PTEN, a tumor suppressor gene, appears to negatively control the phosphoinositide 3-kinase signaling pathway for regulation of cell proliferation and cell survival. Somatic PTEN mutations are involved in a variety of tumors, including endometrial carcinomas, where PTEN expression is diminished. We examined expression of PTEN in a series of cervical adenocarcinomas and precursors, using tissue microarray (TMA) technology. TMA blocks were constructed using paraffin-embedded, formalin-fixed tissues from 273 samples derived from 16 normal cervical biopsies, 119 cases of invasive adenocarcinoma, and 20 high-grade cervical glandular intraepithelial neoplasia (CGIN). Fresh 3-μm sections were cut and immunostained with PTEN, and expression was correlated with clinicopathologic variables, including histologic subtypes of adenocarcinoma. In 137 patients, PTEN expression was positive in 121 (88%). The intensity and distribution of PTEN staining in the tumor tissue were more heterogeneous than those observed in the normal tissues. There were no significant differences in distribution or intensity of PTEN expression between adenocarcinoma in situ and subtypes of invasive adenocarcinoma. Our findings show that unlike the case in most endometrial carcinomas, PTEN expression is retained during the process of carcinogenesis in the glandular cervix. There is, however, evidence of altered distribution and intensity of PTEN expression in cervical adenocarcinoma cells.
- cervical adenocarcinoma
- tissue microarray (TMA)
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