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found a plateau formation in FL3A after six years without late progression-free survival events, in contrast to FL1/2.3 This observation may well relate to the fact that the pres- ent study found GEPs to be distinct between FL1/2 and FL3A, and supports a hypothesis of a differential molecu- lar background that might influence the clinical outcome of patients with FL.
Furthermore, recent clinical data showed that patients with DLBCL/FL3B had clinical features comparable to either FL or DLBCL,28 a notion supported by the GEP find- ings of the present study, pointing to the fact that DLBCL/FL3B may represent a composite form of FL3B and DLBCL with similar gene expression patterns.
Since standardized treatment decisions and distinct therapy strategies for patients with FL still have to be defined, the translation of histological grading into differ-
ent treatment modalities for the moment remains unclear. However, it had previously been postulated that an indi- vidualized approach might be warranted in FL treatment since specific molecular signatures have been shown to reflect a clinical aggressiveness of FL that is independent of histological grade.29
Acknowledgments
We gratefully acknowledge Petra Hitschke, Katja Bräutigam, Daniela Pumm and Thomas Hees for excellent technical assis- tance.
Funding
This study was supported by the Deutsche Krebshilfe and the Robert Bosch Stiftung, Germany. The authors declare no compet- ing interests.
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