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Journal articles on the topic 'BRAF/RAS wild type'

Author: Grafiati

Published: 10 December 2022

Last updated: 31 July 2025

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1

Orive-Ramos, Ana, Christos Adamopoulos, Beau Baars, et al. "Abstract 5734: Designing RAF and MEK inhibitor combinations based on their biochemical properties to effectively target MAPK-driven cancers." Cancer Research 83, no. 7_Supplement (2023): 5734. http://dx.doi.org/10.1158/1538-7445.am2023-5734.

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Abstract Oncogenic alterations of the RAS/RAF/MEK/ERK signaling pathway drives growth of over 40% of human tumors, frequently due to activating mutations of components of the pathway, such as RAS or BRAF. Targeting the pathway using BRAF inhibitors (BRAFi) in combination with MEK inhibitors (MEKi) is now the standard of care for metastatic melanoma patients harboring the BRAF(V600E) mutation. However, effective targeted therapies are lacking for most cancers driven by other pathway alterations, including those with RAS activating mutations. The effectiveness of current clinical BRAFi relies on

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2

Chen, Yuhong, Yixian Qiu, Yanrui Zhang, et al. "Differences of RAS/BRAF mutations between ISCC and RSCC in a Chinese population." Journal of Clinical Oncology 41, no. 16_suppl (2023): e15636-e15636. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.e15636.

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e15636 Background: According to the location and different clinical manifestations, colon cancer can be divided into left-sided colon cancer (LSCC) and right-sided colon cancer (RSCC). There are significant differences in morphology, molecular biology, and drug sensitivity between these two type. In addition, colorectal cancer is associated with the mutation of many essential tumor suppressor genes, such as proto-oncogene (KRAS), serine/threonine protein kinase (BRAF), etc. At that point, this study retrospectively analyzed the RAS/BRAF mutation landscape and studied the gene expression differ

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Osumi, Hiroki, Eiji Shinozaki, Yoshiaki Nakamura, et al. "Survival impact of Neo RAS wild-type metastatic colorectal cancer: A SCRUM-Japan GOZILA substudy." Journal of Clinical Oncology 43, no. 16_suppl (2025): 3530. https://doi.org/10.1200/jco.2025.43.16_suppl.3530.

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3530 Background: The “Neo RAS ’’ phenomenon refers to KRAS or NRAS mutant (MT) metastatic colorectal cancer (mCRC) that becomes RAS wild-type (WT) following treatment and may represent a novel indication for anti-epidermal growth factor receptor monoclonal antibodies. We previously described the incidence and clinicopathological characteristics of Neo RAS WT mCRC (Osumi et al. Nat Commun 2024); here we share the impact of Neo RAS WT on survival for patients with mCRC. Methods: Patients enrolled in the large-scale nationwide screening platform SCRUM-Japan GOZILA who had mCRC, tumor tissue teste

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Schietroma, Francesco, Annunziato Anghelone, Giustina Valente, et al. "Focus on RAS Codon 61 Mutations in Metastatic Colorectal Cancer: A Retrospective Analysis." Cancers 16, no. 5 (2024): 988. http://dx.doi.org/10.3390/cancers16050988.

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RAS mutations involving codon 61 are rare in metastatic colorectal cancer (mCRC), accounting for only 1–4%, but they have recently been identified with high frequency in the circulating tumor DNA (ctDNA) of patients with secondary resistance to anti-EGFRs. This retrospective monocentric study aimed to investigate the clinical phenotype and prognostic performance of codon 61 RAS-mutated mCRC. Fifty patients with codon 61 RAS-mutated mCRC treated at our institution between January 2013 and December 2021 were enrolled. Additional datasets of codon 61 RAS wild-type mCRCs (648 patients) were used a

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Taniguchi, Hiroya, Kay Uehara, Toshiaki Ishikawa, et al. "BRAF V600E and Non-V600E Mutations in RAS Wild-Type Metastatic Colorectal Cancer: Prognostic and Therapeutic Insights from a Nationwide, Multicenter, Observational Study (J-BROS)." Cancers 17, no. 3 (2025): 399. https://doi.org/10.3390/cancers17030399.

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Background/Objectives: BRAF mutations occur in 5–10% of metastatic colorectal cancer (mCRC) cases, but their implications for prognosis and optimal treatment remain unclear. Methods: This multicenter, prospective observational study analyzed 377 RAS wild-type cases from 511 patients across 32 centers, using PCR-based methods. Results: BRAF mutations were identified in 21% (79/377) of cases, predominantly V600E (89.9%) with a minority of non-V600E (10.1%). Microsatellite instability (MSI) testing revealed MSI-high in 11.3%, exclusively among V600E cases. V600E mutations were linked to right-sid

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Terán-Brage, Eduardo, Yolanda Lopez-Mateos, María Mar Abad Hernández, et al. "Role of RAS/BRAF and PIK3CA mutations in tissue and plasma for prognostic assessment in metastatic colorectal cancer (mCRC)." Journal of Clinical Oncology 43, no. 4_suppl (2025): 281. https://doi.org/10.1200/jco.2025.43.4_suppl.281.

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281 Background: Mutations in RAS/BRAF ( RAS/BRAFm ) and PIK3CA ( PIK3CAm ) genes have been described as mechanisms of resistance to anti-EGFR agents in mCRC. However, the utility of liquid biopsy in their baseline detection remains unknown. We aim to analyse oncological outcomes according to RAS/BRAF and PIK3CA mutational status in tissue & plasma in mCRC. Methods: We conducted aretrospective study in patients (pts) with mCRC from 2017 to 2024. RAS/BRAF and PIK3CA mutational status assessment was performed at baseline using Idylla (Biocartis) and Cobas PIK3CA kits, respectively. Cox models

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Maurel, Joan, Vicente Alonso, Pilar Escudero, et al. "Clinical Impact of Circulating Tumor RAS and BRAF Mutation Dynamics in Patients With Metastatic Colorectal Cancer Treated With First-Line Chemotherapy Plus Anti–Epidermal Growth Factor Receptor Therapy." JCO Precision Oncology, no. 3 (December 2019): 1–16. http://dx.doi.org/10.1200/po.18.00289.

