Thursday, February 20, 2014
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Bone marrow niche-sensitizing
chemotherapy to enhance antibody-based acute lymphoblastic leukemia (ALL)
Mouse and human sample
studies suggest targeting tumor type-specific factors that suppress antitumor
immunity could help eliminate residual ALL. In a humanized mouse model of ALL
treated with Campath alemtuzumab,
shRNA screening of residual leukemia cells identified secreted factors that
suppressed antitumor macrophage activity in the bone marrow. In the same
mice, Campath plus low doses of cyclophosphamide led to a synergistic,
near-complete elimination of tumor cells in the bone marrow caused by
cyclophosphamide-dependent blockade of a tumor cell secretory program that
suppressed bone marrow-resident macrophages. Next steps include testing
low-dose cyclophosphamide inhibition with therapeutic antibodies as treatment
for refractory B cell malignancies and investigating specific tumor-secreted,
Campath, an anti-CD52 antibody, is marketed
by Sanofi to treat chronic lymphocytic
leukemia (CLL) and multiple sclerosis (MS).
Cyclophosphamide is a generic chemotherapeutic used to treat cancers
including lymphoma and leukemia.
Published online Feb. 20, 2014
Patents filed covering the
humanized ALL model and treatment with low-dose cyclophosphamide as an
antibody-sensitizing agent; available for licensing
Pallasch, D.P. et al.
Cell; published online Jan. 30, 2014;
Contact: Michael T. Hemann, Massachusetts Institute of
Technology, Cambridge, Mass.
Contact: Jianzhu Chen, same affiliation as above
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