PubMed Health⌕ Search

PubMed · 9755670

Rescreen effect in conventional and PAPNET screening: observed in a study using material enriched with positive smears.

Abstract

OBJECTIVE: To study the rescreen and PAPNET effects on enriched material derived from smears screened routinely using PAPNET and conventional microscopy. STUDY DESIGN: A series of 432 smears (containing 122 atypical squamous cells of undetermined significance [ASCUS] plus 44 at least dysplastic squamous intraepithelial lesion-positive [SIL+] ones), screened routinely with the conventional method, were rescreened using the PAPNET system. Another series of 461 smears (containing 140 ASCUS + 52 SIL+ ones) screened routinely with PAPNET were rescreened conventionally. The rescreen effect, defined as the effect of differences between the rescreen and routine screening situation, was investigated by comparing the rescreen results in both series of smears with the routine results in both series. The effect of using either method of screening was studied by comparing the PAPNET results in both series with the results of conventional screening in both series. RESULTS: The rescreen effect was statistically significant both for a higher number of smears classified as negative (less than ASCUS) and a higher number of smears classified as high grade SIL or more. PAPNET-assisted screening resulted in a significantly higher number of smears classified as high grade SIL+, although for this latter finding there is an unexplained significant difference between conventional and PAPNET-screened cases in the changes made by the cytopathologist in the cytotechnologists' diagnoses. CONCLUSION: The rescreen effect should not be ignored when enriched material is used.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M van Ballegooijen, S Beck, M E Boon, R Boer, J D Habbema. Rescreen effect in conventional and PAPNET screening: observed in a study using material enriched with positive smears.. https://doi.org/10.1159/000332101

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Nonpromoter methylation of the CDKN2A gene with active transcription is associated with improved locoregional control in laryngeal squamous cell carcinoma.

We previously reported a novel association between CDKN2A nonpromoter methylation and transcription (ARF/INK4a) in human papillomavirus associated oropharyngeal tumors. In this study we assessed whether nonpromoter CDKN2A methylation in laryngeal squamous cell carcinomas (LXSCC) conferred a similar association with transcription that predicted patient outcome. We compared DNA methylation and ARF/INK4a RNA expression levels for the CDKN2A locus using the Illumina HumanMethylation27 beadchip and RT-PCR in 43 LXSCC tumor samples collected from a prospective study of head and neck cancer patients treated at Montefiore Medical Center (MMC). Validation was performed using RNAseq data on 111 LXSCC tumor samples from the Cancer Genome Atlas (TCGA). The clinical relevance of combined nonpromoter CDKN2A methylation and transcription was assessed by multivariate Cox regression for locoregional recurrence on a subset of 69 LXSCC patients with complete clinicopathologic data from the MMC and TCGA cohorts. We found evidence of CDKN2A nonpromoter hypermethylation in a third of LXSCC from our MMC cohort, which was significantly associated with increased ARF and INK4a RNA expression (Wilcoxon rank-sum, P&#xa0;=&#xa0;0.007 and 0.003, respectively). A similar association was confirmed in TCGA samples (Wilcoxon rank-sum test P&#xa0;<&#xa0;0.0001 for ARF and INK4a). Patients with CDKN2A hypermethylation or high ARF/INK4a expression were significantly less likely to develop a locoregional recurrence compared to those with neither of the features, independent of other clinicopatholgic risk factors (adjusted hazard ratio=0.21, 95% confidence interval:0.05-0.81). These results support the conclusion that CDKN2A nonpromoter methylation is associated with increased ARF and INK4a RNA expression, and improved locoregional control in LXSCC.

Carcinoma, Squamous Cell↗

HPV integration begins in the tonsillar crypt and leads to the alteration of p16, EGFR and c-myc during tumor formation.

The prevalence of human papillomavirus (HPV) infection is high in the oropharyngeal mucosal regions, of which the tonsil is the most commonly affected. There may be a link between HPV and the pathogenesis of tonsillar cancer (TC), because of common anatomical characteristics between cervical and tonsillar cancer. We aimed to clarify whether HPV directly affects the oncogenesis and biologic behavior of TC by making a comparison between infection prevalence, physical status and viral loading numbers, and clinicopathologic prognostic factors. To compare HPV-related molecules between TC and tonsillitis (CFT), p16, survivin, HIF-1alpha, skp-1, cyclin A, cyclin B1, c-myc and EGFR were investigated. We observed a significant difference in HPV prevalence between 52 TCs and 69 CFTs (73.1% vs. 11.6%), and most of the HPVs were type 16 (87.2%) and nonepisomal (94.1%). Most TCs associated with HPV arose from the tonsillar crypts, and tended to be inverted and poorly differentiated. Compared with HPV-negative TC, HPV-positive TC showed a strong association with p16 overexpression (p<0.0001), and an inverse association with EGFR amplification (p=0.0478). HPV-16 integration status was strongly associated with c-myc amplification (p=0.034) and HIF-1alpha overexpression (p=0.022). HPV-16 integration could be directly related to tonsillar carcinogenesis initially in tonsillar crypts, followed by cell cycle aberration such as p16 overexpression related to the G1-S phase.

Carcinoma, Squamous Cell↗