The effects of neoadjuvant therapy on morbidity and mortality of esophagectomy for esophageal cancer: American college of surgeons national surgical quality improvement program (ACS-NSQIP) 2005-2012.
We reported 4 differentially expressed proteins involved in the pathological process of esophageal cancer, such as annexinA1 (ANXA1), peroxiredoxin-2 (PRDX2), transgelin (TAGLN) andactin-aortic smooth muscle (ACTA2).
We investigated the expression of activin-betaA (Act-betaA) which is a subunit of activin A, its receptor type I and IIb (ActRI, ActRIIb) and its inhibitor, inhibin-alpha (Inh-alpha), which is a subunit of inhibin A in esophageal carcinoma by reverse transcription polymerase chain reaction (RT-PCR) method.
We investigated the expression of activin-betaA (Act-betaA) which is a subunit of activin A, its receptor type I and IIb (ActRI, ActRIIb) and its inhibitor, inhibin-alpha (Inh-alpha), which is a subunit of inhibin A in esophageal carcinoma by reverse transcription polymerase chain reaction (RT-PCR) method.
An ADAM12 and FAK positive feedback loop amplifies the interaction signal of tumor cells with extracellular matrix to promote esophageal cancer metastasis.
In addition, the risk-score model -0.0053*log<sub>2</sub>(<i>CADM2</i>)+0.0168*log<sub>2</sub>(<i>SERPINE1</i>)-0.0073*log<sub>2</sub>(ADAMTS9-AS2)+0.0905*log<sub>2</sub>(PVT1)+0.0047*log<sub>2</sub>(hsa-miR372)-0.0193*log<sub>2</sub>(hsa-miR145), (log<sub>2</sub>[gene count]) could improve diagnosis of EC with an AUC of 0.988.
ADAR1 is commonly overexpressed, for instance in breast, lung, liver and esophageal cancer as well as in chronic myelogenous leukemia, where it promotes cancer progression.
The ADH2(1)/ADH2(1) and ALDH2(1)/ALDH2(2) genotypes were independently and significantly higher in esophageal cancer patients than in healthy controls.
Furthermore, Arg/Arg genotype of ADH1BArg47His variant combined with drinking, smoking and males appeared to show a high risk in patients with esophageal cancer.
The key findings of the earlier studies were that variations (i.e., polymorphisms) in the DNA sequences of the genes encoding alcohol dehydrogenase 1B (i.e., the ADH1B gene), aldehyde dehydrogenase 2 (i.e., the ALDH2 gene), and other alcohol-metabolizing enzymes mediate the risk for alcoholism; moreover, these polymorphisms also have an impact on the risk of alcohol-related cancers, such as esophageal cancer.
A review of case-control studies of the effects of ALDH2, ADH2 and ADH3 genotypes shows consistently positive associations between inactive heterozygous ALDH2 and the less-active ADH2 genotypes and the risk for esophageal cancer in East Asian heavy drinkers and this enzyme-related vulnerability may extend to light-to-moderate drinkers.
The association of lifestyle habits and polymorphism of ADH2 and ALDH2 genes with the risk of esophageal cancer in Thai population was investigated in a hospital-based case-control study: 202 cases and 261 controls.
Inactive ALDH2 encoded by ALDH2*1/2*2 and the low-activity form of alcohol dehydrogenase (ADH)-2 encoded by ADH2*1/2*1 enhance the risk for esophageal cancer in Japanese light to heavy drinkers, a significant association that emphasizes the importance of screening tests for inactive ALDH2 based on alcohol flushing.
Genetic polymorphisms of the alcohol dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (ALDH2) genes are associated with the risk of esophageal cancer.
After adjusting for age, drinking and smoking habits, BMI and ALDH2/ADH2 genotypes, macrocytosis of MCV > or =106 fl was associated with increased risk for esophageal cancer (OR = 2.75).
To determine the effects of ALDH2 and ADH2 genotypes in genetically based cancer susceptibility, lymphocyte DNA samples from 668 Japanese alcoholic men more than 40 years of age (91 with and 577 without esophageal cancer) were genotyped and the results were expressed as odds ratios (ORs).