Selective protection of normal proliferating cells against the toxic effects of chemotherapeutic agents.
A major problem of cancer therapy is to not kill the normal cells essential for life while killing the great majority of cancer cells. Subtle differences that arise during progression of cancer can provide novel therapies, such as targeting normal cells for protection against chemotoxicity. The increasing understanding gained by applying cellular and molecular biological techniques including expression genetics to detect molecular differences is revealing potential targets, related to cell proliferation, apoptosis, and differentiation. The quantitative differences of gene or enzyme expression between normal and tumor cells have provided the basis for drug discovery that can either reversibly target the normal cells or differentially target the tumor cells. Such differences also emphasize the need for the application of multiple drugs, with different modes of action.
Department of Experimental Radiation Oncology, Breast Cancer Research Program, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
Khandan
K
Keyomarsi
Arthur B
AB
Pardee
D000818:Animals; D000970:Antineoplastic Agents / Q000009:adverse effects / Q000037:antagonists & inhibitors* / Q000627:therapeutic use; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D019610:Cytoprotection / Q000187:drug effects / Q000502:physiology*; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects / Q000502:physiology; D006801:Humans; D009369:Neoplasms / Q000188:drug therapy* / Q000378:metabolism; D020011:Protective Agents / Q000494:pharmacology; D016159:Tumor Suppressor Protein p53 / Q000819:agonists / Q000378:metabolism
D000970:Antineoplastic Agents; D020011:Protective Agents; D016159:Tumor Suppressor Protein p53