The point missense mutations at codon 61 were glutamine to arginine (Glu61Arg CAA>CGA) in four cases and glutamine to leucine (Glu61Leu CAA>CTA) in three cases.ConclusionThe significantly higher frequency of codon 61 mutation of the ras oncogene in primary and bilateral pterygium specimens compared with normal conjunctiva supports the tumoral origin of pterygium, and thus set the stage for research into a targeted therapy for pterygium with better outcomes than surgical excision.
Because pterygium is an UV-related uncontrolled cell proliferation, it is logical to assume polymorphisms of Ku70 is associated with genetic predisposition to pterygium.
Pterygium clinical samples were cultured under airlifting conditions with or without APR-246 for 4 days. p63, K10, β-catenin, and TCF-4 expression in pterygial epithelium was determined by immunofluorescent staining and real-time PCR.
Molecular genetic alterations reported in association with pterygium include loss of heterozygosity (LOH), point mutations of proto-oncogenes, such as K-ras and alterations in the expression of tumor suppressor genes, such as p53 or p63.
The correlation between pterygium and TNF-alpha-308 promoter, IL-1beta-511 promoter, IL-1beta exon 5, and IL-1 Ra polymorphisms does not exist and those polymorphisms are not useful genetic markers for pterygium susceptibility.
The point missense mutations at codon 61 were glutamine to arginine (Glu61Arg CAA>CGA) in four cases and glutamine to leucine (Glu61Leu CAA>CTA) in three cases.ConclusionThe significantly higher frequency of codon 61 mutation of the ras oncogene in primary and bilateral pterygium specimens compared with normal conjunctiva supports the tumoral origin of pterygium, and thus set the stage for research into a targeted therapy for pterygium with better outcomes than surgical excision.
Promoter methylation changes of CTLA4 gene were not statistically different in patients with pterygium in comparison with healthy controls (OR=1.614; 95% CI=0.57-4.75; P value=0.37).
Pterygium clinical samples were cultured under airlifting conditions with or without APR-246 for 4 days. p63, K10, β-catenin, and TCF-4 expression in pterygial epithelium was determined by immunofluorescent staining and real-time PCR.
Molecular genetic alterations reported in association with pterygium include loss of heterozygosity (LOH), point mutations of proto-oncogenes, such as K-ras and alterations in the expression of tumor suppressor genes, such as p53 or p63.
Polymorphisms at MMP-8-799C/T, Val436Ala and Lys460Thr may not mainly contribute to determining personal susceptibility to pterygium in the Taiwanese examined.
This study aims to analyze and compare the frequency of the GSTT1 genotypes in relation to pterygium through statistical analyzes in order to build a genotypic profile for the Replicon patients.
Molecular genetic alterations reported in association with pterygium include loss of heterozygosity (LOH), point mutations of proto-oncogenes, such as K-ras and alterations in the expression of tumor suppressor genes, such as p53 or p63.
Molecular genetic alterations reported in association with pterygium include loss of heterozygosity (LOH), point mutations of proto-oncogenes, such as K-ras and alterations in the expression of tumor suppressor genes, such as p53 or p63.
We studied, with immunohistochemistry, the presence and localization of thymine dimers in the epithelial and stromal components of the human primary pterygium and its recurrences with a special emphasis on the vascular network and its interactions with the p53 tumor suppressor gene protein.
We have analyzed the status and expression of the p53 gene in epithelial cells derived from pterygium and have demonstrated that the p53 gene has undergone a monoallelic deletion.
In analysis of specimens from pterygium patients as well as normal conjunctivas, VEGF121 and VEGF165 were identified as the only VEGF splice forms expressed.