V. Brunton
Oncology · 2005–2017
A researcher in the Science corpus: 5 papers; trusts 2 researchers and is trusted by 0 researchers here, as inferred from the citation graph.
Subfields
- Oncology — 58 citations into it
- Cell Biology — 33 citations into it
Whom V. Brunton trusts
Their strongest outbound trust, strongest first, inferred from their citations.
- R. Weinberg (in Oncology)
- Peter Friedl (in Cell Biology)
Papers from V. Brunton's perspective
Ordered by how strongly the researchers V. Brunton trusts endorse each paper. Same corpus, a different order for every researcher.
- The epithelial-mesenchymal transition generates cells with properties of stem cells. (Cell)
- Loss of E-cadherin promotes metastasis via multiple downstream transcriptional pathways. (Cancer Research)
- Migrating cancer stem cells — an integrated concept of malignant tumour progression (Nature Reviews. Cancer)
- The basics of epithelial-mesenchymal transition. (Journal of Clinical Investigation)
- Epithelial–mesenchymal transitions in tumour progression (Nature Reviews. Cancer)
- Prespecification and plasticity: shifting mechanisms of cell migration. (Current Opinion in Cell Biology)
- Collective cell migration in morphogenesis, regeneration and cancer
- FAK–Src signalling through paxillin, ERK and MLCK regulates adhesion disassembly (Nature Cell Biology)
- Reassessing epithelial to mesenchymal transition as a prerequisite for carcinoma invasion and metastasis. (Cancer Research)
- The Snail genes as inducers of cell movement and survival: implications in development and cancer (Development)
Their papers
- The EMT-activator ZEB1 promotes tumorigenicity by repressing stemness-inhibiting microRNAs (2009) — 1,724 citations
- The EMT-activator Zeb1 is a key factor for cell plasticity and promotes metastasis in pancreatic cancer (2017) — 877 citations
- Mutant p53 drives metastasis and overcomes growth arrest/senescence in pancreatic cancer (2010) — 653 citations
- E-cadherin–integrin crosstalk in cancer invasion and metastasis (2013) — 604 citations
- The role of focal-adhesion kinase in cancer — a new therapeutic opportunity (2005) — 1,068 citations