| First Author | Derksen PW | Year | 2006 |
| Journal | Cancer Cell | Volume | 10 |
| Issue | 5 | Pages | 437-49 |
| PubMed ID | 17097565 | Mgi Jnum | J:116152 |
| Mgi Id | MGI:3693058 | Doi | 10.1016/j.ccr.2006.09.013 |
| Citation | Derksen PW, et al. (2006) Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis. Cancer Cell 10(5):437-49 |
| abstractText | Metastatic disease is the primary cause of death in breast cancer, the most common malignancy in Western women. Loss of E-cadherin is associated with tumor metastasis, as well as with invasive lobular carcinoma (ILC), which accounts for 10%-15% of all breast cancers. To study the role of E-cadherin in breast oncogenesis, we have introduced conditional E-cadherin mutations into a mouse tumor model based on epithelium-specific knockout of p53. Combined loss of E-cadherin and p53 resulted in accelerated development of invasive and metastatic mammary carcinomas, which show strong resemblance to human ILC. Moreover, loss of E-cadherin induced anoikis resistance and facilitated angiogenesis, thus promoting metastatic disease. Our results suggest that loss of E-cadherin contributes to both mammary tumor initiation and metastasis. |
