PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 8669186

Sample size calculations for rescreening cytologic smears.

G K Nagy·D N Collins·T A Wilson
View original source ↗Export metadata ↓

Abstract

OBJECTIVE: To describe a method of calculating sample size if rescreening of cytologic material becomes necessary for legal or other reasons. The number of specimens to be reexamined must be large enough to provide adequate confidence in the results and small enough to minimize the cost of investigation. CONCLUSION: Except under very unusual conditions, the sample size is larger than generally thought.

Explore related subjects

Cell BiologyClinical Laboratory TechniquesData Interpretation, StatisticalFalse Negative ReactionsFemaleHumansMass ScreeningQuality ControlSample SizeSpecimen HandlingVaginal SmearsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

G K Nagy, D N Collins, T A Wilson. Sample size calculations for rescreening cytologic smears.. https://doi.org/10.1159/000333906

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

KEEP EXPLORING

Related citations

PubMed2025

MondoA mediates transcriptional coordination between the MYC network and the integrated stress response in pancreatic ductal adenocarcinoma.

MYC amplification contributes to poor survival and outcome in pancreatic ductal adenocarcinoma (PDAC). Here we show that in PDAC cell lines with amplified MYC, MondoA is required for viability, facilitating proliferation while suppressing apoptosis in vitro and in vivo. Transcriptional and genomic profiling demonstrates that loss of MondoA leads to altered expression of direct MondoA targets as well as MYC target genes and is accompanied by shifts in genomic occupancy of MYC, MNT, and the MondoA paralog ChREBP. This altered genomic binding by MYC network members is associated with transcriptional perturbation of multiple metabolic and stress pathways, as well as global changes in N6-methyladenosine modification (m6A) of mRNA. MondoA inhibition disrupts coordination between MYC network members and the Integrated Stress Response (ISR), resulting in decreased translation of ATF4 mRNA, discordant gene regulation of shared targets of MYC and ATF4 and, ultimately, apoptosis. Re-establishing ATF4 protein expression rescues the diminished viability due to loss of MondoA expression or activity, providing direct evidence of a link between deregulated MYC and the transcriptional machinery of the ISR. Lastly, we find that small-molecule inhibition of MondoA is lethal in a subset of PDAC cell lines, including patient-derived organoids, suggesting that the ability to target MYC via chemical inhibition of MondoA transcriptional activity may have broad efficacy.

Cell Biology↗