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Blood, Vol. 95 No. 1 (January 1), 2000:
pp. 314-319
Resistance of ICAM-1-deficient mice to metastasis overcome by
increased aggressiveness of lymphoma cells
Maxime Lalancette,
Fawzi Aoudjit,
Edouard F. Potworowski, and
Yves St-Pierre
From the INRS-Institut Armand-Frappier, Université du
Québec, Québec, Canada
Our recent finding that resistance to lymphoma cell metastasis in
intercellular adhesion molecule-1-(ICAM-1)-deficient mice was
manifested after homing suggested that the mechanism could involve the
capacity of ICAM-1 to induce, via leukocyte function-associated antigen-1 (LFA-1) signaling, the expression of new genes necessary for
migration and survival of lymphoma cells after homing. This hypothesis
would imply that lymphoma cells, on repeated metastatic cycles, would
acquire such a highly aggressive phenotype that they no longer require
contact with ICAM-1 at later stages of metastasis. We addressed this
question by generating highly aggressive lymphoma variants to determine
if increased tumorigenicity would allow lymphoma cells to grow into
tumors in ICAM-1-deficient mice. We found that on repeated in vivo
passages, a selective pressure favored the lymphoma cells that
constitutively express high levels of matrix metalloproteainse-9
(MMP-9), a gene associated with a poor clinical outcome in
non-Hodgkins's lymphoma. We further found that although the parent
lymphoma cells could not grow tumors in ICAM-1-deficient mice, the
aggressive lymphoma variants could. This indicates that, at late stages
of the disease, tumor cells with a high metastatic efficiency, encoded
by the repertoire of selected genes, no longer require some of the
signals normally delivered by cell adhesion molecules. In light of
these findings, the possibility of inhibiting dissemination of lymphoma
cells at the late stage of the disease by acting against cell adhesion molecules must be reconsidered. (Blood.
2000;95:314-319)
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