Evidence map›Paper›PMID 37131652›Full record

ArticlebioRxiv : the preprint server for biology2023

Suprabasal cells retaining stem cell identity programs drive basal cell hyperplasia in eosinophilic esophagitis.

Margarette H Clevenger, Adam L Karami, Dustin A Carlson, Peter J Kahrilas, Nirmala Gonsalves, John E Pandolfino, Deborah R Winter, Kelly A Whelan, Marie-Pier Tétreault

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. 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, 3 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Margarette H ClevengerDepartment of Medicine, Gastroenterology and Hepatology Division, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611-3010, USA.
Adam L KaramiFels Cancer Institute for Personalized Medicine, Temple University Lewis Katz School of Medicine, Philadelphia, PA, USA.
Dustin A CarlsonDepartment of Medicine, Gastroenterology and Hepatology Division, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611-3010, USA.
Peter J KahrilasDepartment of Medicine, Gastroenterology and Hepatology Division, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611-3010, USA.
Nirmala GonsalvesDepartment of Medicine, Gastroenterology and Hepatology Division, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611-3010, USA.
John E PandolfinoDepartment of Medicine, Gastroenterology and Hepatology Division, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611-3010, USA.
Deborah R WinterDepartment of Medicine, Rheumatology Division, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611-3010, USA.
Kelly A WhelanFels Cancer Institute for Personalized Medicine, Temple University Lewis Katz School of Medicine, Philadelphia, PA, USA.
Marie-Pier TétreaultDepartment of Medicine, Gastroenterology and Hepatology Division, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611-3010, USA.
Northwestern University · USTemple University · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LEONIDAS C. PLATANIAS · 1993 to 2026
$153.9M
Investigating the role of mitochondria in Eosinophilic Esophagitis pathogenesis.R01DK121159 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WHELAN, KELLY A · 2019 to 2023
$2.4M
Alternative Mechanisms of Monocyte Transendothelial Migration in InflammationF31HL147413 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CLEVENGER, MARGARETTE HELEN · 2019 to 2024
$211k
The 10x Chromium System for High-Throughput Single Cell GenomicsS10OD025120 · OD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WANG, XINKUN · 2019 to 2019
$79k
NCI NIH HHS P30 CA060553NHLBI NIH HHS F31 HL147413NIDDK NIH HHS R01 DK121159NIH HHS S10 OD025120
6 · The paper itself

Abstract

Eosinophilic esophagitis (EoE) is an esophageal immune-mediated disease characterized by eosinophilic inflammation and epithelial remodeling, including basal cell hyperplasia (BCH) and loss of differentiation. Although BCH correlates with disease severity and with persistent symptoms in patients in histological remission, the molecular processes driving BCH remain poorly defined. Here, we demonstrate that despite the presence of BCH in all EoE patients examined, no increase in basal cell proportion was observed by scRNA-seq. Instead, EoE patients exhibited a reduced pool of

Identifiers

PMID37131652
PMCPMC10153277
OpenAlexW4366772442

What OpenQuestion holds

Textmetadata
LicenceCC BY-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.