Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis.

By P. Derksen, Xiaoling Liu, Francis Saridin, H. van der Gulden, J. Zevenhoven, B. Evers, J. V. van Beijnum, A. Griffioen, J. Vink, P. Krimpenfort and 4 more. Cancer Cell, 2006

629 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/b15f85f1bcc8548872ea7d39fcc22f469ecf5b12

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. Jing Yang
2. J. Tsai
3. C. Gottardi
4. M. Frame
5. David M. Gonzalez
6. D. Medici
7. Angela Jeanes
8. F. van Roy

In Oncology

1. Jing Yang
2. D. Medici
3. David M. Gonzalez
4. M. Frame
5. M. Canel
6. J. Tsai
7. V. Brunton
8. F. van Roy

Citations in the corpus

• Epithelial–mesenchymal plasticity in carcinoma metastasis (2013, background): “Furthermore, mice carrying a genetic deletion of the E-cadherin gene on a mammary-specific p53-null background developed invasive lobular carcinomas, a subtype of breast cancer that presents individual migrating tumor cells (Derksen et al. 2006).”
• Epithelial-mesenchymal transition in breast cancer relates to the basal-like phenotype. (2008, neutral): “For instance, although lobular breast carcinomas have a single-cell invasion pattern and lack E-cadherin (1), they do not show any other evidence of EMT (27, 38) or of the basal phenotype.”
• Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “lobular carcinomas (59), as well as long-standing evidence that loss of E-cadherin can be used as an indicator of carcinoma progression and poor prognosis in multiple tumor types (60).”
• Cadherins and cancer: how does cadherin dysfunction promote tumor progression? (2008, background): “It is important to emphasize, however, that in mouse models loss of E-cadherin alone is not sufficient to induce tumor formation (Tinkle et al., 2004; Tunggal et al., 2005; Derksen et al., 2006).”
• Involvement of members of the cadherin superfamily in cancer. (2009, background): “This was shown by combining a floxed Cdh1 gene with the K14-Cre gene, which is expressed at low, stochastic levels in mammary epithelium (Derksen et al. 2006).”
• EMT and tumor metastasis (2015, background): “For example, a loss of E-cadherin expression and an increase in N-cadherin expression is correlated with anoikis resistance and increased invasiveness [16].”
• E-cadherin–integrin crosstalk in cancer invasion and metastasis (2013, background): “…the downstream consequences of reduced E-cadherin functionality can impact on a number of other tumour-associated phenotypes, such as proliferation, survival, angiogenesis and colonization at metastatic sites (Derksen et al., 2006; Ma et al., 2010; Onder et al., 2008; Wendt et al., 2011).”