ArticleHistopathology2026
Hippo pathway disruption and YAP1 activation in anogenital papillary squamous intraepithelial lesion.
Article in Histopathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsPapillary squamous intraepithelial lesion (PSIL), also known as papillary immature metaplasia, is a rare anogenital lesion associated with low-risk human papillomavirus (HPV) infection. The molecular pathogenesis of PSIL remains unclear. This study aims to investigate the activation of YAP1, a Hippo pathway co-activator, in PSIL and compare it to condyloma and papillary HSIL. METHODS AND
resultsYAP1 activation was evaluated by immunohistochemistry using an antibody specific for activated/unphosphorylated YAP1 (act-YAP1) in 36 PSIL cases, 20 condyloma and 2 papillary HSIL cases. HPV genotyping and chromogenic in situ hybridization (CISH) were performed to determine HPV status. Low-risk HPV, predominantly HPV6, was detected in 78.6% of PSILs. CISH revealed a diffuse fine punctate distribution of low-risk HPV E6/E7 transcripts in PSIL, distinct from the large focal clusters seen in condyloma, but similar to high-risk HPV in HSIL. All PSILs showed non-block p16 expression. Act-YAP1 immunostaining demonstrated YAP1 activation in 86.1% of PSILs (72.2% diffuse, 13.9% focal), resembling the pattern in papillary HSIL but differing from condyloma, which exhibited nuclear act-YAP1 only in basal and granular layers. No significant associations were found between YAP1 activation and HPV status or immunoprofiles of p16, p53, Rb1 and CK7.
conclusionsPSILs demonstrate prominent YAP1 activation, implicating Hippo pathway disruption as a potential driver of PSIL pathogenesis. These findings support a distinct molecular profile of PSIL and provide insight into the biological mechanisms underlying this rare lesion.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.