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PURPOSE RAS and BRAF mutations can be detected as a mechanism of acquired resistance in circulating tumor (ct) DNA in patients with metastatic colorectal cancer treated with anti–epidermal growth factor receptor therapy. METHODS RAS and BRAF mutational status was assessed in ctDNA in a baseline plasma sample and a serum sample collected at the time of the last available determination (named secondary extraction) from patients with KRAS exon 2 wild-type metastatic colorectal cancer treated in two first-line prospective biomarker-designed clinical trials (PULSE, ClinicalTrials.gov identifier: NC

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Calegari, Maria Alessandra, Lisa Salvatore, Brunella Di Stefano, et al. "Clinical, Pathological and Prognostic Features of Rare BRAF Mutations in Metastatic Colorectal Cancer (mCRC): A Bi-Institutional Retrospective Analysis (REBUS Study)." Cancers 13, no. 9 (2021): 2098. http://dx.doi.org/10.3390/cancers13092098.

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Recently, retrospective analysis began to shed light on metastatic colorectal cancers (mCRCs) harboring rare BRAF non-V600 mutations, documenting a distinct phenotype and a favorable prognosis. This study aimed to confirm features and prognosis of rare BRAF non-V600 mCRCs compared to BRAF V600E and BRAF wild-type mCRCs treated at two Italian Institutions. Overall, 537 cases were retrospectively evaluated: 221 RAS/BRAF wild-type, 261 RAS mutated, 46 BRAF V600E and 9 BRAF non-V600. Compared to BRAF V600E mCRC, BRAF non-V600 mCRC were more frequently left-sided, had a lower tumor burden and displ

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9

Bilgetekin, Irem, Mehmet Dogan, Cengiz Karacin, et al. "The temporal evaluation of RAS and BRAF mutation by liquid biopsy at progression after bevacizumab combinations in patients with metastatic colorectal cancer (mCRC)." Journal of Clinical Oncology 39, no. 15_suppl (2021): e15587-e15587. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e15587.

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e15587 Background: Expanded RAS analysis is essential for the selection of biologic agents in mCRC. RAS mutations indicates anti-EGFR unresponsiveness. In this study, we aimed to investigate RAS and BRAF mutations by liquid biopsy at progression in patients with RAS mutant mCRC. Methods: Sixty patients with mCRC who harbored tissue RAS mutations were prospectively analyzed between July 2019 and April 2020. All the patients treated with chemotherapy plus bevacizumab combinations . The plasma samples of the patients were analyzed after progression of bevacizumab combinations. RAS mutation profil

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Wang, Chongkai, Jaideep Sandhu, and Marwan Fakih. "Mucinous Histology Is Associated with Resistance to Anti-EGFR Therapy in Patients with Left-Sided RAS/BRAF Wild-Type Metastatic Colorectal Cancer." Oncologist 27, no. 2 (2022): 104–9. http://dx.doi.org/10.1093/oncolo/oyab028.

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Abstract Background Limited studies have suggested that mucinous histology is associated an attenuated response to anti-epidermal growth factor receptor (EGFR) therapy. Methods We conducted a single-institution, retrospective study to review the anti-EGFR response and the molecular profile of patients with left-sided microsatellite stable RAS/BRAF wild-type mucinous metastatic colorectal cancer. Results In comparison to nonmucinous population (n = 98), mucinous histology (n = 20) was associated with a younger age (48 vs 54, P = .02), wild-type APC (80% vs 15.3%, P &lt; .0001), and wild-typ

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Conroy, Jeffrey M., Sarabjot Pabla, Marc S. Ernstoff, et al. "Comprehensive immune and mutational profile of melanoma." Journal of Clinical Oncology 36, no. 5_suppl (2018): 182. http://dx.doi.org/10.1200/jco.2018.36.5_suppl.182.

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182 Background: The association between tumor mutational profiles and immune signatures has not been well-characterized. Methods: 306 melanoma samples were tested by NGS using a comprehensive cancer panel for mutational status and an immune response panel which interrogates the expression profile of 54 validated immune-related genes. The ranking of gene expression, mutational burden and 7 immune phenotypes was compared to a reference population. 38% cases were positive for activating BRAF mutations, 12% for RAS, and 6% for NF1. The remaining 44% were considered triple wild type. Principal comp

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12

Yoshino, Takayuki, Radka Obermannova, Gyorgy Bodoky, et al. "Are BRAF mutated metastatic colorectal cancer (mCRC) tumors more responsive to VEGFR-2 blockage? Analysis of patient outcomes by RAS/RAF mutation status in the RAISE study—A global, randomized, double-blind, phase III study." Journal of Clinical Oncology 36, no. 4_suppl (2018): 622. http://dx.doi.org/10.1200/jco.2018.36.4_suppl.622.

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622 Background: The RAISE trial (NCT01183780) demonstrated that ramucirumab (RAM) plus leucovorin, fluorouracil, and irinotecan (FOLFIRI) significantly improved overall survival (OS) and progression-free survival (PFS) compared with placebo (PBO) plus FOLFIRI as second-line mCRC treatment. RAS/RAF mutations are associated with resistance to anti-EGFR therapies and poor prognosis, particularly BRAF mutations. The extensive RAISE biomarker program assessed the association of multiple candidate markers with efficacy outcomes. Here we present the results for RAS/ RAF mutations. Methods: Plasma and

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Orive-Ramos, Ana, Bijaya Gaire, Christos Adamopoulos, et al. "Abstract LB424: Mechanistic rationale for combination of RAF/MEK glue avutometinib with a pan-RAF inhibitor for RAS-mutant tumor-selective therapy." Cancer Research 85, no. 8_Supplement_2 (2025): LB424. https://doi.org/10.1158/1538-7445.am2025-lb424.

