Abstract
The antibody-drug conjugate T-DM1 spurs immune cells to infiltrate HER2-positive breast tumors in patients. Treating mice that carry breast tumors with T-DM1 improves survival, but the tumors suppress the infiltrating lymphocytes. Combining T-DM1 with checkpoint inhibitors that block CTLA-4 and PD-1 overcomes this effect, eliminating breast tumors from 95% of the mice.
©2015 American Association for Cancer Research.
MeSH terms
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Ado-Trastuzumab Emtansine
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Antibodies, Monoclonal, Humanized / pharmacology
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Antibodies, Monoclonal, Humanized / therapeutic use*
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use*
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Antineoplastic Combined Chemotherapy Protocols
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Breast Neoplasms / drug therapy*
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Breast Neoplasms / genetics
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Breast Neoplasms / mortality
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Cell Cycle Checkpoints / drug effects
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Cell Cycle Proteins / antagonists & inhibitors*
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Female
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Humans
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Maytansine / analogs & derivatives*
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Maytansine / pharmacology
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Maytansine / therapeutic use
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Mutation
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Neoplasm Metastasis
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Receptor, ErbB-2 / genetics
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Survival Analysis
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Trastuzumab
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Treatment Outcome
Substances
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Antibodies, Monoclonal, Humanized
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Antineoplastic Agents
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Cell Cycle Proteins
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Maytansine
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ERBB2 protein, human
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Receptor, ErbB-2
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Trastuzumab
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Ado-Trastuzumab Emtansine