215
Gene Implications in esophageal adenocarcinoma Ref.
ERBB2 Amplification, substitution, or truncation of receptor tyrosine-protein
kinase (ERBB2) were observed in approximately 23% of patients with
esophageal adenocarcinoma
[ 5 ]
EYA4 Eye absent 4 (EYA4) gene methylation was observed in 83% of esophageal
adenocarcinoma and 77% of BE but only 3% of normal esophageal tissue
and represents a potential candidate marker
[ 35 ]
FGF3/4/19 Amplification of fibroblast growth factor 3/4/19 (FGF3/4/19) was
observed in approximately 12% of patients with esophageal
adenocarcinoma
[ 5 ]
ICAM1 Intercellular Adhesion Molecule 1 (ICAM1) was overexpressed in
esophageal adenocarcinoma compared to normal tissues
[ 34 ]
KRAS Amplification or substitution of V-Ki-ras2 Kirsten rat sarcoma viral
oncogene homolog (KRAS) in approximately 23% of patients with
esophageal adenocarcinoma
[ 5 ]
KRAS amplification due to breakage-fusion-bridge [ 1 ]
MDM2 Mouse double minute 2 homolog (MDM2) amplification was observed in
4% of patients with esophageal adenocarcinoma
[ 36 ]
MDM2 mutation was due to chromothripsis-derived double-minute
chromosome formation or breakage-fusion-bridge
[ 1 ]
MYC MYC (c-Myc) amplification in approximately 16% of patients with
esophageal adenocarcinoma
[ 5 ]
Amplification due to chromothripsis-derived double-minute chromosome
formation
[ 1 ]
RFC3 Amplification of replication factor C (Activator 1) 3 (RFC3) occurred due
to breakage-fusion-bridge
[ 1 ]
SEMA5A Homozygote mutation of semaphorin 5A (SEMA5A) in MFD1 esophageal
adenocarcinoma cell line on chromosome 5 at position 9190519
[ 32 ]
SELENBP1 Expression reduced when Barrett esophagus progresses to esophageal
adenocarcinoma. Overexpression of Selenium Binding Protein 1
(SELENBP1) in Flo-1 cells heightened apoptosis, augmented cellular
senescence, and boosted cisplatin cytotoxicity, indicating its possible
significance as predictor of response towards chemoprevention or
chemosensitization with certain types of selenium in esophageal
adenocarcinoma
[ 8 ]
SMAD4 SMAD family member 4 (SMAD4) mutated in 13% of patients with
esophageal adenocarcinoma
[ 2 , 5 ]
Antiproliferative response was re-established with reactivation of transient
transfection of SMAD4
[ 37 ]
SPG20 Spartin (SPG20) is mutated in 7% of esophageal adenocarcinoma [ 3 ]
Table 1
(continued)
(continued)
Single Gene Mutation in Esophageal Adenocarcinoma