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Cancer Cell. 2011 Dec 13;20(6):728-40. doi: 10.1016/j.ccr.2011.11.006. Epub 2011 Dec 1.

Combined genetic inactivation of β2-Microglobulin and CD58 reveals frequent escape from immune recognition in diffuse large B cell lymphoma.

Author information

1
Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA.

Abstract

We report that diffuse large B cell lymphoma (DLBCL) commonly fails to express cell-surface molecules necessary for the recognition of tumor cells by immune-effector cells. In 29% of cases, mutations and deletions inactivate the β2-Microglobulin gene, thus preventing the cell-surface expression of the HLA class-I (HLA-I) complex that is necessary for recognition by CD8(+) cytotoxic T cells. In 21% of cases, analogous lesions involve the CD58 gene, which encodes a molecule involved in T and natural killer cell-mediated responses. In addition to gene inactivation, alternative mechanisms lead to aberrant expression of HLA-I and CD58 in >60% of DLBCL. These two events are significantly associated in this disease, suggesting that they are coselected during lymphomagenesis for their combined role in escape from immune-surveillance.

PMID:
22137796
PMCID:
PMC3660995
DOI:
10.1016/j.ccr.2011.11.006
[Indexed for MEDLINE]
Free PMC Article

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