NLM Title Abbreviation
Int J Mol Sci
International journal of molecular sciences
DOI of Published Version
The discovery of various driver pathways and targeted small molecule agents/antibodies have revolutionized the management of metastatic breast cancer. Currently, the major targets of clinical utility in breast cancer include the human epidermal growth factor receptor 2 (HER2) and epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF) receptor, mechanistic target of rapamycin (mTOR) pathway, and the cyclin-dependent kinase 4/6 (CDK-4/6) pathway. Brain metastasis, however, remains a thorn in the flesh, leading to morbidity, neuro-cognitive decline, and interruptions in the management of systemic disease. Approximately 20%-30% of patients with metastatic breast cancer develop brain metastases. Surgery, whole brain radiation therapy, and stereotactic radiosurgery are the traditional treatment options for patients with brain metastases. The therapeutic paradigm is changing due to better understanding of the blood brain barrier and the advent of tyrosine kinase inhibitors and monoclonal antibodies. Several of these agents are in clinical practice and several others are in early stage clinical trials. In this article, we will review the common targetable pathways in the management of breast cancer patients with brain metastases, and the current state of the clinical development of drugs against these pathways.
oafund, Antibodies, Monoclonal, Antineoplastic Agents, Blood-Brain Barrier, Brain Neoplasms, Breast Neoplasms, Clinical Trials as Topic, Female, Humans, Molecular Targeted Therapy, Protein Kinase Inhibitors, Signal Transduction, Survival Analysis, Treatment Outcome
Journal Article Version
Version of Record
Published Article/Book Citation
Venur, V.A.; Leone, J.P. Targeted Therapies for Brain Metastases from Breast Cancer. Int. J. Mol. Sci. 2016, 17, 1543. http://doi.org/10.3390/ijms17091543
© 2016 by the authors
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.