ABSTRACT
It appears almost inevitable that following identifi cation of a novel therapeutic agent, shortly thereaft er reports of resistance to the agent will appear in the literature. Among the mechanisms described to mediate drug resistance, cell adhesionmediated drug resistance (CAM-DR) has emerged as an important contributor (reviewed in Hehlgans et al. 2007). Th us, cancer cells deprived of attachment to the ECM can be sensitized to the apoptosis-inducing eff ects of chemotherapeutic agents. Conversely, integrin stimulation can cause drug resistance. Th e infl uence of integrin interaction with the ECM in promoting resistance to chemotherapeutics and radiotherapy has been documented in a broad variety of cancer types (reviewed in Hehlgans et al. 2007). Importantly, elevated levels of FAK expression and/or activity are correlated with CAM-DR, while in contrast suppression of FAK expression can sensitize cells to drug and radiotherapy treatments.
