Evidence map›Paper›PMID 23207606›Full record

ReviewMinerva gastroenterologica e dietologica2012

Discovering the route from inflammation to pancreatic cancer.

N Momi, S Kaur, S R Krishn, S K Batra

Abstract readReview
In one paragraph

Review in Minerva gastroenterologica e dietologica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.4field-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

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Modeling pancreatic cancer in mice for experimental therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2021
    Review
  8. Inactivation of the Euchromatic Histone-LysineFrontiers in cell and developmental biology · 2021
    Article
  9. Article
  10. Article
  11. Observational
  12. Review
  13. Article
  14. Article
  15. Review
  16. Orthotopic inflammation-related pancreatic carcinogenesis in a wild-type mouse induced by combined application of caerulein and dimethylbenzanthracene.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  17. Review
  18. Article
  19. Article
  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 1 institution in 1 country.

N MomiDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA.
S Kaur
S R Krishn
S K Batra
University of Nebraska Medical Center · US

Funding

Tissue CoreP50CA127297 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI HOLLINGSWORTH, MICHAEL A. · 2008 to 2018
$17.1M
Early Diagnosis of Pancreatic CancerU01CA111294 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BATRA, SURINDER K., HOLLINGSWORTH, MICHAEL A. · 2004 to 2015
$7.1M
Role of N-Cadherin in Pancreatic Tumor MicroenvironmentU54CA163120 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI HOLLINGSWORTH, MICHAEL A. · 2011 to 2015
$4.2M
MOLECULAR STUDIES ON MUC4 MUCIN GENER01CA078590 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BATRA, SURINDER K. · 1998 to 2011
$2.5M
Smoking and pancreatic cancerR01CA133774 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BATRA, SURINDER K. · 2008 to 2012
$1.8M
Molecular Markers for the Diagnosis of Pancreatic CancerR01CA131944 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BATRA, SURINDER K. · 2008 to 2012
$1.5M
NCI NIH HHS P50 CA127297NCI NIH HHS R01 CA078590NCI NIH HHS R01 CA131944NCI NIH HHS R01 CA133774NCI NIH HHS R01 CA78590NCI NIH HHS U01 CA111294NCI NIH HHS U54 CA163120
6 · The paper itself

Abstract

Pancreatic cancer (PC) remains a complex malignancy with the worst prognosis, lack of early diagnostic symptoms and resistance to conventional chemo- and radiotherapies. A better understanding of the etiology and early developmental events of PC requires profound attention. The evolution of fully blown PC from initial pancreatic injury is a multi-factorial phenomenon with a series of sequential events. The initial acute infection or tissue damage triggers inflammation that, in conjunction with innate immunity, establishes a state of homeostasis to limit harm to the body. Recurrent pancreatic injuries due to genetic susceptibility, smoking, unhealthy diet, and alcohol abuse induces a pro-inflammatory milieu, consisting of various types of immune cells, cytokines, chemokines, growth factors and restructured extracellular matrix, leading to prolonged inflammatory/chronic conditions. Cells having sustained DNA damage and/or mutagenic assault take advantage of this prolonged inflammatory response and aid in the initiation and development of neoplastic/fibrotic events. Eventually, many tumor-stromal interactions result in a chaotic environment accompanied by a loss of immune surveillance and repair response, thereby leading to PC. A better understanding of the inflammatory markers defining this "injury-inflammation-cancer" pathway would help to identify novel molecular targets for early screening and therapeutic intervention for this lethal malignancy.

Indexed as

Alcohol DrinkingBiomarkersBody Mass IndexChemokinesDiabetes ComplicationsEarly DiagnosisFeeding BehaviorHumansImmunity, InnateInflammationObesityPancreatic NeoplasmsPancreatitis, ChronicPrognosisReceptors, Vascular Endothelial Growth FactorRisk FactorsBiomarkersChemokinesReceptors, Vascular Endothelial Growth Factor

Identifiers

PMID23207606
PMCPMC3556910
OpenAlexW1847835333

What OpenQuestion holds

Textmetadata
LicenceTDM
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.