ArticleVirchows Archiv : an international journal of pathology2025
Abnormal nuclear and nucleolar immunoreactivity of p16INK4a represents a frameshift alteration in CDKN2A: the E6H4 clone recognizes the "p14ARF::p16INK4a" chimeric protein.
Article in Virchows Archiv : an international journal of pathology, 2025. 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
8 authors.
Funding
Abstract
In p16INK4a immunostaining, block positivity (i.e., strong nuclear/nuclear-cytoplasmic staining) is a widely acknowledged surrogate marker of HPV-associated cancers. Thus, immunohistochemistry using the anti-p16INK4a clone E6H4 has been approved as an in vitro diagnostic tool for HPV-associated cancers. This study revealed a distinctive pattern of immunostaining with clone E6H4-strong nuclear with nucleolar staining-which can easily be confused with the HPV-associated pattern. This peculiar pattern can be caused by frameshift deletions or insertions within exon 2 of the INK4a/ARF locus. Since p16INK4a and p14ARF are coded in the same sequence on chromosome 9p21, these mutations may inactivate p16INK4a and convert the reading frame for the 3' region of the p14ARF sequence into p16INK4a, producing a chimeric protein. Recognizing this pattern is essential to avoid misdiagnosis of HPV association and inappropriate treatment.
Indexed as
Identifiers
41339993What OpenQuestion 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 OpenQuestion graph.