Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic.

By Angeliki Voulgari, A. Pintzas. Biochimica et Biophysica Acta, 2009

727 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer (2010, background): “…that reversible epigenetic changes emerging during acquired drug resistance reflect changes in the differentiation state of the tumor, which is likely to reflect EMT and the emergence of chemorefractory cells with stem cell-like features (Voulgari and Pintzas, 2009; Sharma et al., 2010; Figure 4a).”
Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis (2015, background): “Not surprisingly, these cells are being increasingly observed in many aggressive malignancies (105, 198, 219–228), strongly suggesting that partial EMT phenomena are more likely to happen in vivo than complete EMT (169, 229).”
The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis (2022, background): “Mesenchymal cells are distinguished from epithelial cells by their irregular morphology, with an elongated, spindle-shaped form and less rigid topography [26].”
E-cadherin–integrin crosstalk in cancer invasion and metastasis (2013, background): “…trials of the EGFR inhibitor erlotinib in non-small-cell lung cancer have revealed better responses in patients with high E-cadherin expression (Voulgari and Pintzas, 2009), although it remains to be established whether E-cadherin is merely a biomarker of response or whether it participates in…”