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Peripheral T‐cell lymphomas ( PTCL ) are a heterogeneous group of non‐Hodgkin lymphomas with poor prognosis. Their molecular pathogenesis has not been entirely elucidated. We previously showed that 6q24 is one of the most frequently deleted regions in primary thyroid T‐cell lymphoma. In this study, we extended the analysis to other subtypes of  PTCL  and performed functional assays to identify the causative genes of  PTCL  that are located on 6q24. Genomic loss of 6q24 was observed in 14 of 232 (6%)  PTCL  cases. The genomic loss regions identified at 6q24 always involved only two known genes,   STX 11  and   UTRN  . The expression of  STX 11, but not  UTRN , was substantially lower in  PTCL  than in normal T‐cells.   STX 11  sequence analysis revealed mutations in two cases (one clinical sample and one T‐cell line). We further analyzed the function of  STX 11 in 14 cell lines belonging to different lineages.  STX 11 expression only suppressed the proliferation of T‐cell lines bearing genomic alterations at the   STX 11  locus. Interestingly, expression of a novel  STX 11 mutant (p.Arg78Cys) did not exert suppressive effects on the induced cell lines, suggesting that this mutant is a loss‐of‐function mutation. In addition,   STX 11 ‐altered  PTCL  not otherwise specified cases were characterized by the presence of hemophagocytic syndrome (67%  vs  8%,  P =  0.04). They also tended to have a poor prognosis compared with those without   STX 11  alteration. These results suggest that  STX 11 plays an important role in the pathogenesis of  PTCL  and they may contribute to the future development of new drugs for the treatment of  PTCL .

STX 11 functions as a novel tumor suppressor gene in peripheral T‐cell lymphomas