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Abstract The therapeutic window of small-molecule inhibitors targeting the MAPK pathway relies on greater pathway inhibition in the tumor than in normal cells. Inhibitors selective for mutated BRAF (BRAFi) showed clinical activity in BRAF-mutant tumors and combinations of BRAFi with MEK-only inhibitors (MEKi) were successfully administered at full dose for each drug, resulting in clinical success. Next generation pan-RAF inhibitors (pan-RAFi) were subsequently developed that antagonize activated wild-type RAF as well as mutated BRAF and CRAF and have shown clinical activity in RAS-mutant (RAS-

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Landa, Iñigo, Ian Ganly, Timothy A. Chan, et al. "Frequent Somatic TERT Promoter Mutations in Thyroid Cancer: Higher Prevalence in Advanced Forms of the Disease." Journal of Clinical Endocrinology & Metabolism 98, no. 9 (2013): E1562—E1566. http://dx.doi.org/10.1210/jc.2013-2383.

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Background: TERT encodes the reverse transcriptase component of telomerase, which adds telomere repeats to chromosome ends, thus enabling cell replication. Telomerase activity is required for cell immortalization. Somatic TERT promoter mutations modifying key transcriptional response elements were recently reported in several cancers, such as melanomas and gliomas. Objectives: The objectives of the study were: 1) to determine the prevalence of TERT promoter mutations C228T and C250T in different thyroid cancer histological types and cell lines; and 2) to establish the possible association of T

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15

Romano, David, Lucía García-Gutiérrez, Nourhan Aboud, et al. "Proteasomal down-regulation of the proapoptotic MST2 pathway contributes to BRAF inhibitor resistance in melanoma." Life Science Alliance 5, no. 10 (2022): e202201445. http://dx.doi.org/10.26508/lsa.202201445.

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The RAS-RAF-MEK-ERK pathway is hyperactivated in most malignant melanomas, and mutations in BRAF or NRAS account for most of these cases. BRAF inhibitors (BRAFi) are highly efficient for treating patients with BRAFV600E mutations, but tumours frequently acquire resistance within a few months. Multiple resistance mechanisms have been identified, due to mutations or network adaptations that revive ERK signalling. We have previously shown that RAF proteins inhibit the MST2 proapoptotic pathway in a kinase-independent fashion. Here, we have investigated the role of the MST2 pathway in mediating re

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Dillon, Martha, Antonio Lopez, Edward Lin, Dominic Sales, Ron Perets, and Pooja Jain. "Progress on Ras/MAPK Signaling Research and Targeting in Blood and Solid Cancers." Cancers 13, no. 20 (2021): 5059. http://dx.doi.org/10.3390/cancers13205059.

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The mitogen-activated protein kinase (MAPK) pathway, consisting of the Ras-Raf-MEK-ERK signaling cascade, regulates genes that control cellular development, differentiation, proliferation, and apoptosis. Within the cascade, multiple isoforms of Ras and Raf each display differences in functionality, efficiency, and, critically, oncogenic potential. According to the NCI, over 30% of all human cancers are driven by Ras genes. This dysfunctional signaling is implicated in a wide variety of leukemias and solid tumors, both with and without viral etiology. Due to the strong evidence of Ras-Raf invol

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Kotoula, Vassiliki, Elias Sozopoulos, Helen Litsiou, et al. "Mutational analysis of the BRAF, RAS and EGFR genes in human adrenocortical carcinomas." Endocrine-Related Cancer 16, no. 2 (2009): 565–72. http://dx.doi.org/10.1677/erc-08-0101.

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The serine/threonine kinase B-Raf plays a key role in the Ras/Raf/MEK/ERK pathway that relays extracellular signals for cell proliferation and survival. Several types of human malignancies harbor activating BRAF mutations, most frequently a V600E substitution. The epidermal growth factor receptor (EGFR), a transmembrane tyrosine kinase (TK) receptor that mediates proliferation and survival signaling, is expressed in a wide variety of normal and neoplastic tissues. EGFR inhibitors have produced objective responses in patients with non-small cell lung carcinomas harboring activating EGFR TK doma

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Rachiglio, Anna Maria, Laura Forgione, Raffaella Pasquale, et al. "Dynamics of RAS/BRAF Mutations in cfDNA from Metastatic Colorectal Carcinoma Patients Treated with Polychemotherapy and Anti-EGFR Monoclonal Antibodies." Cancers 14, no. 4 (2022): 1052. http://dx.doi.org/10.3390/cancers14041052.

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Analysis of plasma-derived cell-free DNA (cfDNA) might allow for the early identification of resistance in metastatic colorectal carcinoma (mCRC) patients receiving anti-EGFR monoclonal antibodies. We tested plasma samples from the Erbitux Metastatic Colorectal Cancer Strategy (ERMES) phase III trial of FOLFIRI+Cetuximab in first-line treatment of RAS/BRAF wild-type mCRC. Samples were collected at baseline (n = 37), at 8 weeks of treatment (n = 32), progressive disease (PD; n = 36) and 3 months after PD (n = 21). cfDNA testing was performed using the Idylla™ ctKRAS and ctNRAS-BRAF tests and th

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Tang, Wentao, Ye Wei, Li Ren, Qing-Hai Ye, Tianshu Liu, and Jianmin Xu. "mFOLFOXIRI+Bev vs. mFOLFOX6+Bev for RAS mutant unresectable colorectal liver-limited metastases: A study protocol of a multicenter randomized controlled phase 3 (BECOME2) trial." Journal of Clinical Oncology 40, no. 4_suppl (2022): TPS228. http://dx.doi.org/10.1200/jco.2022.40.4_suppl.tps228.

