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H.Y. Lam, K.G. Yen, P. Chevez–Barrios; Histopathology of Radiation Induced and Pediatric Cataracts . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4079.
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Cataract formation is a known sequelae of radiation therapy, usually posterior polar subcapsular type. Radiation has been shown to transiently increase cell mitotic activity and to induce DNA damage. We conducted a pilot study to determine the histologic and immunophenotypic differences between radiation induced cataracts, and non–irradiated cataracts in the pediatric population.
This is a combined prospective and retrospective study. We studied 10 cases, 6 retrospective and 4 prospective specimens. Prospective cases were studied histologically by cell block obtained from the vitrectomy bag of the cataract aspirate. Retrospective cases consisted of archival specimens with and without history of radiation. All specimens were studied by routine H&E, PAS, and by immunohistochemistry using pan–keratin, MIB–1, p53, and vimentin.
Two study groups of radiation and pediatric cataracts and a control group were studied. The radiation cataracts were from three patients with retinoblastoma, and one with rhabdomyosarcoma. The four pediatric cataracts without any history of radiation, included one PHPV associated cataract, one congenital lamellar, one hereditary nuclear, and one non–irradiated retinoblastoma cataract. The control group includes two non–irradiated, non–cataractous lenses: one from an 18 week old embryo, and one from a 72 year old adult.We identified lens epithelial cells (LECs ) and capsule in all of the prospective cases. Immunohistochemical staining of the LECs with p53 was negative in all specimens, however the retinoblastoma specimen without radiation had positive p53 staining in the tumor cells. Each of the three groups had one specimen positive for MIB–1 staining, and there was preferential increased mitotic activity near the anterior capsule. Pan–keratin staining was negative in all specimens, and vimentin was positive in all specimens.
There is no difference in proliferative activity between irradiated versus non–irradiated lenses. The tumor marker, p53 was negative in all specimens, which may imply that there was no specific DNA damage targeted to p53 in the lens epithelial cells induced by irradiation.
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