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Bortezomib disrupts tumour–dendritic cell interactions in myeloma and lymphoma: therapeutic implications
Author(s) -
Kukreja Anjli,
Hutchinson Aisha,
Mazumder Amitabha,
Vesole David,
Angitapalli Revathi,
Jagannath Sundar,
O'Connor Owen A.,
Dhodapkar Madhav V.
Publication year - 2007
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2006.06369.x
Subject(s) - bortezomib , multiple myeloma , clonogenic assay , cancer research , proteasome inhibitor , lymphoma , myeloid , medicine , immunology , biology , apoptosis , biochemistry
Summary Recent studies have shown that the interactions between tumour and dendritic cells (DCs) promote clonogenic growth of lymphoproliferative tumours, particularly myeloma. The present study showed that the proteasome inhibitor, bortezomib, disrupts this interaction. Targeting the drug to DCs was required for optimal suppression of tumour growth, including primary myeloma tumour progenitors in clonogenic assays. Bortezomib lead to dose‐dependent induction of apoptosis in both myeloid and plasmacytoid DCs, and the sensitivity of DCs to bortezomib was comparable with that of tumour cells. These data suggest that disruption of tumour–DC interactions may contribute to the clinical effects of bortezomib.

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