Evidence map›Paper›PMID 42008207›Full record

ArticleHead and neck pathology2026

Malignant Transformation of Sinonasal Papilloma: Assessment of Clinicopathologic Features, p16 and p53 Expression, Transcriptionally Active HPV Status and Underlying Molecular Alterations.

Sara E Amin, Reiri Sono, Zubaidah I Al-Jumaili, Sibel Ak, Jen-Fan Hang, Mahmoud Elsayad, Karan Saluja

Abstract read
In one paragraph

Article in Head and neck pathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Sara E AminDepartment of Pathology and Laboratory Medicine, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX, 77030, USA.
Reiri SonoDepartment of Pathology and Laboratory Medicine, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX, 77030, USA.
Zubaidah I Al-JumailiDepartment of Pathology and Laboratory Medicine, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX, 77030, USA.
Sibel AkDepartment of Pathology and Laboratory Medicine, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX, 77030, USA.
Jen-Fan HangDepartment of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Mahmoud ElsayadDepartment of Pathology and Laboratory Medicine, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX, 77030, USA.
Karan SalujaDepartment of Pathology and Laboratory Medicine, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX, 77030, USA. Karan.saluja@uth.tmc.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeSinonasal papilloma (SP) has a recognized potential for malignant transformation, most commonly into squamous cell carcinoma (SCC). Well-established criteria for malignancy are lacking in SP and often depends on subjective features, such as stromal invasion without desmoplasia or assessment of dysplastic epithelium-to-stroma ratio, which can lead to under- or over-diagnosis, particularly in small biopsies. Additionally, emerging entities that mimic dysplastic papillomas necessitate re-evaluation of previously diagnosed “atypical/dysplastic SP” cases.

methodsWe conducted a retrospective study of 270 SP cases (226 patients) from 01/2010 to 06/2024. Three patients initially reported as “atypical and/or dysplastic SP”, “low-grade papillary sinonasal carcinoma”, and “papillary SCC”, were later found to harbor a DEK::AFF2 fusion were excluded from the study.

resultsIn all, malignant transformation was identified in 17/226 (7.5%) SP patients (including 14/202 (6.9%) inverted papilloma and 3/12 (25%) oncocytic papilloma), of which nine were synchronous and eight were metachronous transformations. Resultant malignancies comprised of SCC (14/17; 82.3%), sinonasal adenocarcinoma (SNAC) (1/17; 5.9%), dedifferentiated squamous cell carcinoma (1/17; 5.9%), and adenosquamous carcinoma (ASC) (1/17; 5.9%). Molecular profiling identified EGFR and KRAS as primary driver mutations, with additional TP53 and CDKN2A loss-of-function alterations implicated in malignant transformation. Immunohistochemical patterns of p53 (overexpression/null) and loss of p16 expression correlated with underlying genetic alterations (TP53 and/or CDKN2A), suggest these can act as surrogate markers for malignant transformation and may aid in risk stratification. Interestingly in our study, among the three oncocytic papillomas with malignant transformation, one showed ASC with transcriptionally active high-risk HPV and a concurrent KRAS mutation, and another transformed into non-intestinal-type SNAC.

conclusionMalignant transformation in SP occurs almost exclusively in IP and OP, warranting comprehensive evaluation of dysplastic SPs to exclude unsampled malignancy and newly defined molecular subsets. HPV appears to play role in malignant transformation. p53 and p16 immunostaining may help in dysplastic SP and guide closer clinical surveillance.

Indexed as

Cell Transformation, NeoplasticPapillomaParanasal Sinus NeoplasmsAdultAgedAged, 80 and overBiomarkers, TumorCyclin-Dependent Kinase Inhibitor p16FemaleHumansMaleMiddle AgedPapillomavirus InfectionsRetrospective StudiesTumor Suppressor Protein p53Biomarkers, TumorCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16TP53 protein, humanTumor Suppressor Protein p53Carcinoma ex-sinonasal papillomaCDKN2AEGFRInvertedKRASMalignant transformationOncocyticSinonasal papillomaTP53

Identifiers

PMID42008207
PMCPMC13096371

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.