![]() ![]() Interestingly, most low-grade SILs were SC junction-negative, implying infection of metaplastic progeny rather than the original SC junction cells. The progressive loss of the embryonic/SC junction markers occurred with 'top down' differentiation during development, remodelling, and early neoplasia. A similar pattern was noted in high-grade squamous intraepithelial lesions (HSILs), suggesting that HPV infection of the cuboidal SC junction cells initiated outgrowth of basally-oriented neoplastic progeny. This downward or basal (rather than upward or apical) evolution from progenitor cell to metaplastic progeny was termed reverse or 'top down' differentiation. In all settings, there was a repetitive scenario in which cuboidal embryonic/SC junction cells gave rise to subjacent metaplastic basal/reserve cells with a switch from the SC junction positive to negative immunophenotype. Early in life, embryonic cervical epithelial cells were seen throughout the cervix and subsequently diminished in number to become concentrated at the SC junction in the adult. In the present study, we analysed the SC junction immunophenotype during pre- and post-natal human and mouse development and in the adult, processes of metaplastic evolution of the SC junction, microglandular change, and early cervical neoplasia. ![]() How this population participates in cervical remodelling and neoplasia is unclear. The cervical squamocolumnar (SC) junction is the site of a recently discovered 'embryonic' cell population that was proposed as the cell of origin for cervical cancer and its precursors. ![]()
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