DLBCL with CD30+ Has Not a Better Prognosis in a Brazilian Coorte Population

Background: CD30 is a well-known diagnostic marker in both anaplastic large cell lymphoma (ALCL) and classical Hodgkin's lymphoma (CHL). The chimeric drug brentuximab vedotin that combines an anti-CD30 monoclonal antibody with the anti-tubulin agent monomethyl auristatin E demonstrated activity in patients with relapsed CHL, ALCL and other lymphomas that express CD30+. Previous observational studies have suggested that CD30 may be expressed in 10 to 20% of DLBCLs. It is possible that CD30+ DLBCLs may show different biologic behavior and be amenable to anti-CD30 therapy. The aim of this study was to determine the prevalence of CD30 expression in DLBCL by immunohistochemistry and explore possible relationships with important clinical and biologic variables of DLBCL.

Methods: We retrospectively identified cases of DLBCL diagnosed between Jan 2007 and march 2014 at our institution. Eligible cases included patients with diagnosis of DLBCL irrespective of anatomic site or tumor stage. The diagnosis of DLBCL was based on the current WHO 2008 criteria. The following large B cell lymphoma subtypes were excluded from this analysis: post-transplant lymphoproliferative disorders with DLBCL morphology, Primary Mediastinal large cell lymphoma and the unclassifiable lymphomas with features intermediate between either DLBCL and Burkitt's lymphoma or between DLBCL and Hodgkin's lymphoma. Immunohistochemistry was performed with TMA (tissue microarray) in all the cases. We use a cut-off of 0%, 5% (expression between 0 and 10%), 10% and 20%. DLBCLs were classified into germinal center (GC) or non-GC subtypes applying the Hans algorithm. Logistic regression analysis was performed to assess association between selected variables and CD30 expression.

Results: A total of 197 cases of DLBCL were eligible for this study and of these 152 cases (77.1%) had paraffin material available to analyse CD30. Clinical and laboratory characteristics of all coorte are shown bellow(table 1). Fifty one patients (33,5%) were positive for CD30, using cut-off>0% and 16 pacients (10,5%) were positives with a cut off ≥ 20%. Nine patients (5,9%) were EBV positives and excluded from the survival analyses. With a follow-up of 34,3 months, according disease free survival, with a cutt off CD30>0%, that was no difference between the groups (71,3% versus 71% p 0,974). According cell origen, no difference was found in the subgroup GC (75% versus 72% p 0,726) nor APC (68,8% versus 64,4% p 0,397).

Usingcut off CD30 ≥ 20% that was also no difference in DFS between groups (75% versus 70,5% p 0,945). Also ocurred when we analysed cell origen, GC with or without CD30 (75% versus 72,7% p 0,519) and for patients ABC with or without CD30 (75% versus 64,2% p 0,524) .

Acoording overall survival, using cutt-off CD30% >0% there was no difference between the groups (86,9% versus 78,2% p 0,257). GC cell origen patients with CD30+ did not have better outcomes than patients CD30- (81,3% versus 77,1% p 0,792). For patients with ABC tumor, there was a slightly better survival for patients with CD30+ (92,3% versus 74,9% p 0,059).

Using cut off CD30 ≥ 20% same results were found according CD30 expression. No difference in overall survival (87,1% versus 80,3% p 0,908). Even versus 78,7% p 0,292) nor ABC (90,9% versus 79,8% p 0,384).

Conclusion: In this present study, DLBCL with CD30+, using cut-off of 0% or 20% did not shown any difference in DFS or overall survival.