(MSI) testing in management of patients with stage II colon cancer Describe the role of KRAS mutational analysis in management of patients with metastatic colorectal cancers Describe the role of BRAF mutational analysis in management of patients with
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Biomarker Use in Colorectal Cancer Therapy
Robin K. Kelley, Grace Wang, and Alan P. Venook
Targeted/Emerging Therapies for Metastatic Non–Small Cell Lung Cancer
Leora Horn
system is an important factor, given that approximately 50% of patients who are on crizotinib will progress with that as their site of disease,” added Dr. Horn. Targeting ROS1 and BRAF Mutations Similar to EGFR and ALK , both ROS1 fusions
Colon Cancer, Version 1.2017, NCCN Clinical Practice Guidelines in Oncology
Al B. Benson III, Alan P. Venook, Lynette Cederquist, Emily Chan, Yi-Jen Chen, Harry S. Cooper, Dustin Deming, Paul F. Engstrom, Peter C. Enzinger, Alessandro Fichera, Jean L. Grem, Axel Grothey, Howard S. Hochster, Sarah Hoffe, Steven Hunt, Ahmed Kamel, Natalie Kirilcuk, Smitha Krishnamurthi, Wells A. Messersmith, 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, Christina S. Wu, Kristina M. Gregory, and Deborah Freedman-Cass
cetuximab or panitumumab. Approximately 5% to 9% of CRCs are characterized by a specific mutation in the BRAF gene (V600E). 155 , 156 BRAF mutations are, for all practical purposes, limited to tumors that do not have KRAS exon 2 mutations. 155 , 157
Targeted Therapy for Metastatic Non–Small Cell Lung Cancer
Presented by: Gregory J. Riely
. “There are multiple molecular targets with agents approved for use in the first-line setting, including EGFR , ALK , ROS1 , RET , MET exon 14, and BRAF mutations. Targeted therapies are addressing targets that we’ve not been able to target before
Genomic Profiling in Patients With Malignant Peripheral Nerve Sheath Tumors Reveals Multiple Pathways With Targetable Mutations
Henry G. Kaplan, Steven Rostad, Jeffrey S. Ross, Siraj M. Ali, and Sherri Z. Millis
Institutional Review Board (IRB)–approved protocol (No. SWD5531S-14). MPNSTs were studied using the QIAGEN QIAamp DNA FFPE Tissue Kit and BRAF mutation was analyzed using a laboratory-developed, allele-specific, real-time PCR assay to detect the major BRAF
Multisystemic and Multiresistant Langerhans Cell Histiocytosis: A Case Treated With BRAF Inhibitor
Letizia Gandolfi, Sarah Adamo, Alessandro Pileri, Alessandro Broccoli, Lisa Argnani, and Pier Luigi Zinzani
BRAF constitutive activation independently of extracellular signals. 15 The BRAF mutation is detected in many malignant diseases, including primary melanoma, hairy cell leukemia, papillary thyroid carcinoma, colorectal cancer, and in approximately
Predictive Biomarkers for Anti-Epidermal Growth Factor Receptor Therapy: Beyond KRAS Testing
Noman Ashraf, Nishi Kothari, and Richard Kim
the same intracellular pathways, it is plausible that BRAF mutation status may also have predictive value for anti-EGFR therapy. 40 , 51 Early studies supported such a role; however, pooled data from the CRYSTAL and OPUS trials showed no
Sessile Serrated Polyps: An Important Route to Colorectal Cancer
Matthew F. Kalady
. The sequence of events is still not completely characterized, but the belief is that a BRAF mutation is the initiating event, with conversion of normal mucosa to either a microvesicular hyperplastic polyp or an SSA/P. DNA hypermethylation (CIMP) of
Right Versus Left Colon Cancer Biology: Integrating the Consensus Molecular Subtypes
Michael S. Lee, David G. Menter, and Scott Kopetz
also enriched for MSI-high, CIMP-high, and BRAF mutation. Although genotypic features such as KRAS and BRAF mutation status are enriched in some subtypes (ie, BRAF in CMS1; KRAS in CMS3), their presence or absence does not specifically define
Management of Patients With Resectable and Metastatic Non–Small Cell Lung Cancer
Presented by: Jane Yanagawa and Gregory J. Riely
rearrangements, BRAF mutations, NTRK1 /2/3 rearrangements, MET exon 14 skipping mutations, and RET rearrangements. EGFR Tyrosine Kinase Inhibitors EGFR mutations are one of the most common oncogenic drivers in NSCLC and have served as the paradigm
