Evidence map›Paper›PMID 21594579›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2011

Novel ARF/p53-independent senescence pathways in cancer repression.

Chia-Hsin Chan, Yuan Gao, Asad Moten, Hui-Kuan Lin

Abstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Nutrients · 2026
    Article
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  6. Review
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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.

Chia-Hsin ChanDepartment of Molecular and Cellular Oncology, The University of Texas, MD Anderson Cancer Center, Houston, TX 77030, USA.
Yuan Gao
Asad Moten
Hui-Kuan Lin

Funding

Regulation of Akt signaling activation by polyubiquitinationR01CA149321 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LIN, HUI-KUAN · 2010 to 2014
$1.6M
The crosstalk between the PI3K/Akt signal and Skp2 in prostate cancer progressionR01CA136787 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LIN, HUI-KUAN · 2010 to 2014
$1.6M
NCI NIH HHS R01 CA136787NCI NIH HHS R01CA136787-01A2NCI NIH HHS R01 CA149321NCI NIH HHS R01CA149321-01
6 · The paper itself

Abstract

Cellular senescence, which can be induced by various stimuli, is a stress response that manifests as irreversible cell cycle arrest. Recent studies have revealed that cellular senescence can serve as a critical barrier for cancer development. Induction of cellular senescence by oncogenic insults, such as Ras overexpression or by inactivation of PTEN tumor suppressor, triggers an ARF/p53-dependent tumor-suppressive effect which can significantly restrict cancer progression. Given the important role of the ARF/p53 pathway in cellular senescence and tumor suppression, drugs that stabilize p53 expression have been developed and tested in clinical trials. However, a major hurdle for p53 targeting in cancer treatment arises from the frequent deficiency or mutation of ARF or p53 in human cancers, which, in turn, profoundly compromises their tumor-suppressive ability. Recent discoveries of novel regulators involved in ARF/p53-independent cellular senescence not only reveal novel paradigms for cellular senescence but also provide alternative approaches for cancer therapy.

Indexed as

ADP-Ribosylation FactorsAnimalsCellular SenescenceHumansNeoplasmsSignal TransductionTumor Suppressor Protein p53ADP-Ribosylation FactorsTumor Suppressor Protein p53

Identifiers

PMID21594579
PMCPMC3296232

What OpenQuestion holds

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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.