Evidence map›Paper›PMID 22984426›Full record

ArticlePloS one2012

Unlike pancreatic cancer cells pancreatic cancer associated fibroblasts display minimal gene induction after 5-aza-2'-deoxycytidine.

Jun Yu, Kimberly Walter, Noriyuki Omura, Seung-Mo Hong, Angela Young, Ang Li, Audrey Vincent, Michael Goggins

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 24% of its field
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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Epigenetic regulation of cancer-associated fibroblast heterogeneity.Biochimica et biophysica acta. Reviews on cancer · 2023
    Review
  5. Article
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  10. Article
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  12. Stromal-derived interleukin 6 drives epithelial-to-mesenchymal transition and therapy resistance in esophageal adenocarcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  13. Review
  14. Article
  15. DNA methylation in the tumor microenvironment.Journal of Zhejiang University. Science. B · 2017
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review
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

8 authors at 2 institutions in 1 country.

Jun YuDepartment of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The John Hopkins Medical Institutions, Baltimore, Maryland, United States of America.
Kimberly Walter
Noriyuki Omura
Seung-Mo Hong
Angela Young
Ang Li
Audrey Vincent
Michael Goggins
Johns Hopkins University · USCancer Research Center · US

Funding

Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI LENNON, ANNE MARIE · 1993 to 2022
$54.6M
CCR NIH HHS RC2148346NCI NIH HHS CA62924NCI NIH HHS P50 CA062924
6 · The paper itself

Abstract

purposeCancer associated stromal fibroblasts (CAFs) undergo transcriptional and phenotypic changes that contribute to tumor progression, but the mechanisms responsible for these changes are not well understood. Aberrant DNA methylation is an important cause of transcriptional alterations in cancer cells but it is not known how important DNA methylation alterations are to CAF behavior. EXPERIMENTAL

designWe used Affymetrix exon arrays to compare genes induced by the DNA methylation inhibitor 5-aza-dC in cultured pancreatic cancer associated fibroblasts, pancreatic control fibroblasts and pancreatic cancer cell lines.

resultsWe found that pancreatic CAFs and control pancreatic fibroblasts were less responsive to 5-aza-dC-mediated gene reactivation than pancreatic cancer cells (mean+/-SD of genes induced ≥ 5-fold was 9 ± 10 genes in 10 pancreatic CAF cultures, 17 ± 14 genes in 3 control pancreatic fibroblast cultures, and 134 ± 85 genes in 4 pancreatic cancer cell lines). We examined differentially expressed genes between CAFs and control fibroblasts for candidate methylated genes and identified the disintegrin and metalloprotease, ADAM12 as hypomethylated and overexpressed in pancreatic CAF lines and overexpressed in fibroblasts adjacent to primary pancreatic adenocarcinomas.

conclusionsCompared to pancreatic cancer cells, few genes are reactivated by DNMT1 inhibition in pancreatic CAFs suggesting these cells do not harbor many functionally important alterations in DNA methylation. CAFs may also not be very responsive to therapeutic targeting with DNA methylation inhibitors.

Indexed as

ADAM12 ProteinADAM ProteinsAzacitidineBase SequenceBlotting, WesternCell Line, TumorDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesFemaleFibroblastsGene Expression Regulation, NeoplasticGenes, NeoplasmGenetic Association StudiesHumansImmunohistochemistryMaleADAM12 ProteinADAM12 protein, humanADAM ProteinsAzacitidineDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNMT1 protein, humanMembrane ProteinsRNA, Messenger

Identifiers

PMID22984426
PMCPMC3439436
OpenAlexW2036217528

What OpenQuestion holds

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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.