BRAF mutations in colorectal cancer have been incorporated into oncology practice for cetuximab and panitumumab therapy since 2008. 26 High-throughput technologies using NGS that enable massively parallel sequencing of nucleic acid (DNA and RNA) at a
Search Results
Multigene Assays in Metastatic Colorectal Cancer
Kristin K. Deeb, Jakub P. Sram, Hanlin Gao, and Marwan G. Fakih
Progress in the Management of Melanoma in 2013
Daniel G. Coit and Anthony J. Olszanski
median overall survival was 13.6 versus 9.7 months, respectively ( P <.001). 11 , 12 Up to 50% of patients with the BRAF mutation show a response to this drug; however, the typical duration of response is approximately 6 months, due to the emergence
Cutaneous Melanoma: Management of Melanoma Brain Metastases and Molecular Testing
Presented by: Douglas B. Johnson, Susan M. Swetter, April K.S. Salama, and Evan Wuthrick
dramatic improvement in relapse-free survival versus placebo. 5 “It’s debated whether BRAF/MEK inhibition or anti–PD-1 is a better treatment option in the adjuvant setting, but it’s certainly clinically indicated to test for BRAF mutations in the stage
BRAF/MEK Dual Inhibitors Therapy in Progressive and Anaplastic Pleomorphic Xanthoastrocytoma: Case Series and Literature Review
Karolina Kata, Juan C. Rodriguez-Quintero, Octavio D. Arevalo, Jackie J. Zhang, Meenakshi Bidwai Bhattacharjee, Cornelius Ware, Antonio Dono, Roy Riascos-Castaneda, Nitin Tandon, Angel Blanco, Yoshua Esquenazi, Leomar Y. Ballester, Mark Amsbaugh, Arthur L. Day, and Jay-Jiguang Zhu
mutation is important for the proper selection of BRAF and MEK inhibitors. BRAF mutations have been grouped into 3 classes: class I comprises V600E mutations resulting in low RAS activity; class II includes BRAF fusions and non-V600E mutations, leading
Interpretation of Genetic Testing for Lynch Syndrome in Patients With Putative Familial Colorectal Cancer
Christina Rybak and Michael J. Hall
. BRAF encodes a kinase involved in response to growth signals. BRAF mutation leads to constitutive activity of the kinase. 33 BRAF V600E accounts for approximately 90% of all activating BRAF mutations. 33 Clinically, most CRCs with dMMR from
NCCN Guidelines Insights: Colon Cancer, Version 2.2018
Al B. Benson III, Alan P. Venook, Mahmoud M. Al-Hawary, Lynette Cederquist, Yi-Jen Chen, Kristen K. Ciombor, Stacey Cohen, Harry S. Cooper, Dustin Deming, Paul F. Engstrom, Ignacio Garrido-Laguna, Jean L. Grem, Axel Grothey, Howard S. Hochster, Sarah Hoffe, Steven Hunt, Ahmed Kamel, Natalie Kirilcuk, Smitha Krishnamurthi, Wells A. Messersmith, Jeffrey Meyerhardt, Eric D. Miller, Mary F. Mulcahy, James D. Murphy, Steven Nurkin, Leonard Saltz, Sunil Sharma, David Shibata, John M. Skibber, Constantinos T. Sofocleous, Elena M. Stoffel, Eden Stotsky-Himelfarb, Christopher G. Willett, Evan Wuthrick, Kristina M. Gregory, and Deborah A. Freedman-Cass
there are not enough data from IDEA to draw any conclusions for patients with rectal or stage II colon cancer. Treatment of RAS Wild-Type/ BRAF Mutation–Positive Metastatic CRC In the 2017 version of the NCCN Guidelines, patients with
Colon Cancer, Version 3.2014
