Cancer cells may acquire the capacity for autonomous and dysregulatedproliferation through the uncontrolled production of specificmolecules that promote cell growth (growth factors) or throughabnormal, enhanced expression of specific proteins (growth factorreceptors) on the cell membranes to which growth factors selectivelybind. Both processes trigger a series of intracellular signalsthat ultimately lead to the proliferation of cancer cells, inductionof angiogenesis, and metastasis.1 The majority of human epithelialcancers are marked by functional activation of growth factorsand receptors of the epidermal growth factor receptor (EGFR)family. Given this phenomenon, EGFR was the first growth factor. . . [Full Text of this Article]
EGFR in Human Carcinogenesis
Development of EGFR Antagonists for Anticancer Therapy
Clinical Efficacy of EGFR Antagonists in Human Cancers
Non–Small-Cell Lung Cancer
Colorectal Cancer
Squamous-Cell Carcinoma of the Head and Neck
Pancreatic Cancer
Predicting the Response to Anti-EGFR Drugs
Clinical and Pathological Predictors
EGFR Protein Expression
Somatic EGFR Gene Mutations
Increased EGFR Copy Number
Resistance to EGFR Antagonists
Intrinsic Resistance
Acquired Resistance
Future Directions
Source Information
From the Division of Medical Oncology, Department of Experimental and Clinical Medicine and Surgery F. Magrassi and A. Lanzara, Second University of Naples (F.C.); and the Division of Medical Oncology, Department of Molecular and Clinical Endocrinology and Oncology, University of Naples Federico II (G.T.) — both in Naples, Italy.
Address reprint requests to Dr. Ciardiello at the Division of Medical Oncology, Department of Experimental and Clinical Medicine and Surgery F. Magrassi and A. Lanzara, Second University of Naples, Via S. Pansini 5, 80131 Naples, Italy, or at fortunato.ciardiello@unina2.it.
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