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.
The purpose of this study is to test whether inhibition of beta-catenin or overexpression of p53 can decrease survivin expression and render esophageal cancer cells more susceptible to apoptosis.
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.
Combination therapy of carbon-ion beam with the far upstream element-binding protein (FBP)-interacting repressor, FIR, which interferes with DNA damage repair proteins, was proposed as an approach for esophageal cancer treatment with low side effects regardless of TP53 status.
Therefore, our results suggested that the survivin expression depended on the p53 status and the C allele in the survivin promoter polymorphism -625G/C might increase the possibility of the survivin overexpression in esophageal cancer patients.
Our recent clinical results from a phase I/II study of adenoviral-mediated p53 gene therapy for patients with un-resectable esophageal cancer are reviewed.
These results suggest that COX-2 may be an important factor for esophageal cancer and inhibition of COX-2 may be helpful for prevention and possibly treatment of this cancer.
Lapatinib inhibits receptor phosphorylation and cell growth and enhances antibody-dependent cellular cytotoxicity of EGFR- and HER2-overexpressing esophageal cancer cell lines.
Our results showed that telomeres were significantly shorter in tumors with somatic p53 mutations compared with tumors with wild-type p53 in both breast tumors (P=0.007) and esophageal cancer (P=0.001).
Potential targets for intervention in esophageal neoplasms include mutations involving retinoblastoma (Rb) and p53 tumor-suppressor pathways as well as tyrosine kinase cascades, which are known to promote cell cycle progression.
When all 11 studies were pooled into the analysis, an increased esophageal cancer risk was significantly associated with the Pro variant of TP53Arg72Pro in three genetic comparison models [odds ratio (OR)Pro vs. Arg=1.21, 95% confidence interval (CI): 1.05-1.39, POR=0.009; ORDominant genetic model=1.22, 95% CI: 1.09-1.37, POR=0.001; ORHomozygote model=1.40, 95% CI: 1.05-1.87, POR=0.024].