cells) were evaluated independently by immunohistochemistry in tissue microarrays of 257 cHL patients and correlated with patient outcome.

RESULTS:

The combined influence of the presence of FOXP3(+) and TIA-1(+) cells distinguished three risk groups of patients with 5-year overall survival of 100%, 88%, and 73%. The presence of a small number of FOXP3(+) cells and a high proportion of TIA-1(+) cells in the infiltrate represent an independent prognostic factor that negatively influenced event-free survival and disease-free survival in cHL. Compared with the features at diagnosis, relapsed samples tended to have more TIA-1(+) cells and a lower proportion of FOXP3(+) cells in the reactive background.

CONCLUSIONS:

These data suggest that low infiltration of FOXP3(+) cells in conjunction with high infiltration of TIA-1(+) cells in cHL may represent biological markers predicting an unfavorable outcome. Moreover, the variation of these markers over the course of the disease implies a possible role for them in the progression of HL cases.

PMID:
15746048
DOI:
10.1158/1078-0432.CCR-04-1869
[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Support Center