ReviewThe Journal of pathology2014
Tumour suppressor gene function in carcinoma-associated fibroblasts: from tumour cells via EMT and back again?
Review in The Journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled 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.
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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- MARCKS contributes to stromal cancer-associated fibroblast activation and facilitates ovarian cancer metastasis.Oncotarget · 2016Pooled it
- Dissecting the multifaceted roles of autophagy in cancer initiation, growth, and metastasis: from molecular mechanisms to therapeutic applications.Medical oncology (Northwood, London, England) · 2024Review
- Elevated mRNA level indicates FSIP1 promotes EMT and gastric cancer progression by regulating fibroblasts in tumor microenvironment.Open medicine (Warsaw, Poland) · 2024Article
- Research status and prospects of pituitary adenomas in conjunction with neurological and psychiatric disorders and the tumor microenvironment.Frontiers in neuroscience · 2024Review
- Tumour microenvironment and pituitary tumour behaviour.Journal of endocrinological investigation · 2023Review
- The microenvironment of pituitary adenomas: biological, clinical and therapeutical implications.Pituitary · 2022Review
- Impact of the Tumor Microenvironment for Esophageal Tumor Development-An Opportunity for Prevention?Cancers · 2022Review
- Regulating tumor suppressor genes: post-translational modifications.Signal transduction and targeted therapy · 2020Review
- Suppression of Stromal Interferon Signaling by Human Papillomavirus 16.Journal of virology · 2019Article
- miR-425 suppresses EMT and the development of TNBC (triple-negative breast cancer) by targeting the TGF-β 1/SMAD 3 signaling pathway.RSC advances · 2018Article
- Inhibition of integrin αCell communication and signaling : CCS · 2018Article
- Article
- miR-1204 targets VDR to promotes epithelial-mesenchymal transition and metastasis in breast cancer.Oncogene · 2018Article
- GRO-α and IL-8 enhance ovarian cancer metastatic potential via the CXCR2-mediated TAK1/NFκB signaling cascade.Theranostics · 2018Article
- Article
- Article
- Autophagy in cancer metastasis.Oncogene · 2017Review
- Transcriptome-wide analysis of compression-induced microRNA expression alteration in breast cancer for mining therapeutic targets.Oncotarget · 2016Article
- The Interaction Between Human Papillomaviruses and the Stromal Microenvironment.Progress in molecular biology and translational science · 2016Review
- Molecular Characterization and Enhancement of Anticancer Activity of Caffeic Acid Phenethyl Ester by γ Cyclodextrin.Journal of Cancer · 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Recent reports indicate that inactivation of the RB, TP53 or PTEN tumour suppressor genes is detected in tumour stroma of oropharyngeal, breast and other human cancers. Mouse models have validated the tumour-promoting effects of deleting Rb, Pten or p53 in fibroblasts that converts them from normal fibroblasts to carcinoma associated fibroblasts (CAFs). The tumour-promoting activity of CAFs in these contexts was associated with increased paracrine signaling to tumour cells through production of specific growth factors, chemokines and MMPs by CAFs. The conversion of NOFs into CAFs through acquisition of specific mutations, such as loss of tumour suppressors, or deregulated expression of microRNAs or key epigenetic events, can clearly occur independently of genetic and epigenetic changes in tumour cells but an alternative source of CAFs that is being reconsidered is that CAFs derive from the tumour cells by EMT. Recent mouse models employing lineage-tracing techniques have suggested that this can take place in vivo and the extent to which this is relevant more broadly is discussed.
Indexed as
Identifiers
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.