Evidence map›Paper›PMID 24411464›Full record

ReviewBMB reports2014

Exploiting tumor cell senescence in anticancer therapy.

Minyoung Lee, Jae-Seon Lee

Open access · goldAbstract readReview
In one paragraph

Review in BMB reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed, 85 citations in OpenAlex.

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  15. Ultra-high dose-rate proton FLASH improves tumor control.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2023
    Article
  16. Review
  17. Tumor treating fields induced senescence on glioblastoma.American journal of cancer research · 2023
    Article
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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

2 authors at 1 institution in 1 country.

Minyoung LeeResearch Center for Radio-senescence, Korea Institute of Radiological and Medical Sciences, Seoul 139-706, Korea.
Jae-Seon LeeResearch Center for Radio-senescence, Korea Institute of Radiological and Medical Sciences, Seoul 139-706, Korea; Department of Biomedical Sciences, College of Medicine, Inha University, Incheon 400-712, Korea.
Korea Institute of Radiological and Medical Sciences · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is a physiological process of irreversible cell-cycle arrest that contributes to various physiological and pathological processes of aging. Whereas replicative senescence is associated with telomere attrition after repeated cell division, stress-induced premature senescence occurs in response to aberrant oncogenic signaling, oxidative stress, and DNA damage which is independent of telomere dysfunction. Recent evidence indicates that cellular senescence provides a barrier to tumorigenesis and is a determinant of the outcome of cancer treatment. However, the senescence-associated secretory phenotype, which contributes to multiple facets of senescent cancer cells, may influence both cancer-inhibitory and cancer-promoting mechanisms of neighboring cells. Conventional treatments, such as chemo- and radiotherapies, preferentially induce premature senescence instead of apoptosis in the appropriate cellular context. In addition, treatment-induced premature senescence could compensate for resistance to apoptosis via alternative signaling pathways. Therefore, we believe that an intensive effort to understand cancer cell senescence could facilitate the development of novel therapeutic strategies for improving the efficacy of anticancer therapies. This review summarizes the current understanding of molecular mechanisms, functions, and clinical applications of cellular senescence for anticancer therapy.

Indexed as

Cellular SenescenceAntineoplastic AgentsHumansNeoplasmsOxidative StressSignal TransductionAntineoplastic Agents

Identifiers

PMID24411464
PMCPMC4163898
OpenAlexW2074053811

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.