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Blockade of CD82 by a monoclonal antibody potentiates anti-leukemia effects of AraC in vivo.

ABSTRACT: We recently found that CD82 inhibits matrix metalloproteinase 9 and augments adhesion of CD34(+) /CD38(-) acute myelogenous leukemia (AML) cells to the bone marrow (BM) microenvironment. The present study found that the use of an anti-CD82 monoclonal antibody (CD82 mAb) mobilized CD34(+) leukemia cells from BM into the peripheral blood in a humanized AML murine model. The use of CD82 mAb in combination with cytarabine (AraC) significantly prolonged survival of immunodeficient mice-bearing human AML cells than did treatment with either AraC or CD82 mAb alone. Taken together, the combination of an anti-leukemic agent and the mobilizing agent CD82 mAb may be a promising treatment strategy to treat patients with AML.

SUBMITTER: Nishioka C

PROVIDER: S-EPMC4567027 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature

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Blockade of CD82 by a monoclonal antibody potentiates anti-leukemia effects of AraC in vivo.

Nishioka Chie C Ikezoe Takayuki T Yokoyama Akihito A

Cancer medicine 20150703 9

We recently found that CD82 inhibits matrix metalloproteinase 9 and augments adhesion of CD34(+) /CD38(-) acute myelogenous leukemia (AML) cells to the bone marrow (BM) microenvironment. The present study found that the use of an anti-CD82 monoclonal antibody (CD82 mAb) mobilized CD34(+) leukemia cells from BM into the peripheral blood in a humanized AML murine model. The use of CD82 mAb in combination with cytarabine (AraC) significantly prolonged survival of immunodeficient mice-bearing human ...[more]

PMID: 26139471

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