Evidence map›Paper›PMID 39112965›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

Stellate cells are in utero markers of pancreatic disease in cystic fibrosis.

Shih-Hsing Leir, Svyatoslav Tkachenko, Alekh Paranjapye, Frederick Meckler, Arnaud J Van Wettere, Jenny L Kerschner, Elizabeth Kuznetsov, Makayla Schacht, Pulak Gillurkar, Misha Regouski and 7 more

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. 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. Cellular imbalance in proximal and distal lung of CFTRMolecular medicine (Cambridge, Mass.) · 2025
    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

17 authors.

Shih-Hsing LeirDepartment of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, 44106-4955, USA.ORCID 0000-0001-9524-3379
Svyatoslav TkachenkoDepartment of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, 44106-4955, USA.
Alekh ParanjapyeDepartment of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, 44106-4955, USA.
Frederick MecklerDepartment of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, 44106-4955, USA.
Arnaud J Van WettereDepartment of Animal, Dairy and Veterinary Sciences, Utah State University, Logan, UT, USA.
Jenny L KerschnerDepartment of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, 44106-4955, USA.
Elizabeth KuznetsovDepartment of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, 44106-4955, USA.
Makayla SchachtDepartment of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, 44106-4955, USA.
Pulak GillurkarDepartment of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, 44106-4955, USA.
Misha RegouskiDepartment of Animal, Dairy and Veterinary Sciences, Utah State University, Logan, UT, USA.
Iuri Viotti PerisseDepartment of Animal, Dairy and Veterinary Sciences, Utah State University, Logan, UT, USA.
Cheyenne M MarriottDepartment of Animal, Dairy and Veterinary Sciences, Utah State University, Logan, UT, USA.
Ying LiuDepartment of Animal, Dairy and Veterinary Sciences, Utah State University, Logan, UT, USA.
Ian BundersonDepartment of Animal, Dairy and Veterinary Sciences, Utah State University, Logan, UT, USA.
Kenneth L WhiteDepartment of Animal, Dairy and Veterinary Sciences, Utah State University, Logan, UT, USA.
Irina A PolejaevaDepartment of Animal, Dairy and Veterinary Sciences, Utah State University, Logan, UT, USA.ORCID 0000-0002-0858-5889
Ann HarrisDepartment of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, 44106-4955, USA. ann.harris@case.edu.ORCID 0000-0002-6541-2546

Funding

Translational Research Training Program in Environmental Health SciencesT32ES019851 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI Kara A Bernstein, Trevor M Penning · 2012 to 2026
$6.0M
Tumor-barcoding coupled with high-throughput sequencing for quantitative radiogenomics of the abscopal response in NSCLCR01CA271540 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Phuoc T. Tran · 2023 to 2026
$2.3M
Quantifying the sources and dynamics of tumor growth variability using Tuba-seqR00CA226506 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MCFARLAND, CHRISTOPHER DENNIS · 2021 to 2023
$747k
Cystic Fibrosis Foundation HARRIS21G0Cystic Fibrosis Foundation Harris 23P0Cystic Fibrosis Foundation LEIR21G0Cystic Fibrosis Foundation POLEJA18G0NCI NIH HHS R00 CA226506NCI NIH HHS R00CA226506NCI NIH HHS R01 CA271540NCI NIH HHS R01CA271540NIEHS NIH HHS T32 ES019851US Department of Agriculture Multistate Project W-4171Utah Agricultural Experiment Station Project 1343
6 · The paper itself

Abstract

backgroundPancreatic fibrosis is an early diagnostic feature of the common inherited disorder cystic fibrosis (CF). Many people with CF (pwCF) are pancreatic insufficient from birth and the replacement of acinar tissue with cystic lesions and fibrosis is a progressive phenotype that may later lead to diabetes. Little is known about the initiating events in the fibrotic process though it may be a sequela of inflammation in the pancreatic ducts resulting from loss of CFTR impairing normal fluid secretion. Here we use a sheep model of CF (CFTR

methodsFetal pancreas was collected at six time points from 50-days of gestation through to term, which is equivalent to ~ 13 weeks to term in human. RNA was extracted from tissue for bulk RNA-seq and single cells were prepared from 80-day, 120-day and term samples for scRNA-seq. Data were validated by immunochemistry.

resultsTranscriptomic evidence from bulk RNA-seq showed alterations in the CFTR

conclusionThe transcriptomic changes and cellular imbalance that we observe likely have pivotal roles in the evolution of CF pancreatic disease and may provide therapeutic opportunities to delay or prevent pancreatic destruction in CF.

Indexed as

BiomarkersCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorDisease Models, AnimalPancreatic Stellate CellsAnimalsFemaleGene Expression ProfilingHumansPancreasPancreatic DiseasesPregnancySheepTranscriptomeBiomarkersCystic Fibrosis Transmembrane Conductance RegulatorCFTRCystic fibrosis (CF)In utero developmentPancreatic diseaseSingle-cell RNA-seqStellate cells

Identifiers

PMID39112965
PMCPMC11304907

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Registered trials

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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.