Ulteriori informazioni
The present volume reviews clinically relevant aspects of the pharmacokinetics of commonly used anticancer agents as well as mechanisms of cellular/experimental resistance to such agents. This extends to technological advances that enable high-throughput studies of genetic polymorphisms, which has opened up new avenues to the study of drug resistance and to the individualization of chemotherapy in order to decrease clinical toxicity and optimize treatment results."This text provides a comprehensive review of the mechanisms of resistance to cancer chemotherapuetic agents. Leading experts discuss molecular and biochemical pathways that influence cytotoxicity. Knowledge of these potential obstacles to therapy will allow for the development of more effective strategies to treat malignant diseases." Steven T. Rosen, M.D., Series Editor
Info autore
David J. P. Murray wurde 1953 in Dublin, Irland, geboren. Er studierte bei den Legionären Christi in Rom und begann 1977 bei der Einrichtung der Audio-Archive der Kongregation mitzuarbeiten. Seit dieser Zeit dokumentiert er die Arbeit von Pater Maciel. Der Autor von Génesis: herramientas esenciales para el educador efectivo lebt als Videoproduzent und pädagogischer Berater in Rom.
Riassunto
Over the last several decades, the introduction of new chemotherapeutic drugs and drug combinations has resulted in increased long term remission rates in several important tumor types. These include childhood leukemia, adult leukemias and lymphomas, as well as testicular and trophoblastic tumors. The addition of high-dose chemotherapy with growth factor and hemopoietic stem cell support has increased clinical remission rates even further. For the majority of patients with some of the more common malignancies, however, palliation (rather than cure) is still the most realistic goal of chemotherapy for metastatic disease. The failure of chemotherapy to cure metastatic cancer is commonly referred to among clinicians as "drug resistance". This phenomenon can, however, often be viewed as the survival of malignant cells that resulted from a failure to deliver an effective drug dose to the (cellular) target because of anyone of or combination of a multitude of individual factors. Clinically, this treatment failure is often viewed as the rapid occurrence of resistance at the single cell level. However, in experimental systems, stable drug resistance is usually relatively slow to emerge.
