Shyhmin Huang

TL;DR: The collective data suggest that the profound in vivo antitumor activity identified in the xenograft setting when C225 is combined with radiation derives from more than simply the antiproliferative and cell cycle effects of EGFR system inhibition.

TL;DR: The data suggest that acquired resistance to cetuximab is accompanied by dysregulation of EGFR internalization/degradation and subsequent EGFR-dependent activation of HER3, suggesting a rationale for the clinical evaluation of combinatorial anti-HER targeting approaches in tumors manifesting acquired resistance.

TL;DR: Combined treatment with distinct EGFR inhibitory agents can augment the potency of EGFR signaling inhibition and this approach suggests potential new strategies to maximize effective target inhibition, which may improve the therapeutic ratio for anti-EGFR-targeted therapies in developing clinical trials.

TL;DR: The capacity of erlotinib to enhance radiation response at several levels, including cell cycle arrest, apoptosis induction, accelerated cellular repopulation, and DNA damage repair is identified and preliminary microarray data suggests additional mechanisms underlying the complex interaction between EGFR signaling and radiation response.

TL;DR: This review focuses primarily on recent progress in the development of anti-EGFR mAbs, and examines their potential in the treatment of cancer.