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TPS228 Background: Colorectal cancer patients with initially unresectable liver-only metastases may be cured after downsizing of metastases by conversion therapy. However, the optimal regimen of conversion therapy for RAS mutant patients has not been defined. Methods: BECOME2 is a multicenter, randomized, phase 3 clinical study. RAS mutant and BRAF wild type colorectal cancer patients with initially unresectable liver-limited metastases are eligible. The (un)resectability status is prospectively assessed by a central multidisciplinary team (MDT) consisting of at least one radiologist and three

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Wang, Chongkai, Ching Ouyang, Jaideep Singh Sandhu, Michael Kahn, and Marwan Fakih. "Wild-type APC and prognosis in metastatic colorectal cancer." Journal of Clinical Oncology 38, no. 4_suppl (2020): 223. http://dx.doi.org/10.1200/jco.2020.38.4_suppl.223.

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223 Background: Somatic mutations at adenomatous polyposis coli ( APC) gene, found in ~75% of colorectal cancers (CRC), are under-represented in microsatellite instable (MSI-H) tumors. While several studies have suggested worse outcomes for CRC patients (pts) with wild-type APC ( APC-WT), the prognostic implication of this genomic alteration in metastatic CRC (mCRC) is not well defined. Methods: APC prognostic value was evaluated in 331 stage IV microsatellite stable (MSS) CRC pts treated in our institution. Next-generation genomic analysis (FoundationOne) was used to characterize the molecula

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Damato, Angela, Angela Damato, Carlo Aschele, et al. "Phase III study to compare bevacizumab or cetuximab plus FOLFIRI in patients with advanced colorectal cancer RAS/BRAF wild type (wt) on tumor tissue and RAS mutated (mut) in liquid biopsy: LIBImAb Study." Journal of Clinical Oncology 40, no. 16_suppl (2022): TPS3636. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.tps3636.

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TPS3636 Background: KRAS, NRAS, and BRAF mutations are well-established negative predictive biomarkers of response to anti-EGFR monoclonal antibodies (MoAbs) in metastatic colorectal cancer (mCRC) patients (pts). In clinical practice, RAS/BRAF wild-type (wt) patients receive first-line therapy regimens containing anti-EGFR agents. However, tumor heterogeneity might drive primary and acquired resistance to anti-EGFR MoAbs. In fact, circulating tumor DNA (ctDNA) testing reveals RAS/BRAF mutations in approximately 10% of pts who resulted in wt at tumor tissue. In addition, 30% to 50% RAS wt pts d

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Damato, Angela, Angela Damato, Carlo Aschele, et al. "Phase III study to compare bevacizumab or cetuximab plus FOLFIRI in patients with advanced colorectal cancer RAS/BRAF wild type (wt) on tumor tissue and RAS mutated (mut) in liquid biopsy: LIBImAb Study." Journal of Clinical Oncology 40, no. 16_suppl (2022): TPS3636. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.tps3636.

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TPS3636 Background: KRAS, NRAS, and BRAF mutations are well-established negative predictive biomarkers of response to anti-EGFR monoclonal antibodies (MoAbs) in metastatic colorectal cancer (mCRC) patients (pts). In clinical practice, RAS/BRAF wild-type (wt) patients receive first-line therapy regimens containing anti-EGFR agents. However, tumor heterogeneity might drive primary and acquired resistance to anti-EGFR MoAbs. In fact, circulating tumor DNA (ctDNA) testing reveals RAS/BRAF mutations in approximately 10% of pts who resulted in wt at tumor tissue. In addition, 30% to 50% RAS wt pts d

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Formica, Vincenzo, Jessica Lucchetti, Elena Doldo, et al. "Clinical Utility of Plasma KRAS, NRAS and BRAF Mutational Analysis with Real Time PCR in Metastatic Colorectal Cancer Patients—The Importance of Tissue/Plasma Discordant Cases." Journal of Clinical Medicine 10, no. 1 (2020): 87. http://dx.doi.org/10.3390/jcm10010087.

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Background: Tumor tissue (T) mutational analysis represents the standard for metastatic colorectal cancer (mCRC); however, circulating tumor DNA (ctDNA) detected by liquid biopsy in plasma (PL) can better represent tumor heterogeneity. Methods: mCRC patients undergoing standard first-line chemotherapy with known T-KRAS/NRAS/BRAF status were enrolled in the present prospective study. PL mutations were assessed within 2 weeks before chemotherapy start with real time PCR and correlated with T status and Progression free survival (PFS). Clinical and biochemical variables including also total numbe

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Rachiglio, Anna Maria, Alessandra Sacco, Matilde Lambiase, et al. "RAS testing of circulating cell-free DNA (cfDNA) from tissue RAS/BRAF wild-type metastatic colorectal carcinoma (mCRC) patients: Preliminary data from the Liquid Biopsy Monoclonal Antibodies in mCRC (LIBImAb) study." Journal of Clinical Oncology 41, no. 16_suppl (2023): 3046. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.3046.

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3046 Background: In mCRC patients RAS/BRAF testing is usually performed on tissue biopsy in order to select patients for treatment with anti-EGFR monoclonal antibodies. Several studies described discordant RAS status between tissue and cfDNA testing from the same patients. In addition, up to 30% of patients with secondary resistance to anti-EGFR therapies become RAS mutant at progression. The LIBImAb study is a phase III, randomized, open-label, comparative, multi-centre trial to assess the superiority in terms of efficacy of bevacizumab versus cetuximab in combination with FOLFIRI chemotherap

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Kotani, Daisuke, Yoshinori Kagawa, Yuki Matsubara, et al. "TRIDENTE trial: A phase II study of rechallenge with encorafenib, binimetinib, and cetuximab in patients with RAS wild-type/BRAF V600E–mutant metastatic colorectal cancer." Journal of Clinical Oncology 41, no. 4_suppl (2023): TPS264. http://dx.doi.org/10.1200/jco.2023.41.4_suppl.tps264.

