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Mutation of CD95 (Fas/Apo-1) Gene in Adult T-Cell Leukemia Cells
Sadahiro Tamiya,
Ken-ichiro Etoh,
Hitoshi Suzushima,
Kiyoshi Takatsuki, and
Masao Matsuoka
From The Second Department of Internal Medicine, Kumamoto University
School of Medicine, Kumamoto, Japan; and the Kitano Hospital, Osaka,
Japan.
CD95 antigen (also known as Fas or Apo-1) and Fas ligand play key
roles in apoptosis of cells of the immune system, function as effector
molecules of cytotoxic T lymphocytes, and function in the elimination
of activated lymphocytes during the downregulation of the immune
response. The critical roles of the Fas-Fas ligand system in apoptosis
suggest that its inactivation may be involved in malignant
transformation. We analyzed the expression of Fas antigen on adult
T-cell leukemia (ATL) cells by flow cytometry and found that Fas
antigen expression was absent in a case of ATL and markedly decreased
in another case among 47 cases examined. Apoptosis could not be induced
in the Fas-negative ATL cells by antibody against Fas antigen.
Sequencing of reverse transcription-polymerase chain reaction products
of the Fas genes in the Fas negative cells showed two types of aberrant
transcripts: one had a 5-bp deletion and a 1-bp insertion in exon 2, and the other transcript lacked exon 4. These mutations caused the
premature termination of both alleles, resulting in the loss of
expression of surface Fas antigen. These aberrant transcripts were not
detected in a nonleukemic B-cell line from the same patient. An RNase
protection assay of the Fas gene showed mutations in 2 additional cases
with Fas-positive ATL cells of 35 cases examined: 1 case lacked exon 4 and the other was a silent mutation. In the Fas antigen-negative case,
leukemic cells were resistant to anticancer drugs in vivo, indicating
that the loss of expression of Fas antigen may be associated with a poor response to anticancer drugs. Indeed, Fas-negative ATL cells were
resistant to adriamycin-induced apoptosis in vitro, which is consistent
with the finding that ATL in this case was resistant to chemotherapy.
These findings indicate that mutation of the Fas gene may be associated
with the progression of ATL and with resistance to anticancer drugs.
Blood, Vol. 91 No. 10 (May 15), 1998:
pp. 3935-3942
© 1998 by The American Society of Hematology.
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