Evidence map›Paper›PMID 40766605›Full record

ArticlebioRxiv : the preprint server for biology2025

Uracil-DNA glycosylase deficiency is associated with repressed tumor cell-intrinsic inflammatory signaling and altered sensitivity to exogenous interferons.

Frank P Vendetti, Pinakin Pandya, Carina R Sclafani, Reyna E Jones, Daniel Ivanov, Robert W Sobol, Christopher J Bakkenist

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. 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

5 · Who and what money

Authors and funding

7 authors.

Frank P VendettiDepartment of Radiation Oncology, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Pinakin PandyaDepartment of Radiation Oncology, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Carina R SclafaniDepartment of Radiation Oncology, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Reyna E JonesDepartment of Radiation Oncology, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Daniel IvanovDepartment of Pathology and Laboratory Medicine, Warren Alpert Medical School & Legorreta Cancer Center, Brown University, Providence, RI.
Robert W SobolDepartment of Pathology and Laboratory Medicine, Warren Alpert Medical School & Legorreta Cancer Center, Brown University, Providence, RI.ORCID 0000-0001-7385-3563
Christopher J BakkenistDepartment of Radiation Oncology, University of Pittsburgh School of Medicine, Pittsburgh, PA.ORCID 0000-0001-9672-0886

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Leonard J. Appleman · 1988 to 2026
$158.0M
Research Project 3P01ES028949 · NIEHS · FLORIDA GULF COAST UNIVERSITY · PI PARSONS, MICHAEL, SOBOL, ROBERT W · 2018 to 2024
$3.8M
Novel approaches to enhance tumor cell cytotoxicity of alkylating agentsR01CA148629 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SOBOL, ROBERT W · 2010 to 2021
$3.4M
Investigating genetic ancestry influences on oral cavity and laryngeal cancer survival disparitiesR01CA238061 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI RAGIN, CAMILLE C., SOBOL, ROBERT W · 2019 to 2023
$3.4M
Measuring genomic DNA damage and DNA repair capacity in longitudinal population samples - a step towards precision preventionU01ES029518 · NIEHS · UNIVERSITY OF SOUTH ALABAMA · PI SOBOL, ROBERT W · 2018 to 2022
$2.7M
The Impact of ATR Kinase Inhibitors on CD8+ T Cell Expansion and Memory DevelopmentR01CA266172 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHRISTOPHER J. BAKKENIST · 2022 to 2026
$2.3M
Barcoded human cells engineered with heterozygous genetic diversity to uncover toxicodynamic variabilityR44ES032522 · NIEHS · AMELIA TECHNOLOGIES, LLC · PI GEORGE, JAY, SOBOL, ROBERT W · 2021 to 2023
$1.9M
DNA damage signaling to dormant origins of replicationR01CA236367 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BAKKENIST, CHRISTOPHER J. · 2020 to 2024
$1.8M
NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA148629NCI NIH HHS R01 CA236367NCI NIH HHS R01 CA238061NCI NIH HHS R01 CA266172NIEHS NIH HHS P01 ES028949NIEHS NIH HHS R44 ES032522NIEHS NIH HHS U01 ES029518
6 · The paper itself

Abstract

2'-deoxyuridine (dU) is a common DNA lesion resulting from cytosine deamination and from dUMP incorporation by DNA polymerases, both of which are prevalent in cancer. The primary mechanism that repairs dU lesions in genomic DNA is base excision repair initiated by Uracil-DNA Glycosylase 1 (UNG1). We generated

Indexed as

deoxyuridineglycosylasetumor microenvironmenttype-II interferontype-I interferonUNG

Identifiers

PMID40766605
PMCPMC12324335

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.