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TPS264 Background: The BEACON CRC trial demonstrated survival benefit of combination therapy with encorafenib (ENCO) + cetuximab (CET) +/- binimetinib (BINI) in patients with RAS wild-type (WT)/ BRAF V600E mutant metastatic colorectal cancer (mCRC). However, prognosis of those patients still be poor after the refractoriness to the BEACON combination therapy. One of resistant mechanisms to BRAF inhibitor has been reported as MAPK alterations including RAS mutation, similar to those for anti-EGFR antibody in patients with RAS/ BRAF V600E WT mCRC. Promising results of rechallenge therapy with ant

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Tóth, Béla, Norbert Kiss, Judit Hársing, et al. "Frequent KIT mutations in skin lesions of patients with BRAF wild-type Langerhans cell histiocytosis." Virchows Archiv 477, no. 5 (2020): 749–53. http://dx.doi.org/10.1007/s00428-020-02820-w.

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Abstract Langerhans cell histiocytosis (LCH) is characterized by mutations of the RAS-RAF-MAPK signaling pathway. We analyzed MAP2K1, NRAS and KIT mutation incidence in skin lesions of BRAF wild-type (wt) LCH patients. We evaluated the occurrence of MAP2K1, NRAS and KIT mutations in seven LCH and one indeterminate cell histiocytosis (ICH) patients. MAP2K1 mutation frequency was found to be 3/7 (42.9%) in LCH and also found in ICH. Similarly, the KIT mutation frequency was found to be equally prevalent (4/7, 57.1%) in LCH and also occurred in ICH. Involvement of KIT exons in LCH-ICH indicated t

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Hwang, Kwangwoo, SeoHyun Jo, Jieun Choi, et al. "Abstract LB521: Antitumor activity of potent RAF inhibitors in solid tumors with activated RAS-RAF axis." Cancer Research 82, no. 12_Supplement (2022): LB521. http://dx.doi.org/10.1158/1538-7445.am2022-lb521.

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Abstract FDA approved three RAF inhibitors for the treatment of tumors containing BRAFV600 mutations, but one of the major drawbacks of these type I RAF inhibitors is to activate MAPK signaling pathway, instead of inhibiting signaling, which is referred to as paradoxical activation. Such undesired paradoxical activation not only leads to renewed tumor growth but also spurs additional cancer growth in non-cancerous wild-type BRAF tissue. Plus, these first-generation RAF inhibitors targeting BRAFV600 mutants are unable to inhibit oncogenic RAF dimers. This has led to the development of type II R

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ESER, KADIR. "The Effect of Tumor Sideness and Mutational Status on First Line Treatment Response and Survival in The Patients with Metastatic Colorectal Cancer." International Journal of Hematology and Oncology 30, no. 4 (2020): 197–206. http://dx.doi.org/10.4999/uhod.204659.

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RAS and BRAF mutation and primary tumour sideness are prognostic and predictive factors in metastatic colorectal cancer (mCRC). We aimed to investigate RAS-BRAF mutation rates and responses to biologic agents the effects of tumour sideness on survival. This was a retrospective study conducted at three Turkish institutes. 303 patients with mCRC who were examined for tumour RAS and 172 examined for tumour BRAF mutations between 2006-2018. A total of 303 (M/F= 186/117) patients were included to study. Median age was 63 (range: 23-86) years. Median follow-up was 22.8 (range: 19.1-26.4) months. In

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Tsuji, Akihito, Yu Sunakawa, Manabu Shiozawa, et al. "Final analysis of modified (m)-FOLFOXIRI plus cetuximab versus bevacizumab for RAS wild-type and left-sided metastatic colorectal cancer: The DEEPER trial (JACCRO CC-13)." Journal of Clinical Oncology 43, no. 4_suppl (2025): 17. https://doi.org/10.1200/jco.2025.43.4_suppl.17.

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17 Background: The DEEPER trial (NCT02515734), which evaluated m-FOLFOXIRI (irinotecan 150 mg/m², oxaliplatin 85 mg/m², 5-FU 2400 mg/m²) plus cetuximab (cet) vs. bevacizumab (bev) as initial therapy in terms of depth of response (DpR) as the primary endpoint in RAS wild-type metastatic colorectal cancer (mCRC), has demonstrated a significantly better DpR in the cet arm (ASCO 2021). Moreover, favorable progression-free survival (PFS) was reported in the cet arm for patients (pts) with RAS / BRAF wild-type and left-sided tumors (ESMO 2023). Due to the small number of overall survival (OS) events

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Gouda, Mohamed Alaa, Heather Y. Lin, Lei Kang, et al. "Response to RAF/MEK/ERK inhibitors in patients with RAS altered and wild-type tumors." Journal of Clinical Oncology 42, no. 16_suppl (2024): 3099. http://dx.doi.org/10.1200/jco.2024.42.16_suppl.3099.

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3099 Background: The MAPK pathway is frequently activated in different cancers. Inhibitors of different molecules across this pathway have been developed and approved including BRAF, MEK, and ERK inhibitors. However, limited data are available regarding response in patients with upstream RAS alterations. The interplay between RAS and downstream RAF/MEK/ERK has been commonly noted; although distinct conclusions have been debated. In this study, we aimed to explore possible associations between RAS status and therapeutic outcomes to RAF/MEK/ERK inhibition in patients with advanced solid tumors.

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Ciardiello, Davide, Stefania Napolitano, Vincenzo Famiglietti, et al. "Pretreatment Plasma Circulating Tumor DNA RAS/BRAF Mutational Status in Refractory Metastatic Colorectal Cancer Patients Who Are Candidates for Anti-EGFR Rechallenge Therapy: A Pooled Analysis of the CAVE and VELO Clinical Trials." Cancers 15, no. 7 (2023): 2117. http://dx.doi.org/10.3390/cancers15072117.

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Rechallenge with anti-EGFR drugs represents a promising strategy in refractory RAS/BRAF wild-type (WT) metastatic colorectal cancer (mCRC). We performed the pooled analysis of the CAVE and VELO studies to evaluate the percentage of patients with WT circulating tumor DNA (ctDNA) tumors and the association of mutational status with time from the last anti-EGFR drug administration. At baseline, 97/129 patients had RAS/BRAF WT plasma ctDNA, while 32/129 had RAS/BRAF mutated plasma ctDNA. Median anti-EGFR drug-free interval was 10.6 (CI 95%, 8.9–13.4) months in the plasma RAS/BRAF mutant group as c

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Hill, Kristen S., Evan R. Roberts, Xue Wang, et al. "Abstract PR13: PTPN11 plays oncogenic roles and is a therapeutic target for BRAF wild-type melanomas." Cancer Research 80, no. 19_Supplement (2020): PR13. http://dx.doi.org/10.1158/1538-7445.mel2019-pr13.

