P53 expression and histopathological changes in primary and recurrent pterygia among Egyptian cases

The aim of this work is to assess P53 expression and histopathologic features in the epithelia of both primary and recurrent pterygia cases, searching for the pathogenesis of this common lesion. The pterygia specimens from 22 patients [twelve primary and ten recurrent cases] were studied by both routine hematoxylin and eosin stain and immunohistochemically using antibodies against P53 protein. Cases included in this study were 16 males and 6 females. Their ages ranged from 20 to 55 years. Positive family history was recorded in 18.2% of patients and positive parental consanguinity in 9.1% of them. Twenty cases [90.1%] had a history of chronic exposure to solar light i.e prolonged outdoor exposure time [8-12 hours/day] for more than 5 years. Epithelial hyperplasia was more common in recurrent pterygium samples [8 cases] than primary pterygium [only one case]. But, squamous metaplasia with mild dysplasia was more common in Primary pterygium samples [10 cases] than recurrent samples [2 cases]. Ten out of twelve studied specimens with primary pterygium [83.4%] were positive for abnormal P53 expression and two specimens [16.6%] were negative, while only 2 specimens [20%] of recurrent pterygium showed the abnormal positive expression and 8 cases [80%] were negative. Cases with marked and moderate P53 immunostaining [12 cases] showed squamous metaplasia with mild dysplastic changes, nine out of ten cases with negative immunostaining showed epithelial hyperplasia and the remaining sample showed squamous metaplasia without dysplasia. P53 protein is expressed at a high rate in primary pterygia as compared to cases of recurrence. Hence the possible role of P53 in the original development of pterygium, suggesting that pterygium could be a result of uncontrolled cell proliferation and unregulated cell apoptosis which can be proposed a type of benign tumour or even a precancerous condition and not as a degenerative lesion. It seems to be no correlation between P53 expression and recurrence. Recurrent pterygium was related to hyperplastic changes and this may explain the pathogenesis of recurrence especially if the pterygium was not excised completely and the remained epithelial cells continued to grow and formed a new pterygium

study of p53 protein and DNA ploidy in retinoblastoma

Retinoblastoma is the most common primary intraocular cancer in children. It arises from cells that are defective in both copies of the retinoblastoma susceptibility gene [RB I]. Loss of both RB1 and p53 functions may be required for cell immortalization and tumor development. The pattern of p53 expression in retinoblastoma appears to depend on the state of differentiation of the tumor. p53 and RB pocket proteins are important to control DNA ploidy, which may have a value in estimating the prognosis of retinoblastoma. The aim of this work was to assess p53 expression, DNA ploidy, and their relations with histopathologic features in retinoblastoma cases. The study was done on eight patients with retinoblastoma [seven males and one female]. Personal and family history with pedigree analysis were done for all cases. Ophthalmic examination with follow up of tumor regression rate during therapy was performed. Eight primary retinoblastoma samples were obtained from enucleated eyes of all patients. Retinoblastoma sections were stained by hematoxylin and eosin stain and scoring of histopathologic features was performed. Sections were immunohistochemically stained for the protein product of the tumor suppressor gene p53 and quantified for the extent and intensity of the staining. DNA ploidy was examined by assessment of type of DNA histogram and DNA index using cytometric analysis system [CAS 200] after feulgen staining. The proliferative activity was automatically expressed by the CAS 200 as the percentage of cells engaged in the S-phase of the cycle. Our results indicated that p53 protein was immunohistochemically detectable in most retinoblastoma cases [7/8 cases], and was only negative in one case. DNA was aneuploid in 6 out of 8 cases, while 2 cases [one of them was p53 negative, and the other showed weak positivity] were diploid with high proliferative activity. Histopathologic examination revealed that 3 cases were poorly differentiated and 5 cases showed intermediate differentiation with increased necrotic changes and mitotic figures. Retinoblastoma samples showed high degree of p53 protein expression and high degree of aneuploidy which were related to the aggressiveness of histopathologic changes of retinoblastoma. Thus both p53 expression and DNA ploidy have been shown to be markers of aggressiveness of tumor behaviour in retinoblastoma and can help in the prediction of its prognosis