SYK expression in monomorphic epitheliotropic intestinal T-cell lymphoma

Mod Pathol. 2018 Mar;31(3):505-516. doi: 10.1038/modpathol.2017.145. Epub 2017 Oct 20.

Abstract

Monomorphic epitheliotropic intestinal T-cell lymphoma (MEITL), formerly known as type II enteropathy associated T-cell lymphoma (type II EATL), is a rare, aggressive primary intestinal T-cell lymphoma with a poor prognosis and an incompletely understood pathogenesis. We collected 40 cases of MEITL and 27 cases of EATL, formerly known as type I EATL, and comparatively investigated the T-cell receptor (TCR) itself and associated signaling molecules using immunohistochemistry, amplicon deep sequencing and bisulfite pyrosequencing. The TCR showed both an αβ-T-cell origin (30%) and a γδ-T-cell derivation (55%) resulting in a predominant positive TCR phenotype in MEITL compared with the mainly silent TCR phenotype in EATL (65%). The immunohistochemical expression of the spleen tyrosine kinase (SYK) turned out to be a distinctive feature of MEITL (95%) compared with EATL (0%). Aberrant SYK overexpression in MEITL is likely caused by hypomethylation of the SYK promoter, while no common mutations in the SYK gene or in its promoter could be detected. Using amplicon deep sequencing, mutations in DNMT3A, IDH2, and TET2 were infrequent events in MEITL and EATL. Immunohistochemical expression of linker for activation of T-cells (LAT) subdivided MEITL into a LAT expressing subset (33%) and a LAT silent subset (67%) with a potentially earlier disease onset in LAT-positive MEITL.

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics*
  • Adult
  • Aged
  • Aged, 80 and over
  • Biomarkers, Tumor / genetics*
  • DNA (Cytosine-5-)-Methyltransferases / genetics
  • DNA Methyltransferase 3A
  • DNA-Binding Proteins / genetics
  • Dioxygenases
  • Enteropathy-Associated T-Cell Lymphoma / genetics*
  • Female
  • Humans
  • Immunohistochemistry / methods
  • Isocitrate Dehydrogenase / genetics
  • Male
  • Membrane Proteins / genetics*
  • Middle Aged
  • Mutation
  • Proto-Oncogene Proteins / genetics
  • Receptors, Antigen, T-Cell / metabolism*
  • Syk Kinase / genetics*
  • Syk Kinase / metabolism

Substances

  • Adaptor Proteins, Signal Transducing
  • Biomarkers, Tumor
  • DNA-Binding Proteins
  • DNMT3A protein, human
  • LAT protein, human
  • Membrane Proteins
  • Proto-Oncogene Proteins
  • Receptors, Antigen, T-Cell
  • IDH2 protein, human
  • Isocitrate Dehydrogenase
  • Dioxygenases
  • TET2 protein, human
  • DNA (Cytosine-5-)-Methyltransferases
  • DNA Methyltransferase 3A
  • SYK protein, human
  • Syk Kinase