Correlations of recurrence after radical surgery for esophageal cancer with glucose-lipid metabolism, insulin resistance, inflammation, stress and serum p53 expression.
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.
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.
We used 9 kinds of human squamous esophageal carcinoma cells with different <i>p53</i> genotypes and examined expression of p53 and the related molecules in CP-31398-treated cells.
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.
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.
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.
<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).
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.
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.
In contrast, replication-competent Ad produced greater cytotoxicity in p53 mutated than in wild-type esophageal carcinoma cells, suggesting a possible association between the cytotoxicity and the p53 genotype.
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.
We also observed a significant increase in ERCC1 expression, and decrease in p53 and EGFR expression, in EC-9706 cells treated with SNX-2112 (P < 0.05), indicating the regulation of EC by SNX-2112.