Guoli Chen
Research Subjects
Guoli Chen has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Christopher D. Gocke
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
1 shared publication - Gang Zheng
Division of Laboratory Genetics and Genomics, Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota
1 shared publication - James R. Eshleman
Johns Hopkins University 1 Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center Baltimore, Maryland
1 shared publication - Li-Hui Tseng
Department of Medical Genetics, National Taiwan University Hospital, Taipei, Taiwan
1 shared publication - Lisa Haley
Johns Hopkins Medical Institutions
1 shared publication - Ming-Tseh Lin
From the Departments of Pathology (Drs De Marchi, Ibrahim, Zheng, Gocke, Eshleman, Belchis, Illei, and Lin, Ms Haley, Mr Fryer, and Ms Beierl) and Oncology (Drs Gocke and Eshleman), Johns Hopkins University School of Medicine, Baltimore, Maryland; and the Division of Hematology and Bone Marrow Transplantation, Hospital-University of Udine, Udine, Italy (Dr De Marchi)
1 shared publication
Latest Publications
- Open Access
- 24 October 2015
- Published by Springer Nature in BMC Cancer
- Vol. 15 (1) , 1-10
Clinical detection and categorization of uncommon and concomitant mutations involving BRAF
Selective BRAF inhibitors, vemurafenib and dabrafenib, and the MEK inhibitor, trametinib, have been approved for treatment of metastatic melanomas with a BRAF p.V600E mutation. The clinical significance of non-codon 600 mutations remains unclear, in part, due to variation of kinase activity for different mutants. In this study, we categorized BRAF mutations according to the reported mutant kinase activity. A total of 1027 lung cancer, colorectal cancer or melanoma specimens were submitted for clinical mutation detection by next generation sequencing. Non-codon 600 mutations were observed in 37 % of BRAF-mutated tumors. Of all BRAF mutants, 75 % were kinase-activated, 15 % kinase-impaired and 10 % kinase-unknown. The most common kinase-impaired mutant involves codon 594, specifically, p.D594G (c.1781A > G) and p.D594N (c.1780G > A). Lung cancers showed significantly higher incidences of kinase-impaired or kinase-unknown mutants. Kinase-impaired BRAF mutants showed a significant association with concomitant activating KRAS or NRAS mutations, but not PIK3CA mutations, supporting the reported interaction of these mutations. BRAF mutants with impaired or unknown kinase activity as well as concomitant kinase-impaired BRAF mutations and RAS mutations were detected in lung cancers, colorectal cancers and melanomas. Different therapeutic strategies based on the BRAF mutant kinase activity and the concomitant mutations may be worthwhile.
- 24 October 2015
- Published by Springer Nature in BMC Cancer
- Vol. 15 (1) , 1-10
Open AccessClinical detection and categorization of uncommon and concomitant mutations involving BRAF
Selective BRAF inhibitors, vemurafenib and dabrafenib, and the MEK inhibitor, trametinib, have been approved for treatment of metastatic melanomas with a BRAF p.V600E mutation. The clinical significance of non-codon 600 mutations remains unclear, in part, due to variation of kinase activity for different mutants. In this study, we categorized BRAF mutations according to the reported mutant kinase activity. A total of 1027 lung cancer, colorectal cancer or melanoma specimens were submitted for clinical mutation detection by next generation sequencing. Non-codon 600 mutations were observed in 37 % of BRAF-mutated tumors. Of all BRAF mutants, 75 % were kinase-activated, 15 % kinase-impaired and 10 % kinase-unknown. The most common kinase-impaired mutant involves codon 594, specifically, p.D594G (c.1781A > G) and p.D594N (c.1780G > A). Lung cancers showed significantly higher incidences of kinase-impaired or kinase-unknown mutants. Kinase-impaired BRAF mutants showed a significant association with concomitant activating KRAS or NRAS mutations, but not PIK3CA mutations, supporting the reported interaction of these mutations. BRAF mutants with impaired or unknown kinase activity as well as concomitant kinase-impaired BRAF mutations and RAS mutations were detected in lung cancers, colorectal cancers and melanomas. Different therapeutic strategies based on the BRAF mutant kinase activity and the concomitant mutations may be worthwhile.