[Resistance to target-based therapy and its circumvention].
Intrinsic and acquired resistance to molecular target therapy critically limits the outcome of cancer treatments. Target levels including quantitative and gene alteration should be determinants for the resistance. Downstream of the target molecules, drug metabolism, and drug transport influences the tumor sensitivity to molecular target therapy. The mechanisms of resistance to antibody therapy have not been fully clarified. Correlative clinical studies using these biomarkers of resistance are extremely important for circumvention of clinical resistance to target based therapy.
Nishio
Kazuto
K
Pharmacology Division, National Cancer Center Research Institute.
D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D058846:Antibodies, Monoclonal, Murine-Derived; D000970:Antineoplastic Agents / Q000627:therapeutic use; D001549:Benzamides; D000068818:Cetuximab; D016503:Drug Delivery Systems; D019008:Drug Resistance, Neoplasm; D000069347:Erlotinib Hydrochloride; D000077156:Gefitinib; D006801:Humans; D000068877:Imatinib Mesylate; D010879:Piperazines / Q000627:therapeutic use; D011743:Pyrimidines / Q000627:therapeutic use; D011799:Quinazolines / Q000627:therapeutic use; D000069283:Rituximab; D000068878:Trastuzumab
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D058846:Antibodies, Monoclonal, Murine-Derived; D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D011743:Pyrimidines; D011799:Quinazolines; D000069283:Rituximab; D000068877:Imatinib Mesylate; D000069347:Erlotinib Hydrochloride; D000068878:Trastuzumab; D000068818:Cetuximab; D000077156:Gefitinib