ReviewNature reviews. Cancer2012
To differentiate or not--routes towards metastasis.
Review in Nature reviews. Cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 372 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
372 citing papers in PubMed, 1 synthesis or guideline pooled it, 624 citations in OpenAlex.
- Guidelines and definitions for research on epithelial-mesenchymal transition.Nature reviews. Molecular cell biology · 2020Guideline
- Entinostat, a class I selective histone deacetylase inhibitor, plus exemestane for Chinese patients with hormone receptor-positive advanced breast cancer: A multicenter, randomized, double-blind, placebo-controlled, phase 3 trial.Acta pharmaceutica Sinica. B · 2023Trial
- Article
- Antitumor effect of dipyridamole mediated by inhibiting the interaction between platelets and tumor cells.Discover oncology · 2026Review
- miRNA-lncRNA Cross-Regulation Landscape in Cancer: From Molecular Mechanisms to Therapeutic and Diagnostic Applications.Cancers · 2026Review
- Hyperglycaemia-Induced Metabolic Stress Promotes EMT-Driven Therapeutic Resistance in Cancer: Evidence of a Deleterious Feed-Forward Cycle.Pharmaceuticals (Basel, Switzerland) · 2026Review
- The Anti-EMMPRIN Monoclonal Antibody hMR18-mAb Induces Tumor Dormancy and Inhibits the EMT Process in Human Carcinoma Cell Lines Co-Cultured with Macrophages.Biomedicines · 2025Article
- RBMX2 linkseLife · 2025Article
- Clinical applications of circulating tumor cells in metastasis and therapy.Journal of hematology & oncology · 2025Review
- Vimentin intermediate filaments as structural and mechanical coordinators of mesenchymal cells.Nature cell biology · 2025Review
- Epithelial-to-mesenchymal transition (EMT) and cancer metastasis: the status quo of methods and experimental models 2025.Molecular cancer · 2025Review
- The invadosome of stem-like cancer cells: metastasis machinery and targetable vulnerability.Cancer metastasis reviews · 2025Review
- A potential therapeutic molecule target: lncRNA AK023507 inhibits the metastasis of breast cancer by regulating the WNT/DOCK4/β-catenin axis.Breast cancer research and treatment · 2025Article
- Molecular Mechanisms Regulating Epithelial Mesenchymal Transition (EMT) to Promote Cancer Progression.International journal of molecular sciences · 2025Review
- Circulating tumor cells share RNA modules with early embryo trophectoderm and with metastatic cancer.Cancer communications (London, England) · 2025Article
- Effects ofMarine drugs · 2025Article
- Hypoxia-induced MIR31HG expression promotes partial EMT and basal-like phenotype in pancreatic ductal adenocarcinoma based on data mining and experimental analyses.Journal of translational medicine · 2025Article
- Design of an In Vitro Model for Epithelial-to-Mesenchymal Transition in Gastric Cancer.Biochemical genetics · 2025Article
- Emerging roles of CircRNA-miRNA networks in cancer development and therapeutic response.Non-coding RNA research · 2025Review
- Inhibition of CHI3L1 decreases N-cadherin and VCAM-1 levels in glioblastoma.Pharmacological reports : PR · 2025Article
312 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Why are many metastases differentiated? Invading and disseminating carcinoma cells can undergo an epithelial-mesenchymal transition (EMT), which is associated with a gain of stem cell-like behaviour. Therefore, EMT has been linked to the cancer stem cell concept. However, it is a matter of debate how subsequent mesenchymal-epithelial transition (MET) fits into the metastatic process and whether a MET is essential. In this Opinion article, I propose two principle types of metastatic progression: phenotypic plasticity involving transient EMT-MET processes and intrinsic genetic alterations keeping cells in an EMT and stemness state. This simplified classification integrates clinically relevant aspects of dormancy, metastatic tropism and therapy resistance, and implies perspectives on treatment strategies against metastasis.
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.