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Abstract Melanoma is one of the most highly mutated cancer types, harboring numerous alterations with unknown significance. To identify functional drivers of melanoma, we searched for cross-species conserved mutations utilizing a mouse melanoma model driven by loss of PTEN and CDKN2A, and identified mutations in Kras, Erbb3, and Ptpn11. PTPN11 encodes the SHP2 protein tyrosine phosphatase (PTP) that activates the RAS/RAF/MAPK pathway. Although PTPN11 is an oncogene in leukemia, lung, and breast cancers, its roles in melanoma are not clear. In this study, we found that PTPN11 is frequently acti

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Miller, Nichol L. G., Tim S. Wang, Paul Severson, et al. "Abstract 2674: Antitumor activity of KIN-2787, a next-generation pan-RAF inhibitor, in preclinical models of human RAF/RAS mutant melanoma." Cancer Research 82, no. 12_Supplement (2022): 2674. http://dx.doi.org/10.1158/1538-7445.am2022-2674.

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Abstract Background: In the US in 2021, invasive melanoma will account for an estimated 106,000 new cases and &gt; 7,000 deaths. Somatic mutations that activate the MAPK signaling pathway are a leading cause of melanoma with 50% harboring oncogenic BRAF alterations and another 20% with activating NRAS mutations. Of note, NRAS mutant melanoma has been shown to be dependent upon RAF signaling via CRAF dimers for downstream activation of MEK/ERK. While targeted therapies are approved for V600 (Class I, monomer-driven) BRAF mutant melanoma, no approved targeted therapy exists for patients with

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da Silva Soley, Bruna, Radhika Athalye, Ryan Zhang, Thomas Andl та Yuhang Zhang. "Abstract 296: BRAFi-induced ROCK-mediated non-canonical nuclear β-catenin shuttling drives a phenotypic switch in cancer-associated fibroblasts". Cancer Research 84, № 6_Supplement (2024): 296. http://dx.doi.org/10.1158/1538-7445.am2024-296.

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Abstract The discovery of BRAF mutations in around 60% of melanoma patients and the subsequent development of targeted inhibitors to counter the hyperactive BRAF-driven pro-tumorigenic signaling pathway have marked a significant milestone in melanoma therapy. However, despite this progress, the long-term outcomes remain unsatisfactory for many patients due to the occurrence of drug resistance. We previously reported that cancer-associated fibroblasts (CAFs) are stimulated by BRAF inhibitors (BRAFi) to drive matrix remodeling and therapeutic escape pathways in melanoma cells. However, the under

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Desaunay, Mathieu, Tara L. Peters, Beau Baars, et al. "Abstract LB294: Mechanism of tumor-selective inhibition of dimeric RAF by a Type 1 RAF inhibitor." Cancer Research 85, no. 8_Supplement_2 (2025): LB294. https://doi.org/10.1158/1538-7445.am2025-lb294.

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Abstract Over a third of human tumors are driven by deregulated RAS/MAPK signaling, frequently by mutations in RAS or BRAF. First generation RAF inhibitors bind in the Type 1.5 mode (αC-OUT/DFG-IN) and are effective in inhibiting monomeric BRAF(V600X), while inducing paradoxical RAF and MAPK activation in contexts where RAF signals as dimer, including wild-type and RAS-Mutant (RAS-MUT) settings. Thus, these inhibitors are only active against BRAF(V600X), and paradoxical MAPK activation in normal cells enables vertical MAPK-targeting combinations with MEK or EGFR antagonists. These combinations

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Karimi, Misagh, Chongkai Wang, Bahareh Bahadini, George Hajjar, and Marwan Fakih. "Integrating Academic and Community Practices in the Management of Colorectal Cancer: The City of Hope Model." Journal of Clinical Medicine 9, no. 6 (2020): 1687. http://dx.doi.org/10.3390/jcm9061687.

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Colorectal cancer (CRC) management continues to evolve. In metastatic CRC, several clinical and molecular biomarkers are now recommended to guide treatment decisions. Primary tumor location (right versus left) has been shown to predict benefit from anti-epidermal growth factor receptors (EGFRs) in rat sarcoma viral oncogene homologue (RAS) and v-raf murine sarcoma viral oncogene homolog B1 (BRAF) wild-type patients. Anti-EGFR therapy has not resulted in any benefit in RAS-mutated tumors, irrespective of the primary tumor location. BRAF-V600E mutations have been associated with poor prognosis a

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Mariani, Stefano, Marco Puzzoni, Nicole Liscia, et al. "Liquid biopsy-driven anti-EGFR rechallenge in patients with metastatic colorectal cancer." Journal of Clinical Oncology 39, no. 15_suppl (2021): 3577. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.3577.

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3577 Background: The rechallenge with EGFR inhibitors represents an emerging strategy for anti-EGFR pre-treated patients with RAS wild type colorectal cancer (CRC). Unfortunately definitive selection criteria for anti-EGFR rechallenge in this setting are lacking. Very recently RAS wild type status on circulating tumor DNA (ct-DNA) at the time of rechallenge along with already known clinical criteria emerged as a potential watershed for this strategy. In the present study we explored liquid biopsy-driven anti-EGFR rechallenge strategy in the clinical practice for patients with metastatic colore

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Mazurenko, N. N., V. V. Yugay, and I. V. Tsyganova. "Molecular features of gastrointestinal stromal tumors “wild-type” (<i>KIT/PDGFRA</i> WT)." Advances in Molecular Oncology 10, no. 4 (2023): 61–75. http://dx.doi.org/10.17650/2313-805x-2023-10-4-61-75.

