ReviewSeminars in cell & developmental biology2010
Involvement of stromal p53 in tumor-stroma interactions.
Review in Seminars in cell & developmental biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 43 citations in OpenAlex.
- Stromal fibroblastic mutant Trp53 promotes mammary tumor development via enhanced secretion of paracrine factors.NPJ breast cancer · 2025Article
- Advances in Anti-Cancer Activities of Flavonoids inInternational journal of molecular sciences · 2022Review
- Predicting clinical outcomes of cancer patients with a p53 deficiency gene signature.Scientific reports · 2022Article
- Immunotherapy response modeling by ex-vivo organ culture for lung cancer.Cancer immunology, immunotherapy : CII · 2021Article
- Depletion of Trp53 and Cdkn2a Does Not Promote Self-Renewal in the Mammary Gland but Amplifies Proliferation Induced by TNF-α.Stem cell reports · 2021Article
- Dysregulation of lysophospholipid signaling by p53 in malignant cells and the tumor microenvironment.Cellular signalling · 2021Review
- A Different Facet of p53 Function: Regulation of Immunity and Inflammation During Tumor Development.Frontiers in cell and developmental biology · 2021Review
- Loss of p53 in mesenchymal stem cells promotes alteration of bone remodeling through negative regulation of osteoprotegerin.Cell death and differentiation · 2021Article
- Exosomal microRNAs derived from colon cancer cells promote tumor progression by suppressing fibroblast TP53 expression.Cancer science · 2019Article
- A ZEB1/p53 signaling axis in stromal fibroblasts promotes mammary epithelial tumours.Nature communications · 2019Article
- Mutant p53-a potential player in shaping the tumor-stroma crosstalk.Journal of molecular cell biology · 2019Review
- Paracrine Induction of Epithelial-Mesenchymal Transition Between Colorectal Cancer Cells and its Suppression by a p53/miR-192/215/NID1 Axis.Cellular and molecular gastroenterology and hepatology · 2019Article
- Androgen receptor functions as transcriptional repressor of cancer-associated fibroblast activation.The Journal of clinical investigation · 2018Article
- The evolving relationship of wound healing and tumor stroma.JCI insight · 2018Review
- p53-Autophagy-Metastasis Link.Cancers · 2018Review
- Multiplexed Electrochemical Immunosensors for Clinical Biomarkers.Sensors (Basel, Switzerland) · 2017Review
- Therapeutic strategies of drug repositioning targeting autophagy to induce cancer cell death: from pathophysiology to treatment.Journal of hematology & oncology · 2017Review
- Reversible p53 inhibition prevents cisplatin ototoxicity without blocking chemotherapeutic efficacy.EMBO molecular medicine · 2017Article
- Reprogramming pancreatic stellate cells via p53 activation: A putative target for pancreatic cancer therapy.PloS one · 2017Article
- Novel p53 target genes secreted by the liver are involved in non-cell-autonomous regulation.Cell death and differentiation · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
p53 is a major tumor-suppressor gene, inactivated by mutations in about half of all human cancer cases, and probably incapacitated by other means in most other cases. Most research regarding the role of p53 in cancer has focused on its ability to elicit apoptosis or growth arrest of cells that are prone to become malignant owing to DNA damage or oncogene activation, i.e. cell-autonomous activities of p53. However, p53 activation within a cell can also exert a variety of effects upon neighboring cells, through secreted factors and paracrine and endocrine mechanisms. Of note, p53 within cancer stromal cells can inhibit tumor growth and malignant progression. Cancer cells that evolve under this inhibitory influence acquire mechanisms to silence stromal p53, either by direct inhibition of p53 within stromal cells, or through pressure for selection of stromal cells with compromised p53 function. Hence, activation of stromal p53 by chemotherapy or radiotherapy might be part of the mechanisms by which these treatments cause cancer regression. However, in certain circumstances, activation of stromal p53 by cytotoxic anti-cancer agents might actually promote treatment resistance, probably through stromal p53-mediated growth arrest of the cancer cells or through protection of the tumor vasculature. Better understanding of the underlying molecular mechanisms is thus required. Hopefully, this will allow their manipulation towards better inhibition of cancer initiation, progression and metastasis.
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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.