Use of p63 for distinction of glandular versus squamous lesions in cervicovaginal specimens

Abstract

Perinatal hypoxic‐ischemic encephalopathy (HIE) is a significant cause of mortality and morbidity in infants and young children. Therapeutic opportunities are very limited for neonatal and pediatric HIE. Specific neural systems and populations of cells are selectively vulnerable in HIE; however, the mechanisms of degeneration are unresolved. These mechanisms involve oxidative stress, excitotoxicity, inflammation, and the activation of several different cell death pathways. Decades ago the structural and mechanistic basis of the cellular degeneration in HIE was thought to be necrosis. Subsequently, largely due to advances in cell biology and to experimental animal studies, emphasis has been switched to apoptosis or autophagy mediated by programmed cell death (PCD) mechanisms as important forms of degeneration in HIE. We have conceptualized based on morphological and biochemical data that this degeneration is better classified according to an apoptosis‐necrosis cell death continuum and that programmed cell necrosis has prominent contribution in the neurodegeneration of HIE in animal models. It is likely that neonatal HIE evolves through many cell death chreodes influenced by the dynamic injury landscape. The relevant injury mechanisms remain to be determined in human neonatal HIE, though preliminary work suggests a complexity in the cell death mechanisms greater than that anticipated from experimental animal models. The accurate identification of the various cell death chreodes and their mechanisms unfolding within the immature brain matrix could provide fresh insight for developing meaningful therapies for neonatal and pediatric HIE. Ann Neurol 2011;69:743–758

P634A4 and TAp73 immunocytochemistry in liquid-based cervical cytology—potential biomarkers for diagnosis and progress prediction of cervical neoplasia

“…The antibody can also detect isolated small HSIL cells and can improve the sensitivity of detecting these 'litigation' cells that are potentially easy to be missed. P63 has been suggested to be useful to distinguish squamous and glandular lesions in cervical samples 39 and the endocervical glandular cells in this study was found to be negative for p634A4. In the squamous mucosa, p63 expression is often localized to the basal and parabasal cells of mature or metaplastic stratified squamous epithelium but may be present in all cell layers in atrophic epithelium.…”

Gynecologic cytology on conventional and liquid‐based preparations: A comprehensive review of similarities and differences

“…This antibody is not expressed in AGC, adenocarcinoma, or normal glandular cells. p63 stains basal cells and may be a diagnostic pitfall in atrophic Pap tests 118…”