Correlations of recurrence after radical surgery for esophageal cancer with glucose-lipid metabolism, insulin resistance, inflammation, stress and serum p53 expression.
In summary, shikonin can sensitize esophageal cancer cells to paclitaxel-treatment by promoting cell mitotic arrest and reinforcing the susceptibility of esophageal cancer cells to apoptosis induced by paclitaxel, which is potentially associated with altered levels of Bcl-2 and p53.
Methylation‑associated silencing of miR‑128 promotes the development of esophageal cancer by targeting COX‑2 in areas with a high incidence of esophageal cancer.
Among the down-regulated miRNAs in SCI, 21, 19 and 20 miRNAs were potentially associated with hematological, bladder and esophageal cancer, respectively, and three target genes (<i>TP53, CCND1 and KRAS</i>) were common to all three types of cancer.
Data on the combined effect of p53 protein accumulation and <i>TP53</i> genomic deactivation in large scale studies for esophageal cancer are currently lacking.
Nimotuzumab is a humanized monoclonal antibody against epidermal growth factor receptor (EGFR), the efficacy of nimotuzumab added to nCRT for esophageal cancer is uncertain.
Esophageal cancer (ESC) is one of the most deadly diseases for human. p53 in most cancers, including ESC cell, is mutated, and the mutated p53 losses its original function and acquires "gain of function" that allows for promoting the hallmarks of cancer, such as antiapoptosis, metastasis, invasion, angiogenesis, and resistance to chemotherapy.
Results indicated that PT shows more effective antitumor activity as compared with Pan both on EGFR-overexpressed KYSE-450 and KYSE-150 esophageal cancer cells, especially on KYSE-450 cells.
Zerumbone can inhibit the proliferation and induce apoptosis of esophageal cancer EC-109 cells, and its induction of apoptosis may be realized through upregulating the mRNA expression of P53 and downregulating the mRNA expression of Bcl-2, and upregulating the protein expression of P53 and downregulating the protein expression of Bcl-2.
Evaluating the expression of cyclooxygenase-2 enzyme by immunohistochemistry in normal and tumoral tissue before and after neoadjuvant chemoradiotherapy in patients with esophageal cancer in Khorasan Province.
These phase 3 trial results point to little benefit to current EGFR-targeted agents in an unselected patient population, and highlight the need for predictive biomarkers in the treatment of esophageal cancer.
Results of this study suggest that anti-EGFR therapies should be investigated in prospective clinical trials in different settings in EGFR FISH-positive and, in particular, EGFR-amplified esophageal cancer.
<b>MATERIALS AND METHODS:</b> The prevalence of HPV in individuals with and without esophageal cancer (EC) was determined by using multiplex PCR; p16 and p53 protein levels were assessed by immunohistochemistry (IHC).
We searched PubMed, Ovid MEDLINE, Embase, and Current Contents Connect to identify studies published between January 1990 and February 2016 of esophageal cancer populations that measured p53 expression and/or mutation status and reported hazard ratios (HRs), or adequate data for estimation of HRs for survival for p53-defined subgroups.
A ligand-based and enediyne-energized bispecific fusion protein targeting epidermal growth factor receptor and insulin-like growth factor-1 receptor shows potent antitumor efficacy against esophageal cancer.
The sensitivity of the p53 fluorescent in situ hybridization probe was13.3 % for any abnormality, 10 % for intestinal metaplasia, and 0 % for dysplasia or esophageal cancer.
These results indicated that miR-133a could inhibit the MEK/ERK pathway to promote cell apoptosis and enhance radio-sensitivity by targeting EGFR in EC..