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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

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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

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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

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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

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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

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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

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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

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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

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Presented by: Midhun Malla, Katrina S. Pedersen, and Aparna R. Parikh

Molecular biomarker testing for all patients with metastatic colorectal cancer (CRC) has become increasingly important because identifying targetable alterations can lead to meaningful clinical benefits. At a minimum, testing should include RAS, BRAF mutational status, microsatellite instability status, HER2 expression, NTRK, and RET mutations. For HER2-amplified cancer, the NCCN Guidelines offer multiple treatment options, including trastuzumab in combination with tucatinib or pertuzumab, and trastuzumab-deruxtecan. Combination trastuzumab + tucatinib has recently received approval by the FDA for refractory RAS wild-type, HER2-amplified CRC. The addition of bevacizumab to trifluridine/tipiracil treatment has significantly prolonged median overall survival compared with trifluridine/tipiracil alone, regardless of molecular subtypes. KRAS G12C–targeted therapies are on the horizon, with several agents in ongoing studies. Furthermore, bilevel blockade is important when addressing MAP kinase pathway alterations.

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Alan N. Houghton