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Gastrointestinal stromal tumors (GIST) are the most common mesenchymal tumors of the gastrointestinal tract. Their main features are the expression of CD117 (KIT) and mutations of KIT or PDGFRA in 85 % of patients. however, 10–15 % of adult GIST and 85 % of pediatric GIST do not have KIT/PDGFRA mutations (KIT/PDGFRA WT GIST or “wild-type” GIST). The prognosis and clinical course of these tumors and GIST with KIT/PDGFRA mutations differ. “Wild-type” GIST are quite heterogeneous group of tumors in terms of clinical phenotype, genetic etiology, and molecular pathways. Gastrointestinal stromal tum

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Guan, Michelle, R. Joseph Bender, Michael J. Pishvaian, et al. "Molecular and clinical characterization of BRAF mutations in pancreatic ductal adenocarcinomas (PDACs)." Journal of Clinical Oncology 36, no. 4_suppl (2018): 214. http://dx.doi.org/10.1200/jco.2018.36.4_suppl.214.

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214 Background: The activation of the RAS/RAF/MEK/ERK pathway is critical for the proliferation, survival, and tumorigenesis of PDACs. Oncogenic mutations in KRAS (90%) or BRAF (3%) are recurrent genomic alterations, but their co-occurrence is not well described. We reviewed BRAF alterations and clinical outcomes in consecutive PDAC patients (pts). Methods: Perthera, Inc. deploys an IRB-approved registry that was utilized in partnership with PanCAN’s “Know Your Tumor” program. Perthera uses CAP/CLIA accredited multi-Omic profiling, including next generation DNA sequencing (NGS, Foundation Medi

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Peeters, Marc, Frédéric Forget, Meinolf Karthaus, et al. "Exploratory pooled analysis evaluating the effect of sequence of biological therapies on overall survival in patients with RAS wild-type metastatic colorectal carcinoma." ESMO Open 3, no. 2 (2018): e000297. http://dx.doi.org/10.1136/esmoopen-2017-000297.

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BackgroundThe aim of this study was to evaluate the optimal sequence of targeted therapies (epidermal growth factor receptor inhibitors (EGFRi) and vascular endothelial growth factor inhibitors (VEGFi)), combined with chemotherapy, in patients with RAS wild-type (WT) metastatic colorectal carcinoma (mCRC). Exploratory analyses of overall survival (OS) for patients treated with either first-line panitumumab (EGFRi) and second-line VEGFi therapy, or first-line bevacizumab (VEGFi) and second-line EGFRi, were conducted.MethodsPatients from PEAK (NCT00819780), PRIME (NCT00364013) and Study 181 (NCT

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Chibaudel, Benoist, Hubert Richa, Elisabeth Carola, et al. "Clinical/molecular features and prognostic significance of RAS mutant-low versus RAS mutant-high in patients with metastatic colorectal cancer." Journal of Clinical Oncology 42, no. 3_suppl (2024): 187. http://dx.doi.org/10.1200/jco.2024.42.3_suppl.187.

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187 Background: Addressing tumor heterogeneity is one of the main advantage of liquid biopsy over tissue biopsy, as liquid biopsy is likely to better reflect the global molecular profile (primary tumor site and metastatic disease). Variant Allele Frequency (VAF) represents the fraction of sequencing reads in which a variant is observed. The aim was to evaluate the prognostic value of circulating tumor (ct) VAF for KRAS and NRAS genes in patients with ctRAS mutant metastatic colorectal cancer (MCRC). Methods: Circulating comprehensive genomic profiling using FoundationOne Liquid CDx (FO-Liq) wa

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Kotani, Daisuke, Sebastián Mondaca, Aparna Parikh, et al. "Clinicopathological features, efficacy of anti-EGFR therapy, and survival outcomes in patients with BRAF non-V600 mutated metastatic colorectal cancer." Journal of Clinical Oncology 37, no. 4_suppl (2019): 659. http://dx.doi.org/10.1200/jco.2019.37.4_suppl.659.

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659 Background: BRAF non-V600 mutations occur in 2-3% of colorectal cancer. These mutants can be classified as RAS independent (class 2) or RAS dependent (class 3). We reported BRAF non-V600 mutations could be a negative predictive factor for anti-EGFR therapy in patients (pts) with pretreated metastatic colorectal cancer (mCRC), while mCRC pts with class 3 BRAF mutations could respond to anti-EGFR therapy because of its dependency on receptors and RAS. Methods: This study evaluates the efficacy to anti-EGFR therapy in a large cohort of pts with BRAF non-V600 mutated mCRC. Pts with mCRC referr

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Jasmine, Farzana, Briseis Aschebrook-Kilfoy, Mohammad M. Rahman, et al. "Association of DNA Promoter Methylation and BRAF Mutation in Thyroid Cancer." Current Oncology 30, no. 3 (2023): 2978–96. http://dx.doi.org/10.3390/curroncol30030227.

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The BRAF V600E mutation and DNA promoter methylation play important roles in the pathogenesis of thyroid cancer (TC). However, the association of these genetic and epigenetic alterations is not clear. In this study, using paired tumor and surrounding normal tissue from the same patients, on a genome-wide scale we tried to identify (a) any association between BRAF mutation and DNA promoter methylation, and (b) if the molecular findings may provide a basis for therapeutic intervention. We included 40 patients with TC (female = 28, male = 12) without distant metastasis. BRAF mutation was present

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Lee, Darren, Yazan Abu-Shihab, Deedra Nicolet, et al. "BRAF-Mutated Acute Myeloid Leukemia (AML) Represents a Prognostically Poor Subgroup Enriched for Myelodysplasia-Related Subtypes and Distinct from Other RAS Pathway Mutant AML." Blood 144, Supplement 1 (2024): 2921. https://doi.org/10.1182/blood-2024-210110.