Al B. Benson III, Alan P. Venook, Tanios Bekaii-Saab, Emily Chan, Yi-Jen Chen, Harry S. Cooper, Paul F. Engstrom, Peter C. Enzinger, Moon J. Fenton, Charles S. Fuchs, Jean L. Grem, Steven Hunt, Ahmed Kamel, Lucille A. Leong, Edward Lin, Wells Messersmith, Mary F. Mulcahy, James D. Murphy, Steven Nurkin, Eric Rohren, David P. Ryan, Leonard Saltz, Sunil Sharma, David Shibata, John M. Skibber, Constantinos T. Sofocleous, Elena M. Stoffel, Eden Stotsky-Himelfarb, Christopher G. Willett, Kristina M. Gregory, and Deborah A. Freedman-Cass
characterized by a specific mutation in the BRAF gene (V600E). 130 , 203 BRAF mutations are, for all practical purposes, limited to tumors that do not have KRAS exon 2 mutations. 203 , 204 Activation of the protein product of the nonmutated BRAF gene
Colon Cancer, Version 3.2024, NCCN Clinical Practice Guidelines in Oncology
Al B. Benson III, Alan P. Venook, Mohamed Adam, George Chang, Yi-Jen Chen, Kristen K. Ciombor, Stacey A. Cohen, Harry S. Cooper, Dustin Deming, Ignacio Garrido-Laguna, Jean L. Grem, Paul Haste, J. Randolph Hecht, Sarah Hoffe, Steven Hunt, Hisham Hussan, Kimberly L. Johung, Nora Joseph, Natalie Kirilcuk, Smitha Krishnamurthi, Midhun Malla, Jennifer K. Maratt, Wells A. Messersmith, Jeffrey Meyerhardt, Eric D. Miller, Mary F. Mulcahy, Steven Nurkin, Michael J. Overman, Aparna Parikh, Hitendra Patel, Katrina Pedersen, Leonard Saltz, Charles Schneider, David Shibata, Benjamin Shogan, John M. Skibber, Constantinos T. Sofocleous, Anna Tavakkoli, Christopher G. Willett, Christina Wu, Lisa A. Gurski, Jenna Snedeker, and Frankie Jones
regarding biomarker testing. Currently, determination of tumor gene status for KRAS/NRAS and BRAF mutations, as well as HER2 amplifications and microsatellite instability (MSI)/mismatch repair (MMR) status (if not previously done), are recommended for
NCCN Task Force Report: Evaluating the Clinical Utility of Tumor Markers in Oncology
Phillip G. Febbo, Marc Ladanyi, Kenneth D. Aldape, Angelo M. De Marzo, M. Elizabeth Hammond, Daniel F. Hayes, A. John Iafrate, R. Kate Kelley, Guido Marcucci, Shuji Ogino, William Pao, Dennis C. Sgroi, and Marian L. Birkeland
or predictive strength for the disease or class of therapy. One recent example of co-approval of a drug and companion diagnostic is the BRAF V600E mutation test coapproved with the kinase inhibitor vemurafenib. BRAF mutations are found in 30% to
Colon Cancer, Version 2.2021, NCCN Clinical Practice Guidelines in Oncology
Al B. Benson III, Alan P. Venook, Mahmoud M. Al-Hawary, Mustafa A. Arain, Yi-Jen Chen, Kristen K. Ciombor, Stacey Cohen, Harry S. Cooper, Dustin Deming, Linda Farkas, Ignacio Garrido-Laguna, Jean L. Grem, Andrew Gunn, J. Randolph Hecht, Sarah Hoffe, Joleen Hubbard, Steven Hunt, Kimberly L. Johung, Natalie Kirilcuk, Smitha Krishnamurthi, Wells A. Messersmith, Jeffrey Meyerhardt, Eric D. Miller, Mary F. Mulcahy, Steven Nurkin, Michael J. Overman, Aparna Parikh, Hitendra Patel, Katrina Pedersen, Leonard Saltz, Charles Schneider, David Shibata, John M. Skibber, Constantinos T. Sofocleous, Elena M. Stoffel, Eden Stotsky-Himelfarb, Christopher G. Willett, Kristina M. Gregory, and Lisa A. Gurski
NCCN.org ). Currently, determination of tumor gene status for KRAS/NRAS and BRAF mutations, as well as HER2 amplifications and microsatellite instability high (MSI)/mismatch repair (MMR) status (if not previously done), are recommended for patients
