Evidence map›Paper›PMID 36522745›Full record

ReviewCell & bioscience2022

Distinct mechanisms mediating therapy-induced cellular senescence in prostate cancer.

Julia Kallenbach, Golnaz Atri Roozbahani, Mehdi Heidari Horestani, Aria Baniahmad

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.8field-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

33 citing papers in PubMed, 49 citations in OpenAlex.

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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 at 1 institution in 1 country.

Julia Kallenbach *Institute of Human Genetics, Jena University Hospital, Friedrich Schiller University, Am Klinikum 1, 07740, Jena, Germany.
Golnaz Atri Roozbahani *Institute of Human Genetics, Jena University Hospital, Friedrich Schiller University, Am Klinikum 1, 07740, Jena, Germany.
Mehdi Heidari Horestani *Institute of Human Genetics, Jena University Hospital, Friedrich Schiller University, Am Klinikum 1, 07740, Jena, Germany.
Aria BaniahmadInstitute of Human Genetics, Jena University Hospital, Friedrich Schiller University, Am Klinikum 1, 07740, Jena, Germany. aria.baniahmad@med.uni-jena.de.ORCID http://orcid.org/0000-0003-1085-9161
Jena University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProstate cancer (PCa) is an age-related malignancy in men with a high incidence rate. PCa treatments face many obstacles due to cancer cell resistance and many bypassing mechanisms to escape therapy. According to the intricacy of PCa, many standard therapies are being used depending on PCa stages including radical prostatectomy, radiation therapy, androgen receptor (AR) targeted therapy (androgen deprivation therapy, supraphysiological androgen, and AR antagonists) and chemotherapy. Most of the aforementioned therapies have been implicated to induce cellular senescence. Cellular senescence is defined as a stable cell cycle arrest in the G1 phase and is one of the mechanisms that prevent cancer proliferation.

resultsIn this review, we provide and analyze different mechanisms of therapy-induced senescence (TIS) in PCa and their effects on the tumor. Interestingly, it seems that different molecular pathways are used by cancer cells for TIS. Understanding the complexity and underlying mechanisms of cellular senescence is very critical due to its role in tumorigenesis. The most prevalent analyzed pathways in PCa as TIS are the p53/p21

conclusionThus, dependent on the type of senescence inducer and the specific senescence-induced cellular pathway, it is useful to develop pathway-specific senolytic compounds to specifically targeting senescent cells in order to evict senescent cells and thereby to reduce SASP side effects.

Indexed as

Androgen receptorCancer cell senescenceChemotherapyExosomeProstate cancerRadiotherapySenescence-associated secretory phenotype

Identifiers

PMID36522745
PMCPMC9753376
OpenAlexW4311860591

What OpenQuestion holds

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LicenceCC BY
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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.