ReviewCancer research2012
Microenvironmental regulation of epithelial-mesenchymal transitions in cancer.
Review in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 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
161 citing papers in PubMed, 1 synthesis or guideline pooled it, 301 citations in OpenAlex.
- Risk prediction for late-stage ovarian cancer by meta-analysis of 1525 patient samples.Journal of the National Cancer Institute · 2014Pooled it
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- Mesenchymal-epithelial transition reduces proliferation but increases immune evasion in tumor spheroids.iScience · 2025Article
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- Exploring the role of EMT in ovarian cancer progression using a multiscale mathematical model.NPJ systems biology and applications · 2025Article
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- Comparative Analysis of Transcription Factors TWIST2, GATA3, and HES5 in Glioblastoma Multiforme : Evaluating Biomarker Potential and Therapeutic Targets Using in Silico Methods.Journal of Korean Neurosurgical Society · 2025Article
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- PI3K/AKT pathway as a pivotal regulator of epithelial-mesenchymal transition in lung tumor cells.Cancer cell international · 2024Review
- Cancer-associated fibroblasts rewire the estrogen receptor response in luminal breast cancer, enabling estrogen independence.Oncogene · 2024Article
- Forces at play: exploring factors affecting the cancer metastasis.Frontiers in immunology · 2024Review
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- A Deep Learning Decision Support Tool to Improve Risk Stratification and Reduce Unnecessary Biopsies in BI-RADS 4 Mammograms.Radiology. Artificial intelligence · 2023Article
- Ferroptosis and EMT: key targets for combating cancer progression and therapy resistance.Cellular and molecular life sciences : CMLS · 2023Review
- Tumor-derived small extracellular vesicles promote breast cancer progression by upregulating PD-L1 expression in macrophages.Cancer cell international · 2023Article
- Hepatic stellate cell-released CXCL1 aggravates HCC malignant behaviors through the MIR4435-2HG/miR-506-3p/TGFB1 axis.Cancer science · 2023Article
101 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The evolution of the cancer cell into a metastatic entity is the major cause of death in patients with cancer. Activation of the epithelial-to-mesenchymal transition (EMT) endows invasive and metastatic properties upon cancer cells that favor successful colonization of distal target organs. The observation that in many cancers distant metastases resemble the epithelial phenotype of primary tumors has led to speculation that the disseminated tumor cells recruited to the target organs undergo mesenchymal-to-epithelial transition (MET). However, the MET cascade has not been recapitulated in vivo, and the cellular and molecular regulators that promote MET remain unknown. In a recent report, using a model of spontaneous breast cancer, we have shown that bone marrow-derived myeloid progenitor cells in the premetastatic lung secrete the proteoglycan versican, which induces MET of metastatic tumor cells and accelerates metastases. This review summarizes recent progress in MET research, outlines a unique paracrine cross-talk between the microenvironment and the cancer cells, which promotes tumor outgrowth in the metastatic organ, and discusses opportunities for novel antimetastatic approaches for cancer therapy.
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.