Tumor antigen-specific monoclonal antibodies and induction of T cell immunity
Identifieur interne : 004051 ( Ncbi/Curation ); précédent : 004050; suivant : 004052Tumor antigen-specific monoclonal antibodies and induction of T cell immunity
Auteurs : Sumita Trivedi [États-Unis] ; H-B Jie [États-Unis] ; Robert L. Ferris [États-Unis]Source :
- Seminars in oncology [ 0093-7754 ] ; 2014.
Descripteurs français
- KwdFr :
- MESH :
- immunologie : Anticorps monoclonaux, Antigènes néoplasiques, Lymphocytes T, Tumeurs.
- usage thérapeutique : Anticorps monoclonaux.
- Animaux, Humains, Tumeurs.
English descriptors
- KwdEn :
- MESH :
- chemical , immunology : Antibodies, Monoclonal, Antigens, Neoplasm.
- chemical , therapeutic use : Antibodies, Monoclonal.
- immunology : Neoplasms, T-Lymphocytes.
- therapy : Neoplasms.
- Animals, Humans.
Abstract
For decades the primary available cancer therapies were relatively nonspecific cytotoxic agents which, while effective in some patients, were limited by narrow therapeutic indices, extensive toxicity and development of resistance, likely due to tumor heterogeneity. Although these chemotherapies remain common tools of conventional treatment, the approval of a growing number of tumor antigen (TA) specific monoclonal antibodies (mAb) by the FDA, has driven a shift in the paradigm of cancer therapy. For a subset of patients with lymphoma, colorectal, head and neck and breast cancer, the inclusion of rituximab (anti-CD20), cetuximab (anti–human epidermal growth factor 1), and trastuzumab (anti–human epidermal growth factor2 ) has resulted in overall improved clinical response rates and survival advantages. The mechanisms which contribute to these effects are not only limited to inhibition of signaling pathways, but also by cell-mediated cytotoxicity by innate immune cells and priming of effector cells of adoptive immunity triggered by the TA-specific mAb. As the use of these therapeutic mAb has become more widespread, however, it has been observed that there is significant variability of response in patients who have received treatment with these agents. Thus, the factors which mediate this variability in clinical response of the treated patients must be elucidated, in order to optimize the use of TA-specific mAb.
Url:
DOI: 10.1053/j.seminoncol.2014.08.003
PubMed: 25440612
PubMed Central: 4254440
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PMC:4254440Le document en format XML
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<front><div type="abstract" xml:lang="en"><p id="P1">For decades the primary available cancer therapies were relatively nonspecific cytotoxic agents which, while effective in some patients, were limited by narrow therapeutic indices, extensive toxicity and development of resistance, likely due to tumor heterogeneity. Although these chemotherapies remain common tools of conventional treatment, the approval of a growing number of tumor antigen (TA) specific monoclonal antibodies (mAb) by the FDA, has driven a shift in the paradigm of cancer therapy. For a subset of patients with lymphoma, colorectal, head and neck and breast cancer, the inclusion of rituximab (anti-CD20), cetuximab (anti–human epidermal growth factor 1), and trastuzumab (anti–human epidermal growth factor2 ) has resulted in overall improved clinical response rates and survival advantages. The mechanisms which contribute to these effects are not only limited to inhibition of signaling pathways, but also by cell-mediated cytotoxicity by innate immune cells and priming of effector cells of adoptive immunity triggered by the TA-specific mAb. As the use of these therapeutic mAb has become more widespread, however, it has been observed that there is significant variability of response in patients who have received treatment with these agents. Thus, the factors which mediate this variability in clinical response of the treated patients must be elucidated, in order to optimize the use of TA-specific mAb.</p>
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