S100A6 expression was strong in the superficial layer of pterygium epithelium but relatively weaker in the suprabasal and superficial cells of normal conjunctiva epithelium.
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.
Other findings in pterygium include the frequent detection of HPV DNA, ocular surface changes such as the overexpression of various proteins, including defensins and phospolipases D, as well as the up-regulation of growth factors, such as bFGF or VEGF.
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.
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.
Antibodies raised against VEGF and p53 were used to analyze the distribution and expression of these markers in pterygium and normal human conjunctiva were used as negative control.
HPV 16/18 E6 contributes to HPV-mediated pterygium pathogenesis as it is partly involved in p53 inactivation and is expressed in HPV DNA-positive pterygium.
The most abundant complementary DNAs from pterygium include clusterin, keratins 13 (Krt13) and 4 (Krt4), S100A9/calgranulin B, and spermidine/spermine N1-acetyltransferase (SAT1).
The most abundant complementary DNAs from pterygium include clusterin, keratins 13 (Krt13) and 4 (Krt4), S100A9/calgranulin B, and spermidine/spermine N1-acetyltransferase (SAT1).
The most abundant complementary DNAs from pterygium include clusterin, keratins 13 (Krt13) and 4 (Krt4), S100A9/calgranulin B, and spermidine/spermine N1-acetyltransferase (SAT1).
The most abundant complementary DNAs from pterygium include clusterin, keratins 13 (Krt13) and 4 (Krt4), S100A9/calgranulin B, and spermidine/spermine N1-acetyltransferase (SAT1).
The higher levels of FGF2 or VEGFA mRNA in pterygium imply that these factors may be involved in the pathogenesis or clinical behavior of the pterygium, including postoperative recurrence.
Because the polymorphism of hOGG1 was reported to be associated with pterygium, it is logical to assume the correlation between XRCC1, XPA, and XPD polymorphisms and pterygium formation.
Higher prevalence of G6PD- was found in patients affected by primary pterygium than in control subjects, both men and women, suggesting that this enzymatic defect may be a predisposing factor for pterygium.