Cynthia Shepherd
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Cynthia Shepherd has a total of 2 co-authors. Here are the top co-authors by number of shared publications:
- Igor Puzanov
Department of Medicine, Roswell Park Comprehensive Cancer Center, Buffalo, USA
1 shared publication Jeffrey A. Sosman
Vanderbilt University Medical Center
1 shared publication
Latest Publications
- 24 March 2010
- Published by Springer Nature in Current Oncology Reports
- Vol. 12 (3) , 146-152
B-RAF Inhibitors: An Evolving Role in the Therapy of Malignant Melanoma
Immunotherapy and chemotherapy benefit few patients with metastatic melanoma, and even fewer experience durable survival benefit. These poor results come from treating melanoma as a single homogeneous disease. Recently, it has been shown that targeting activated tyrosine kinases (oncogenes) can mediate striking clinical benefits in several cancers. In 2002, a mutation at the V600E amino acid of the BRAF serine/threonine kinase was described as present in over 50% of melanomas. The mutation appeared to confer a dependency by the melanoma cancer cell on its activation of the MAP kinase pathway. The frequency and specificity of this mutation (95% at V600E of BRAF) suggests that it may be a potential target for therapy, and recent results with one inhibitor, PLX4032/RG7204, bare this out. This review updates the status of BRAF inhibitors in melanoma and what may be on the horizon.
- 24 March 2010
- Published by Springer Nature in Current Oncology Reports
- Vol. 12 (3) , 146-152
B-RAF Inhibitors: An Evolving Role in the Therapy of Malignant Melanoma
Immunotherapy and chemotherapy benefit few patients with metastatic melanoma, and even fewer experience durable survival benefit. These poor results come from treating melanoma as a single homogeneous disease. Recently, it has been shown that targeting activated tyrosine kinases (oncogenes) can mediate striking clinical benefits in several cancers. In 2002, a mutation at the V600E amino acid of the BRAF serine/threonine kinase was described as present in over 50% of melanomas. The mutation appeared to confer a dependency by the melanoma cancer cell on its activation of the MAP kinase pathway. The frequency and specificity of this mutation (95% at V600E of BRAF) suggests that it may be a potential target for therapy, and recent results with one inhibitor, PLX4032/RG7204, bare this out. This review updates the status of BRAF inhibitors in melanoma and what may be on the horizon.