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Mutational Analysis Reinforces the Diagnosis of Nodal Marginal Zone Lymphoma With Robust PD1-positive T-Cell Hyperplasia.

To the Editor: We found the recent article by Egan et al1 titled “Expansion of PD1-positive T cells in nodal marginal zone lymphoma: a potential diagnostic pitfall” of significant interest. The authors describe a series of cases of marginal zone lymphoma (MZL) in which an atypical infiltrate of T-follicular helper cells initially prompted suspicion for a diagnosis of peripheral T-cell lymphoma. Three general patterns of programmed cell death protein 1 (PD1)– positive T-cell growth were enumerated, highlighting diversity in these MZLassociated T-cell infiltrates and exemplifying the potential to misdiagnose these cases as peripheral T-cell lymphoma. We have similarly reviewed several comparable cases of MZL with robust PD1-positive T-cell hyperplasia at our institution. In each, the diagnostic biopsy was preceded by at least 1 prior inconclusive specimen, illustrating the elusive nature of many MZLs. In fact, a diagnosis of follicular T-cell lymphoma or angioimmunoblastic T-cell lymphoma was either made or seriously considered in 2 of these cases. A summary of histologic and immunophenotypic findings, immunoglobulin heavy chain and T-cell receptor rearrangement studies, and high-throughput sequencing results for each case is represented in Table 1 and Figure 1. In addition to the immunophenwotypic and antigen receptor gene rearrangement studies evaluated likewise by Egan et al,1 targeted mutational analyses were performed in our cases and were found to be particularly informative. Genetic analyses of 2 cases detected mutational variants in NOTCH2 and KLF2 that are among the most frequently mutated genes in MZL, particularly in splenic MZL, but also in nodal and extranodal MZL.2–7 Truncating mutations in exon 34 involving the transactivation domain of NOTCH2, as seen in both cases, appear to be enriched in MZL compared with other indolent B-cell lymphomas.4 Similarly, KLF2 mutations have been reported in up to 44% of MZLs, but are infrequent in T-cell lymphomas or non-MZL B-cell lymphomas.6 Frameshift mutations in TNFAIP3, inactivating TP53 mutations, and EZH2 aberrations were detected in the third case; these variants have been demonstrated to be enriched in MZLs compared with other small B-cell lymphoma entities.2,3,6 All 3 cases lacked recurrent genetic aberrations described