@article{88231,
  keywords = {Animals, Humans, chemotaxis, Cell Proliferation, Mice, Female, Cell Line, Tumor, Breast Neoplasms, Cell Differentiation, Antibodies, Monoclonal, Cell Adhesion, Stem Cells, Integrin alpha4beta1, Mice, Inbred BALB C, NF-kappa B, Transplantation, Heterologous, Molecular Targeted Therapy, Osteoclasts, Mice, Nude, Neoplasm Transplantation, Bone Neoplasms, Osteolysis, Neoplasm Micrometastasis, Radiography, Vascular Cell Adhesion Molecule-1},
  author = {Xin Lu and Euphemia Mu and Yong Wei and Sabine Riethdorf and Qifeng Yang and Min Yuan and Jun Yan and Yuling Hua and Benjamin Tiede and Xuemin Lu and Bruce Haffty and Klaus Pantel and Joan Massagu{\'e} and Yibin Kang},
  title = {VCAM-1 promotes osteolytic expansion of indolent bone micrometastasis of breast cancer by engaging α4β1-positive osteoclast progenitors.},
  abstract = {<p>Breast cancer patients often develop locoregional or distant recurrence years after mastectomy. Understanding the mechanism of metastatic recurrence after dormancy is crucial for improving the cure rate for breast cancer. Here, we characterize a bone metastasis dormancy model to show that aberrant expression of vascular cell adhesion molecule 1 (VCAM-1), in part dependent on the activity of the NF-κB pathway, promotes the transition from indolent micrometastasis to overt metastasis. By interacting with the cognate receptor integrin α4β1, VCAM-1 recruits monocytic osteoclast progenitors and elevates local osteoclast activity. Antibodies against VCAM-1 and integrin α4 effectively inhibit bone metastasis progression and preserve bone structure. These findings establish VCAM-1 as a promising target for the prevention and inhibition of metastatic recurrence in bone.</p>
},
  year = {2011},
  journal = {Cancer Cell},
  volume = {20},
  pages = {701-14},
  month = {12/2011},
  issn = {1878-3686},
  doi = {10.1016/j.ccr.2011.11.002},
  language = {eng},
}