ArticleAging2019
The senescence-associated secretory phenotype (SASP) from mesenchymal stromal cells impairs growth of immortalized prostate cells but has no effect on metastatic prostatic cancer cells.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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.
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.
Who cites it
43 citing papers in PubMed, 57 citations in OpenAlex.
- Innovative niosome screening for efficient gene delivery in senescent primary umbilical cord stroma-derived MSCs.Drug delivery · 2026Article
- Single-cell immunoprofiling reveals a dysfunctional-like immune microenvironment and malignant phenotype in aging penile squamous cell carcinoma.Cell biology and toxicology · 2026Article
- Human adipose-derived mesenchymal stromal cells in vitro expansion for regenerative applications: tracking small genetic variants reveals dynamic changes within a genetically stable framework.Stem cell research & therapy · 2026Article
- Towards a personalized perspective on gliomas: an epigenetic-immuno-inflammatory aging framework.Frontiers in immunology · 2026Review
- Immunosenescence in prostate cancer: from aging-related immune dysfunction to therapeutic opportunities.Frontiers in immunology · 2026Review
- The controversial role of senescence-associated secretory phenotype (SASP) in cancer therapy.Molecular cancer · 2025Review
- Exploring TGF-β signaling in benign prostatic hyperplasia: from cellular senescence to fibrosis and therapeutic implications.Biogerontology · 2025Review
- Methods to Detect and Compare Cellular and Mitochondrial Changes in Senescent and Healthy Mesenchymal Stem Cells.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Cellular senescence in metastatic prostate cancer: A therapeutic opportunity or challenge (Review).Molecular medicine reports · 2024Review
- Cellular senescence and SASP in tumor progression and therapeutic opportunities.Molecular cancer · 2024Review
- Emerging roles for stromal cells in bone metastasis.Journal of bone oncology · 2024Article
- Therapy-induced secretion of spliceosomal components mediates pro-survival crosstalk between ovarian cancer cells.Nature communications · 2024Article
- Arctigenin fromAntioxidants (Basel, Switzerland) · 2024Article
- The senescence journey in cancer immunoediting.Molecular cancer · 2024Review
- Article
- Mesenchymal Stem Cells in the Pathogenesis and Therapy of Autoimmune and Autoinflammatory Diseases.International journal of molecular sciences · 2023Review
- An unbiased proteomics approach to identify the senescence-associated secretory phenotype of human bone marrow-derived mesenchymal stem cells.Bone reports · 2023Article
- Involvement of ACACA (acetyl-CoA carboxylase α) in the lung pre-metastatic niche formation in breast cancer by senescence phenotypic conversion in fibroblasts.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Phenotyping senescent mesenchymal stromal cells using AI image translation.Current research in biotechnology · 2023Article
- Senescence induces fundamental changes in the secretome of mesenchymal stromal cells (MSCs): implications for the therapeutic use of MSCs and their derivates.Frontiers in bioengineering and biotechnology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescent cells secrete inflammatory cytokines, proteases, and other factors, which are indicated as senescence-associated secretory phenotype (SASP). There are contrasting studies on the role of the SASP in cancer. Studies suggested that cancer cells may misuse the senescent secretome for their growth. Other investigations evidenced that the SASP may induce cancer growth arrest, senescence, or apoptosis. These conflicting data can be reconciled considering that cancer cells can coax senescent cells to secrete factors for their survival, thus abrogating the SASP's anti-cancer effect. Cancer stage may also have an impact on the capacity of the SASP to block tumor proliferation and promote senescence. Indeed, senescence is associated with a permanent cell cycle arrest, which needs functional cell cycle checkpoints. We evaluated the SASP effect on the
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What OpenQuestion holds
Registered trials
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.