the RAS/RAF/MEK/ERK pathway, a key oncogenic signaling cascade for many human malignancies. 3 Activating BRAF mutations are the most common cause for this activation in PTC, occurring in 25% to 49% of tumors. Moreover, the presence of this mutation
Search Results
Dwight H. Owen, Bhavana Konda, Jennifer Sipos, Tom Liu, Amy Webb, Matthew D. Ringel, Cynthia D. Timmers, and Manisha H. Shah
R. Michael Tuttle and R. Leboeuf
Clin Endocrinol Metab 2003 ; 88 : 1947 – 1960 . 20. Shchemelinin I Sefc L Necas E . Protein kinase inhibitors . Folia Biol (Praha) 2006 ; 52 : 137 – 148 . 21. Solit DB Garraway LA Pratilas CA . BRAF mutation predicts
Karam Khaddour, Michael R. Chicoine, Jiayi Huang, Sonika Dahiya, and George Ansstas
best sensitivity and specificity to detect somatic BRAF mutations in papillary craniopharyngioma, we recommend an approach using DNA-based testing (such as PCR or NGS) and antibody-based testing (immunohistochemistry to detect mutant BRAF protein
Presenters: Dara L. Aisner and Gregory J. Riely
in 5% to 7%, ROS1 rearrangements in 1% to 3%, and BRAF mutations in 2% to 5%. “The best therapeutic outcome is seen if therapy is targeted to the first 3 mutations— EGFR , ALK , and ROS1 . It is critically important to perform testing for
characteristics, such as microsatellite instability-high (MSI-H), BRAF mutation, or HER2 overexpression. Hereditary risk assessment and screening are also essential components in caring for patients with intestinal cancers, since many are potentially preventable
: Determine the objective response rate of the combination sorafenib and temsirolimus in I-131 refractory thyroid cancer Secondary Outcome Measures: Evaluate if the presence of BRAF mutations, with or without concomitant mutations in the PI3K AKT, mTOR
rate of combination sorafenib and temsirolimus in I-131 refractory thyroid cancer Secondary Outcome Measures: Evaluate if the presence of BRAF mutations, with or without concomitant mutations in the PI3K AKT, mTOR pathway, predicts
develop studies to scientifically evaluate and define GSK2118436, a BRAF inhibitor, and GSK1120212, a MEK1 and MEK2 inhibitor. Previous research has indicated that BRAF mutations are strong targets for therapies in the treatment of advanced melanoma
Shailender Bhatia and John A. Thompson
V600R). 25 The absolute and relative frequencies of the different mutations of BRAF are age-dependent, with an inverse relationship between age and BRAF mutation rate and a higher proportion of V600K mutations in older patients. 26 Earlier
Daniel G. Coit, John A. Thompson, Alain Algazi, Robert Andtbacka, Christopher K. Bichakjian, William E. Carson III, Gregory A. Daniels, Dominick DiMaio, Ryan C. Fields, Martin D. Fleming, Brian Gastman, Rene Gonzalez, Valerie Guild, Douglas Johnson, Richard W. Joseph, Julie R. Lange, Mary C. Martini, Miguel A. Materin, Anthony J. Olszanski, Patrick Ott, Aparna Priyanath Gupta, Merrick I. Ross, April K. Salama, Joseph Skitzki, Susan M. Swetter, Kenneth K. Tanabe, Javier F. Torres-Roca, Vijay Trisal, Marshall M. Urist, Nicole McMillian, and Anita Engh
with single-agent ipilimumab. Both these trials also showed substantially increased toxicity with immune checkpoint combination therapy versus monotherapy. Anti–PD-1 Therapy in Patient Subpopulations: BRAF Mutation Status: Subgroup analyses in the