Expression of @entity13433 and XXXX in @entity978 at Initial Diagnosis May Predict Clinical Outcome.

@entity5953 @entity404 @entity5 @entity3538 @entity3138 @entity5893 @entity14546 @entity13433 @entity8395 @entity2902 @entity978 @entity4587 @entity6755 @entity1349
UNASSIGNED: Although the expression of T-cell antigens and proteins associated with @entity5 -infiltrating T-lymphocytes (TILs), regulatory T cells (T-regs), and B-cell development have been evaluated in classical @entity978 (cHL), few studies correlate these proteins' expression patterns with clinical outcome. The purpose of this study was to evaluate proteins expressed in the Reed-Sternberg cells (RSCs) and TILs of cHLs at initial diagnosis to determine their prognostic significance. The expression of 12 proteins in RSCs and TILs from 88 diagnostic cHL biopsies was quantitated and correlated to @entity1349 ( @entity1349 ) and progression-free survival (PFS). @entity3138 , CD3, @entity404 , @entity5893 , @entity4587 , @entity2902 , @entity8395 , @entity13433 , @entity14546 , and @entity6755 expression in RSCs did not correlate with @entity1349 or PFS, nor did programmed death 1 ( @entity8395 ) expression in TILs. High numbers of @entity13433 -positive TILs (>= 50%) correlated with @entity1349 (P=0.027), but not PFS (P=0.993) in univariate analysis. Expression of @entity3138 , CD3, @entity404 , @entity5893 , and/or @entity13433 (6%) in RSCs was associated with lymphocyte-rich/mixed-cellularity subtype (P=0.032). High @entity3538 ( @entity3538 ; P=0.036), and high stage (P=0.046) were independent predictors of worse PFS in univariate analysis. Low @entity3538 (P=0.003) and nodular sclerosing subtype (P=0.022) were associated with better @entity1349 in univariate analysis. Only the @entity3538 predicted @entity1349 in multivariate (P=0.009) analysis. High @entity13433 + TILs correlated with worse clinical outcomes for cHLs, as did @entity5953 -RSCs (P=0.024), although only 2/74 cases were shown to be negative for this marker, suggesting that the @entity5 microenvironment and a transcription factor crucial for B-cell development are critical biological determinants of the disease course.
