Evidence map›Paper›PMID 21075310›Full record

ArticleCancer cell2010

Oncogenic KRas suppresses inflammation-associated senescence of pancreatic ductal cells.

Kyoung Eun Lee, Dafna Bar-Sagi

Open access · bronzeAbstract read
In one paragraph

Article in Cancer cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

79 citing papers in PubMed, 127 citations in OpenAlex.

  1. Article
  2. KRAS Withdrawal in Cholangiocarcinoma Leads to Immune Infiltration and Tumor Regression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Article
  4. MultiplexedbioRxiv : the preprint server for biology · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Frontiers in cell and developmental biology · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Cancer-Mediated Muscle Cachexia: Etiology and Clinical Management.Trends in endocrinology and metabolism: TEM · 2021
    Review
  18. Review
  19. Inactivation of the Euchromatic Histone-LysineFrontiers in cell and developmental biology · 2021
    Article
  20. Review

19 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Kyoung Eun LeeCell and Molecular Biology Program, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA.
Dafna Bar-Sagi
New York University · US

Funding

MECHANISMS OF SIGNAL TRANSDUCTION BY RAS PROTEINSR37CA055360 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI BAR-SAGI, DAFNA · 2001 to 2008
$3.4M
MECHANISMS OF SIGNAL TRANSDUCTION BY RAS PROTEINSR01CA055360 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI BAR-SAGI, DAFNA · 1991 to 2015
$2.6M
Mechanisms of Signal Transduction by Ras ProteinsR56CA055360 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BAR-SAGI, DAFNA · 2009 to 2009
$484k
NCI NIH HHS CA055360NCI NIH HHS R01 CA055360NCI NIH HHS R37 CA055360NCI NIH HHS R56 CA055360
6 · The paper itself

Abstract

Mutational activation of KRas is the first and most frequently detected genetic lesion in pancreatic ductal adenocarcinoma (PDAC). However, the precise role of oncogenic KRas in the pathogenesis of PDAC is not fully understood. Here, we report that the endogenous expression of oncogenic KRas suppresses premature senescence in primary pancreatic duct epithelial cells (PDEC). Oncogenic KRas-mediated senescence bypass is conferred by the upregulation of the basic helix-loop-helix transcription factor Twist that in turn abrogates p16(INK4A) induction. Moreover, the KRas-Twist-p16(INK4A) senescence bypass pathway is employed in vivo to prevent inflammation-associated senescence of pancreatic ductal epithelium. Our findings indicate that oncogenic KRas could contribute to PDAC initiation by protecting cells from entering a state of permanent growth arrest.

Indexed as

Animalsbeta-GalactosidaseCarcinoma, Pancreatic DuctalCell ProliferationCells, CulturedCellular SenescenceCyclin-Dependent Kinase Inhibitor p16MiceNuclear ProteinsPancreatic DuctsPancreatic NeoplasmsPancreatitisProto-Oncogene Proteins p21(ras)RNA, MessengerTumor Suppressor Protein p53Twist-Related Protein 1beta-GalactosidaseCyclin-Dependent Kinase Inhibitor p16Hras protein, mouseNuclear ProteinsProto-Oncogene Proteins p21(ras)RNA, MessengerTumor Suppressor Protein p53Twist1 protein, mouseTwist-Related Protein 1

Identifiers

PMID21075310
PMCPMC3397918
OpenAlexW2116602759

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.