EGFR mutations in esophageal carcinoma are rare but do exist, and thus gefitinib could be included in esophageal cancer treatment regimens by selecting those patients who possess such mutations.
EGFR mutations in esophageal carcinoma are rare but do exist, and thus gefitinib could be included in esophageal cancer treatment regimens by selecting those patients who possess such mutations.
Influence of apoptosis (BCL2, FAS), cell cycle (CCND1) and growth factor (EGF, EGFR) genetic polymorphisms on survival outcome: an exploratory study in squamous cell esophageal cancer.
The selection of esophageal cancer patients for future studies with EGFR-TKIs based on the level of EGFR expression in their tumors or SCC histology should be considered.
While more primary esophageal tumors remain to be screened for the mutations at the tyrosine kinase domain of EGFR, current observation implies that gefitinib may be worth further investigation for treatment of esophageal cancers.
We review six aspects of the research literature on esophageal cancer: epidemiology and etiology, epidermal growth factor receptor and related growth factor receptors, cell cycle regulatory proteins, transforming growth factor-beta/Smad proteins, mismatch repair genes, and other genes.
Northern blot analysis revealed a fourfold increase (p < 0.01) in EGF-R mRNA levels in the esophageal cancer samples in comparison with normal tissue samples.
Thus, changes in gene copy number or level of expression of HER-I or c-myc DNA sequences may play an important role in the pathogenesis of esophageal cancer in this high-risk region.