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Endogenous tumor necrosis factor as a predictor of doxorubicin sensitivity
in leukemic patients
D Kobayashi, N Watanabe, N Yamauchi, N Tsuji, T Sato and Y Niitsu
Department of Laboratory Diagnosis, Sapporo Medical University, School of
Medicine, Chuo-ku, Japan.
We have previously reported that intracellular tumor necrosis factor
(enTNF) is responsible for resistance, in established cell lines to
doxorubicin (DOX), exogenous TNF, and heat stress by inducing manganous
superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free
radicals. Leukemic cells from 19 patients (6 acute lymphoblastic leukemia,
13 acute myeloid leukemia) were examined for their sensitivity to DOX and
TNF in relation to their enTNF expression and MnSOD activity. Sensitivity
to DOX and the expression of enTNF or MnSOD activity were inversely
correlated. In a case with acquired resistance to chemotherapy which
included DOX, enTNF expression and MnSOD activity were increased.
Furthermore, in 14 cases treated with a regimen including an anthracycline,
4 cases that failed to respond to chemotherapy showed relatively high
amounts of enTNF expression. KG-1 (human acute myelogenous leukemia) cells
transfected with a nonsecretory-type TNF expression vector (pTNF delta pro)
showed resistance to DOX. A significant increase in MnSOD levels was also
noted in the transfectants. TNF antisense cDNA was transfected into
isolated leukemic cells from five patients. Sensitivity of the antisense
transfectants to DOX was increased, approximately 1.4- to 2.5- fold. These
results suggest that enTNF acts as a resistance factor against DOX in
leukemia, and that enTNF may be useful as a predictor of DOX sensitivity in
leukemia.
Volume 89,
Issue 7,
pp. 2472-2479,
04/01/1997
Copyright © 1997 by The American Society of Hematology
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