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Background: MAPK/RAS signaling pathway mutations are common somatic events in de novo and secondary acute myeloid leukemia (AML), occurring mainly in NRAS, KRAS, and/or PTPN11. BRAF mutations occur with lower frequency in AML and are reported to be universally associated with poor outcome. To date, no comprehensive analysis exists that decisively assesses clinical and molecular characteristics of BRAF-mutated (BRAFm) AML, including insights into clonal architecture, co-occurring mutations, and disease immunophenotype. Methods: We identified 42 AML pts harboring BRAF mutations through targeted

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Brodowicz, Thomas, Damir Vrbanec, Klaus Kaczirek, et al. "FOLFOX4 plus cetuximab administered weekly or every two weeks in first-line treatment of patients with KRAS and NRAS wild-type (wt) metastatic colorectal cancer (mCRC)." Journal of Clinical Oncology 32, no. 3_suppl (2014): LBA391. http://dx.doi.org/10.1200/jco.2014.32.3_suppl.lba391.

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LBA391^ Background: Efficacy and safety of first-line FOLFOX4 plus either cetuximab (weekly or every two weeks) have been reported to be similar in 152 patients with KRAS exon 2 wt mCRC within the randomized phase II CECOG/CORE2 study. Recent analyses have shown that also mutations in KRAS exons 3/4 and NRAS (exons 2, 3, and 4) are associated with an inferior PFS and OS with EGFR-targeted monoclonal antibody containing therapy. The impact of these additional mutations on the reported findings in the CECOG/CORE2 study were investigated. Methods: Tumor samples of 148 randomized KRAS exon 2 wild-

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Garawin, Tamer, Kimberly Lowe, George Kafatos, and Samuel Murray. "The prevalence RAS and BRAF mutations among patients in the Middle East and Northern Africa with metastatic colorectal cancer." Journal of Clinical Oncology 34, no. 4_suppl (2016): 598. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.598.

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598 Background: Anti-EGFR therapies are recommended for metastatic colorectal cancer (mCRC) patients with confirmed wild-type RAS (exons 2, 3, 4 of KRAS and NRAS) status. There is limited published information on the prevalence of RAS mutations using real world data. The objective of this study was estimate the prevalence of RAS and BRAF mutations among patients with mCRC in the Middle East and Northern Africa (MENA) in an effort to inform the rationale for biomarker testing and treatment choice. Methods: The study included 1,669 patients from August 2013 to July 2015 with mCRC from Algeria, B

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Nakayama, Izuma, Eiji Shinozaki, Takeru Wakatsuki, et al. "The significance of EGFR pathway mutations for the efficacy of first line treatment with bevacizumab in metastatic colonrectal cancer." Journal of Clinical Oncology 33, no. 3_suppl (2015): 699. http://dx.doi.org/10.1200/jco.2015.33.3_suppl.699.

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699 Background: After analysis of minor RAS mutations (KRAS exon3, 4/NRAS) in FIRE-3 or PRIME study, so called all RAS mutation would be being regarded as a biomarker for anti-EGFR antibodies. BRAF and PIK3CA mutation would be a candidate of biomarkers for anti EGFR targeted therapies. However it remains unknown whether EGFR pathway mutations affect the efficacy of bevacizumab in Stage.‡W CRC. Methods: Of the 1,001 consecutive patients of CRC in our institute between Nov 2006 and Dec 2013, we examined RAS, PIK3CA and BRAF mutational status, 141 patients received systemic chemotherapy for the f

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Mesti, Tanja, Marko Boc, Martina Rebersek, Zvezdana Hlebanja, Neva Volk, and Janja Ocvirk. "KRAS, NRAS and BRAF mutational status and first line treatment patterns in Slovenian population with metastatic colorectal carcinoma: Five year results." Journal of Clinical Oncology 39, no. 15_suppl (2021): e15546-e15546. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e15546.

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e15546 Background: A phase IV non-interventional study was performed from 2013 till 2018 including 650 patients with primary aim to assess KRAS, NRAS and BRAF mutational status in Slovenian population with metastatic colorectal carcinoma (mCRC) suitable for first-line treatment. The evaluation of decisions for first-line treatment regarding the biomarkers status and assessing the possible impact of the time period of the biomarker status analysis report on the treatment decision were also incorporated in the analysis. The molecular analyses for KRAS and NRAS gene mutations were performed on ex

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Giordano, Guido, Pietro Parcesepe, Giuseppina Bruno, et al. "Evidence-Based Second-Line Treatment in RAS Wild-Type/Mutated Metastatic Colorectal Cancer in the Precision Medicine Era." International Journal of Molecular Sciences 22, no. 14 (2021): 7717. http://dx.doi.org/10.3390/ijms22147717.

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Target-oriented agents improve metastatic colorectal cancer (mCRC) survival in combination with chemotherapy. However, the majority of patients experience disease progression after first-line treatment and are eligible for second-line approaches. In such a context, antiangiogenic and anti-Epidermal Growth Factor Receptor (EGFR) agents as well as immune checkpoint inhibitors have been approved as second-line options, and RAS and BRAF mutations and microsatellite status represent the molecular drivers that guide therapeutic choices. Patients harboring K- and N-RAS mutations are not eligible for

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Morano, Federica, Salvatore Corallo, Sara Lonardi, et al. "Negative Hyperselection of Patients With RAS and BRAF Wild-Type Metastatic Colorectal Cancer Who Received Panitumumab-Based Maintenance Therapy." Journal of Clinical Oncology 37, no. 33 (2019): 3099–110. http://dx.doi.org/10.1200/jco.19.01254.

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PURPOSE We assessed the prognostic/predictive role of primary tumor sidedness and uncommon alterations of anti–epidermal growth factor receptor (EGFR) primary resistance (primary resistance in RAS and BRAF wild-type metastatic colorectal cancer patients treated with anti-EGFR monoclonal antibodies [PRESSING] panel) in patients with RAS/ BRAF wild-type (wt) metastatic colorectal cancer (mCRC) who were randomly assigned to panitumumab plus fluorouracil, leucovorin, and oxaliplatin (FOLFOX-4) induction followed by maintenance with panitumumab with or without fluorouracil (FU) plus leucovorin (LV)

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