期刊
CANCER CELL
卷 10, 期 4, 页码 295-307出版社
CELL PRESS
DOI: 10.1016/j.ccr.2006.08.025
关键词
-
资金
- NCI NIH HHS [R01 CA96569, R01 CA103978, P01 CA55819] Funding Source: Medline
We discovered that monoclonal antibodies (mAbs) specific to human beta(2)-microglobulin (beta M-2) induce apoptosis in vitro and were therapeutic in mouse models of myeloma and other hematological tumor cells. Cell death occurred rapidly, without the need for exogenous immunological effector mechanisms. The mAbs induced cell death via recruiting MHC class I molecules to lipid rafts and activating Lyn and PLC gamma 2, leading to activated JNK and inhibited PI3K/Akt and ERK, compromised mitochondrial integrity, and caspase-9-dependent cascade activation. Although the expression of beta M-2 on normal hematopoietic cells is a potential safety concern, the mAbs were selective to tumor-transformed cells and did not induce apoptosis of normal cells. Therefore, such mAbs offer the potential for a therapeutic approach to hematological malignancies.
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