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Blood, Vol. 96 No. 1 (July 1), 2000:
pp. 282-287
Endostatin, an antiangiogenic drug, induces tumor stabilization
after chemotherapy or anti-CD20 therapy in a NOD/SCID mouse model
of human high-grade non-Hodgkin lymphoma
Francesco Bertolini,
Lisa Fusetti,
Patrizia Mancuso,
Alberto Gobbi,
Chiara Corsini,
Pier
Francesco Ferrucci,
Giovanni Martinelli, and
Giancarlo Pruneri
From the Divisions of Hematology-Oncology, Experimental Oncology,
and Pathology-Laboratory Medicine, IRCCS European Institute of
Oncology, Milan, Italy.
Both chemotherapy and chimeric anti-CD20 monoclonal antibodies are
effective agents against B-cell non-Hodgkin lymphoma (NHL). However,
patients achieving remission are at risk of relapse. To evaluate the
effect of the antiangiogenic drug endostatin used alone and after the
administration of cyclophosphamide (CTX) or the anti-CD20 antibody
rituximab, we generated a new model of human NHL by transplanting
Namalwa cells intraperitoneally into nonobese diabetic/severe combined
immunodeficient (NOD/SCID) mice. First, we determined the most
effective treatment schedule for the drugs assessed. When administered
alone, CTX (3 courses of 75 mg/kg of body weight given
intraperitoneally), rituximab (3 courses of 25 mg/kg given
intraperitoneally), and endostatin (5 courses of 50 µg given
subcutaneously) delayed tumor growth, and CTX was the most effective in
controlling bulky disease. When given after chemotherapy or
immunotherapy, endostatin effectively induced tumor stabilization. When
mice given CTX or rituximab on days 3, 5, and 7 after transplantation
were randomly assigned to receive endostatin or phosphate-buffered
saline on days 15 to 19, tumor growth was prevented in
endostatin-treated mice as long as the drug was administered.
Furthermore, administration of endostatin on days 25 to 29 after tumor
regrowth still induced significant tumor regression, whereas CTX and
rituximab were not effective. The specific antiangiogenic action of
endostatin was confirmed by in vitro and in vivo studies indicating
that the drug inhibited proliferation and induced apoptosis of
endothelial (but not of NHL) cells. In conclusion, sequential
administration of chemotherapy and endostatin seems promising for
treating bulky NHL, and the less toxic sequential administration of
rituximab and endostatin is promising for treating limited disease.
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