Evidence map›Paper›PMID 19714813›Full record

ArticleJournal of proteome research2009

Mucin glycosylation is altered by pro-inflammatory signaling in pancreatic-cancer cells.

Yi-Mi Wu, D David Nowack, Gilbert S Omenn, Brian B Haab

Open access · greenAbstract read
In one paragraph

Article in Journal of proteome research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. The Role of Mucins in Esophageal Inflammatory Diseases.Journal of personalized medicine · 2026
    Review
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  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Cancers · 2020
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Assessment of tumor characteristics based on glycoform analysis of membrane-tethered MUC1.Laboratory investigation; a journal of technical methods and pathology · 2017
    Article
  19. Glycoproteins and glycoproteomics in pancreatic cancer.World journal of gastroenterology · 2016
    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

4 authors at 2 institutions in 1 country.

Yi-Mi WuVan Andel Research Institute, Grand Rapids, Michigan 49503, USA.
D David Nowack
Gilbert S Omenn
Brian B Haab
Van Andel Institute · USAndrews University · US

Funding

Defining Secreted Glycan Alterations in Pancreatic CancerR33CA122890 · NCI · VAN ANDEL RESEARCH INSTITUTE · PI HAAB, BRIAN B. · 2008 to 2010
$894k
Defining Secreted Glycan Alterations in Pancreatic CancerR21CA122890 · NCI · VAN ANDEL RESEARCH INSTITUTE · PI HAAB, BRIAN B. · 2006 to 2006
$325k
Induced Glycan Alterations in Sub-populations of Pancreatic TumorsR03CA139225 · NCI · VAN ANDEL RESEARCH INSTITUTE · PI HAAB, BRIAN B. · 2009 to 2010
$182k
NCI NIH HHS R03 CA139225NCI NIH HHS R21 CA122890NCI NIH HHS R33 CA122890
6 · The paper itself

Abstract

Altered glycosylation on the surfaces or secreted proteins of tumor cells is common in pancreatic cancer and is thought to promote cancer progression, but the factors leading to the changes in carbohydrate structures are incompletely understood. We hypothesized that pro-inflammatory conditions can lead to alterations in cancer-associated glycans on mucins produced by pancreatic-cancer cells. With the use of a novel antibody-glycan microarray method, we measured the effects of pro-inflammatory stimuli (oxidative stress and treatment with the cytokines IFNgamma, IL-1alpha, and TNFalpha) on the expression and glycosylation of the mucins MUC1, MUC5AC, and MUC16 in multiple pancreatic cancer cell lines. Mucin glycosylation was significantly affected in specific cell lines, particularly in structures involving terminal galactose or N-acetylgalactosamine. In addition, the responses of the cell lines grouped according to the expression of cell-surface markers that are associated with tumorigenicity, as cell lines bearing minimal surface markers, showed evidence of increased O-glycan extension and decreased presentation of terminal beta1,4-linked galactose, opposite to cell lines bearing multiple markers. These results suggest mechanisms whereby inflammation might influence tumor behavior in a cell-type specific manner through modulating the presentation of cancer-associated glycans.

Indexed as

Cell Line, TumorCell MembraneCytokinesGlycosylationHumansInflammationMucinsOxidative StressPancreatic NeoplasmsSignal TransductionCytokinesMucins

Identifiers

PMID19714813
PMCPMC2893235
OpenAlexW1991268162

What OpenQuestion holds

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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.