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Blood, Vol. 92 No. 9 (November 1), 1998:
pp. 3018-3024
RAPID COMMUNICATION
Somatic Fas Mutations in Non-Hodgkin's Lymphoma:
Association With Extranodal Disease and Autoimmunity
Kirsten Grønbæk,
Per thor Straten,
Elisabeth Ralfkiaer,
Vibeke Ahrenkiel,
Mette Klarskov Andersen,
Niels Ebbe Hansen,
Jesper Zeuthen,
Klaus Hou-Jensen, and
Per Guldberg
From the Department of Tumor Cell Biology, Institute of Cancer
Biology, Danish Cancer Society; the Departments of Pathology and
Hematology, Herlev Hospital; and the Departments of Hematology and
Pathology, Rigshospitalet, Copenhagen, Denmark.
Fas (APO-1/CD95) is a cell-surface receptor involved in cell death
signaling. Germline mutations in the Fas gene have been associated with autoimmune lymphoproliferative syndrome, and somatic Fas mutations have been found in multiple myeloma. We have
examined the entire coding region and all splice sites of the
Fas gene in 150 cases of non-Hodgkin's lymphoma. Overall,
mutations were identified in 16 of the tumors (11%). Missense
mutations within the death domain of the receptor were associated with
retention of the wild-type allele, indicating a dominant-negative
mechanism, whereas missense mutations outside the death domain were
associated with allelic loss. Fas mutations were identified in
3 (60%) MALT-type lymphomas, 9 (21%) diffuse large B-cell lymphomas,
2 (6%) follicle center cell lymphomas, 1 (50%) anaplastic large cell
lymphoma, and 1 unusual case of B-cell chronic lymphocytic leukemia
with a marked tropism for skin. Among the 16 patients with somatic Fas mutations, 15 showed extranodal disease at presentation,
and 6 relapsed in extranodal areas. Ten of 13 evaluable patients showed features suggestive of autoreactive disease. Our data indicate that
somatic disruption of Fas may play a role in the pathogenesis of some lymphomas, and suggest a link between Fas mutation,
cancer and autoimmunity.
© 1998 by The American Society of Hematology.
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