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. 2017 Apr;102(4):e148-e151.
doi: 10.3324/haematol.2016.158428. Epub 2017 Jan 12.

Integrative clinicopathological and molecular analyses of angioimmunoblastic T-cell lymphoma and other nodal lymphomas of follicular helper T-cell origin

Maria Pamela Dobay  1 , Francois Lemonnier  2   3 , Edoardo Missiaglia  1   4 , Christian Bastard  5 , David Vallois  4 , Jean-Philippe Jais  6 , Laurianne Scourzic  7 , Aurélie Dupuy  2   3 , Virginie Fataccioli  2   3   8 , Anais Pujals  2   3   8 , Marie Parrens  9 , Fabien Le Bras  10 , Thérèse Rousset  11 , Jean-Michel Picquenot  12 , Nadine Martin  2   3 , Corinne Haioun  2   3   10 , Richard Delarue  13 , Olivier A Bernard  7 , Mauro Delorenzi  1   14 , Laurence de Leval  15 , Philippe Gaulard  16   3   8
Affiliations

Integrative clinicopathological and molecular analyses of angioimmunoblastic T-cell lymphoma and other nodal lymphomas of follicular helper T-cell origin

Maria Pamela Dobay et al. Haematologica. 2017 Apr.
No abstract available

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Figures

Figure 1.
Figure 1.
Morphological, immunophenotypical and molecular features of AITL and other PTCL of TFH origin. (A) Heatmap representation of TFH marker expression, AITL-like features and mutation status for epigenetic modifiers and RHOA in 74 AITL and 21 other nodal lymphomas of TFH cell origin including five F-PTCL. Of note, among the 16 cases with a diffuse pattern (TFH-like PTCL), 7 comprised some FDC expansion. Cases are arranged as a function of increasing column sums of the IHC scores; details on IHC scoring are included in Online Supplementary Information. Detailed score information is in Online Supplementary Table S1. TFH marker protein and mRNA expression correlations are in Online Supplementary Table S2. The mutational status for RHOA, TET2, DNMT3A and IDH2 indicated for each case. (B) Representative example of a follicular PTCL (F-PTCL). Low-power view of the lymph node shows multiple nodules with pale centers surrounded by a rim of small, darker lymphocytes; CD21 staining underlines FDC meshworks in association with the nodules, but no extrafollicular FDC expansion; CD3 stains the cells in the center of the follicles, while CD20 is negative in the nodules and stains the cells forming the mantles. High-power view of the nodules shows pale lymphoid cells, expressing CD3, and the TFH markers BCL6 and PD1. (C-D) Representative examples of two TFH-like PTCL cases with (C) or without (D) FDC expansion. (C) At low-power, the lymph node shows diffuse architectural effacement, and extranodal infiltration without preservation of the peripheral sinus; high-power view of the lymphoproliferation shows a predominance of large transformed lymphoid cells featuring mitotic figures, and a minor reactive component of histiocytes and plasmacytoid cells. CD21 focally highlights the presence of a follicular dendritic cell meshwork in association with the neoplastic infiltrate; the large lymphoid cells are CD4+ and immunostaining confirms the abundance of the neoplastic component; many cells are CXCL13-positive; CD20 shows the presence of aggregates of small B cells and occasional larger B-cell blasts (arrow). In situ hybridization with EBER probes demonstrates Epstein-Barr virus in a small number of small lymphoid cells and occasional blastic cells. This case was also strongly positive for both PD1 and ICOS but negative for CD10 and BCL6. (D) Low-power view of the lymph node showing a diffuse lymphoma infiltrate; CD21 highlights small residual foci of follicular dendritic cells but no follicular dendritic cell expansion. High-power view of the lymphoproliferation composed of diffuse sheets of large lymphoid cells which are positive for CD3, negative for CD2, and feature a high proliferation index (Ki67). The lymphoma cells express several TFH markers including CXCL13 in scattered cells, BCL6 in most nuclei, and PD1. (E) Projection of samples on the first three component axes from principal component analysis (PCA) performed on 6000 genes with the most variable expression. Notably, with Consensus Clustering, which allows us to evaluate cluster stability based on ~1000 random subsamplings of 80% of the data, F-PTCL cases consistently clustered with AITLs. (F) Median levels of expression of the normal TFH cell signature, global AITL tumor signature and AITL microenvironment signature in AITL, other nodal PTCL of TFH origin, and PTCL-NOS. All but one (ns = not significant) of pairwise comparisons yielded statistically significant differences (P<0.01) between classes.
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