Migrating cancer stem cells — an integrated concept of malignant tumour progression

By Thomas Brabletz, A. Jung, S. Spaderna, F. Hlubek, T. Kirchner. Nature Reviews. Cancer, 2005

1,415 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/cef36e4592675906fedc276cf68861f30430408d

How researchers see this paper

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

In Molecular Biology

1. R. Weinberg
2. M. Nieto
3. Thomas Brabletz
4. Jing Yang
5. J. P. Thiery
6. Simone Brabletz
7. A. Cano
8. D. Hanahan

In Oncology

1. R. Weinberg
2. M. Nieto
3. Thomas Brabletz
4. D. Hanahan
5. Jing Yang
6. J. P. Thiery
7. Simone Brabletz
8. A. Cano

Citations in the corpus

• Hallmarks of cancer: the next generation. (2011, positive): “This concordance suggests that the EMT program not onlymay enable cancer cells to physically disseminate from primary tumors but also can confer on such cells the self-renewal capability that is crucial to their subsequent clonal expansion at sites of dissemination (Brabletz et al., 2005).”
• Tetraspanins: push and pull in suppressing and promoting metastasis (2009, background): “and have recently been extended to include theepithelial-to-mesenchymal transition (EMT) as an initiating even”
• CAFs secreted exosomes promote metastasis and chemotherapy resistance by enhancing cell stemness and epithelial-mesenchymal transition in colorectal cancer (2019, background): “Cancer stem cells (CSCs) are self-renewable cell types that contribute to initiation, metastasis, relapse, and chemotherapy resistance of cancer cells [22, 23].”
• Generation of Breast Cancer Stem Cells through Epithelial-Mesenchymal Transition (2008, background): “. When exposed to microenvironmental signals, these cancer stem cells would display motility capacities due to EMT, lending support to the notion of “mobile cancer stem cells” initially proposed by T. Brabletz”
• Wnt activity defines colon cancer stem cells and is regulated by the microenvironment (2010, background): “This suggests a framework in which stromal components, in this case HGF-producing myofibroblasts, stimulate CSC features of cancer cell populations mainly at the tumour edges and simultaneously promote the invasion and spread of the malignancy into the surrounding tissue, as has also been suggested ”
• Transcriptional regulation of cell polarity in EMT and cancer (2008, background): “These recent observations are in line with previous studies indicating that EMT occurs at invasive regions of colorectal tumours (Brabletz et al., 2005) where ZEB1 may have an important function (Spaderna et al., 2006).”
• A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells (2008, background): “Metastases often recapitulate the differentiated phenotype of the primary tumour; therefore, EMT seems to be transiently activated by the inductive tumour environment at the invasive tumour edge, but is reversed in growing metastases (Brabletz et al, 2001, 2005).”
• Classification of colorectal cancer based on correlation of clinical, morphological and molecular features (2007, background): “Furthermore, budding cells have the properties of malignant stem cells, including the potential for re-differentiation both locally and at sites of metastasis.(153) In other words, the morphological and immunophenotypic features associated with budding cells are reversible and therefore likely to be”
• Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype? (2007, background): “Importantly, cell survival properties might also be linked to tumour invasion, EMT and stem-cell properties, as suggested by the recent description of 'migratory cancer stem cells' (MSCs) in colorectal cance”
• Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “In parallel, buds show reduced E-cadherin expression, nuclear β-catenin activation [153] and cancer stem cells characteristics [154], suggesting that it may indeed reflect the presence of invasive mesenchymal-like cells.”
• Epithelial-mesenchymal transitions in development and disease. (2009, background): “…was previously formulated from an analysis of the progression of colon primary tumors and liver metastases, where it was proposed that cancer stem cells could acquire a mesenchymal phenotype, and thereby become migratory cancer stem cells that will form metastasis (Brabletz et al., 2005).”