Evidence map›Paper›PMID 40508015›Full record

ArticleInternational journal of molecular sciences2025

The Predictive Impact of HPV Genotypes, Tumor Suppressors and Local Immune Response in the Regression of Cervical Intraepithelial Neoplasia 2-3: A Prospective Population-Based Cohort Study.

Pavla Sustova, Birgit Engesæter, Irene Tveiterås Øvestad, Einar G Gudlaugsson, Reza Ghiasvand, Ivar Skaland, Jan P A Baak, Ameli Tropé, Emiel A M Janssen, Ane Cecilie Munk

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

10 authors.

Pavla SustovaDepartment of Laboratory Medicine, St. Olav's Hospital, Trondheim University Hospital, 7006 Trondheim, Norway.
Birgit EngesæterDepartment of Cervical Cancer Screening, Cancer Registry of Norway, Norwegian Institute of Public Health, 0304 Oslo, Norway.ORCID 0000-0002-0956-8378
Irene Tveiterås ØvestadDepartment of Pathology, Stavanger University Hospital, 4011 Stavanger, Norway.
Einar G GudlaugssonDepartment of Pathology, Stavanger University Hospital, 4011 Stavanger, Norway.
Reza GhiasvandOslo Centre for Biostatistics and Epidemiology, Oslo University Hospital, 0424 Oslo, Norway.
Ivar SkalandDepartment of Pathology, Stavanger University Hospital, 4011 Stavanger, Norway.
Jan P A BaakDepartment of Pathology, Stavanger University Hospital, 4011 Stavanger, Norway.ORCID 0000-0002-4018-9085
Ameli TropéDepartment of Cervical Cancer Screening, Cancer Registry of Norway, Norwegian Institute of Public Health, 0304 Oslo, Norway.
Emiel A M JanssenDepartment of Pathology, Stavanger University Hospital, 4011 Stavanger, Norway.ORCID 0000-0002-7760-5396
Ane Cecilie MunkDepartment of Obstetrics and Gynecology, Sørlandet Hospital Kristiansand, 4604 Kristiansand, Norway.

Funding

Western Norway Regional Health Authority 190202
6 · The paper itself

Abstract

Cervical intraepithelial neoplasia (CIN) is caused by human papillomavirus (HPV); however, factors such as HPV genotype and individual immune response may also contribute to its development. The loop electrosurgical excision procedure (LEEP) is a treatment for high-grade cervical intraepithelial neoplasia (CIN), as approximately 30% of these cases may progress to cancer. However, 20-40% of cases will regress spontaneously. HPV16 infection constitutes the highest risk for progression to cervical cancer and a lower probability of regression. Knowledge regarding the regression of lesions caused by other high-risk genotypes alone or in association with biomarker expression and lesion length has been limited. In the present study, the regression rates of high-grade squamous intraepithelial lesions were calculated. Twenty-one percent of the 161 women diagnosed with CIN2-3 on colposcopy-directed biopsies exhibited regression (defined as CIN1 or less) in the subsequent cone excisions. The mean interval between biopsy and treatment was 113 days (range of 71-171). High-grade lesions of the squamous epithelium caused by HPV16, together with lesions caused by HPV31, 52 and 58, showed significantly lower regression rates (HR 0.54, 0.22-0.75; low-regression group) than lesions caused by HPV18, 33, 35, 39, and 45 (HR 2.85, 1.54-5.28; high-regression group). A multivariate analysis of HPV genotypes, epithelial expressions of pRb and p53, immune cell proportions in the stroma (CD4/CD25 and CD4/CD8), and lesion lengths correctly predicted regression in 78% (Harrell's C). A Harrell's C value of 82% for the low-regression group indicates that different HPV genotypes or groups, together with divergent patterns of tumor suppressors, immune cells, and lesion size, can give prognostic information regarding the outcome of CIN2-3.

Indexed as

PapillomaviridaePapillomavirus InfectionsUterine Cervical DysplasiaUterine Cervical NeoplasmsAdultAgedFemaleGenotypeHumansMiddle AgedProspective StudiesYoung Adultbiomarkerscervical intraepithelial neoplasiaCIN lesion sizehigh-risk HPVHPV genotypesregression

Identifiers

PMID40508015
PMCPMC12155477

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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.