Relevant bibliographies by topics / BRAF/RAS wild type

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'BRAF/RAS wild type'

Author: Grafiati
Published: 10 December 2022
Last updated: 31 July 2025

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

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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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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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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 < .0001), and wild-typ
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Dissertations / Theses on the topic "BRAF/RAS wild type"

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Rebecca, Vito William. "Potential Targeted Therapeutic Strategies for Overcoming Resistance in BRAF Wild Type Melanoma." Scholar Commons, 2014. http://scholarcommons.usf.edu/etd/5112.

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Melanoma manifests itself from the malignant transformation of melanocytes and represents the deadliest form of skin cancer, being responsible for the disproportionate majority of all skin cancer deaths. The 2002 discovery that 50% of all melanoma patients possess activating BRAF mutations ignited a significant paradigm shift in the way the melanoma field approached research and how patients were treated [1]. The era of targeted therapy had begun and with it came successful targeted BRAF inhibitor therapy regimens, which have accomplished improved clinical benefit (response rate, progression f
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Moka, Nagaishwarya, Kelley cross, Marianne Brannon, et al. "Delta-tocotrienol and simvastatin induces differential cytotoxicity and synergy in BRAF wild-type SK-MEL-2 and mutant BRAF SK-MEL-28 melanoma cancer cells." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/215.

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Targeting the mutant BRAF and immunotherapy are new approaches to the treatment of metastatic malignant melanoma that has significantly improved survival but is associated with significant toxicity and cost. Potent and specific BRAF inhibitors like vemurafenib and dabrafenib are superior to chemotherapy in treatment of BRAF mutant melanomas which represent nearly 50% of all melanomas. A less toxic approach to treatment of malignant melanoma is hence appealing. Delta-tocotrienol (DT3), an unsaturated vitamin E isoform, and simvastatin, an HMG-CoA reductase inhibitor have been shown to have anti
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PUZZONI, MARCO. "Selection with a molecUlar PanEl foR Panitumumab EfficAcy in K-RAS and N-RAS wild type metastatic colorectal cancer (SUPER-PEAK)." Doctoral thesis, Università degli Studi di Cagliari, 2021. http://hdl.handle.net/11584/305679.

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BACKGROUND: Clinical reports with the use of monoclonal antibodies directed against the ligand-binding site of the epidermal growth factor receptor (EGFR) have shown practice-changing results in the treatment of colorectal cancer. However if on the one hand we are now able to exclude from anti-EGFR treatment more patients with putative refractory colorectal tumours (i.e. those harboring a RAS mutant status), on the other hand we are still incapable to accurately select responding patients among those without RAS mutations. Most of the biological factors analysed in the attempt to improve patie
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Ferguson, Robert. "Wild-type N-Ras complements mutant K-Ras in pancreatic cancer cell lines but K-Ras has a specific role in cell cycle independent regulation of G2 cyclins." Thesis, University of Liverpool, 2015. http://livrepository.liverpool.ac.uk/2032380/.

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Pancreatic Ductal Adenocarcinoma (PDAC) is nearly always associated with mutant K-Ras. Nevertheless, targeting oncogenic K-Ras has so far proved ineffective in treating this form of cancer and pancreatic cancer cell lines can become K-Ras independent. Other forms of Ras are rarely mutated but wild type N-Ras and H-Ras have been shown to be present alongside functional K-Ras mutations and have been demonstrated to increase responsiveness to growth factors. Beyond this little evidence had previously been gathered on the activity or function of N-Ras and H-Ras in PDAC. Therefore, this thesis aime
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Sree, Kumar Shalini. "Biomarkers of resistance to anti-EGFR in wild type KRAS/BRAF colorectal cancer cell lines." Thesis, 2015. http://hdl.handle.net/2440/104679.

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Colorectal cancer (CRC) is a leading cause of cancer death worldwide and despite significant improvement the median survival remains relatively poor. The use of targeted therapies like cetuximab and panitumumab inhibiting the epidermal growth factor receptor (EGFR) offer promise in improving patient outcomes. However, a high proportion of CRC patients show resistance to anti-EGFR therapy. Biomarkers such as mutant KRAS or BRAF predict resistance to anti-EGFR therapy in only a subset of patients and we hypothesise that other biomarkers for resistance to EGFR targeted therapies exist. The studie
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Weyandt, Jamie Dawn. "Investigatiing the Role of the Wild-Type Ras Isoforms in KRas-driven Cancer." Diss., 2015. http://hdl.handle.net/10161/11392.

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<p>The RAS family is a group of small GTPases that can become constitutively activated by point mutations that are found in about 30% of all cancer patients. There are three well-characterized RAS family members: HRAS, NRAS, and KRAS, the latter of which is alternatively spliced at the C-terminus into KRAS4A and KRAS4B. The RAS proteins are all nearly identical at their N-termini and core effector binding domains, but have divergent C-terminal membrane-binding regions that impart different subcellular localization and subtle differences in signaling. Although the role of constitutively acti
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Chun-ILi and 李俊毅. "The effect of miR-146a and target gene vimentin on tumorigenesis of esophageal squamous cell carcinoma cell lines overexpressing wild-type K-Ras gene." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/b64k4e.

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Book chapters on the topic "BRAF/RAS wild type"

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Chandra, Sunandana, Grant McArthur, and Jeffrey Sosman. "Molecularly Targeted Therapy for Patients with BRAF Wild-Type Melanoma." In Cutaneous Melanoma. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-46029-1_55-1.

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Chandra, Sunandana, Grant A. McArthur, and Jeffrey Sosman. "Molecularly Targeted Therapy for Patients with BRAF Wild-Type Melanoma." In Cutaneous Melanoma. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-05070-2_55.

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Wittinghofer, Alfred, Sybille M. Franken, Axel J. Scheidig, et al. "Three-Dimensional Structure and Properties of Wild-Type and Mutant H-ras-Encoded p21." In Ciba Foundation Symposium 176 - The GTPase Superfamily. John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514450.ch2.

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Wittinghofer, Alfred, and Alfonso Valencia. "Three-dimensional structure of Ras and Ras-related proteins." In Guidebook to the Sinall GTPases. Oxford University PressOxford, 1995. http://dx.doi.org/10.1093/oso/9780198599456.003.0003.

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Abstract The structures of several different wild-type and mutantp21 complexes have been determined by two groups. A listof the published structures is shown in Table 1 togetherwith the resolutions obtained in the crystallographic analyses.For wild-type and one oncogenic mutant both thetriphosphate and diphosphate structures have been determined.For the triphosphate complex of p21 the non-cleavableanalogues GppNHp and Gpp(CH2)p were used,because GTP and even GTPy.i are hydrolysed by p21 duringcrystallization.
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Babu, Geethu, R. Rejnish Ravi Kumar, Malu Rafi, et al. "Systemic Therapy in Thyroid Cancer." In Thyroid Cancer - The Road From Genes to Successful Treatment [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106462.

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The standard treatment for patients with differentiated thyroid cancer (DTC) is a combination of surgery, radioactive iodine (RAI), and long-term thyroid hormone–suppression therapy. Treatment of patients whose diseases persist, recur, or metastasize remains a challenge. The role of cytotoxic chemotherapy in the treatment of thyroid cancer is limited. The key signaling pathways involved in the pathogenesis of thyroid cancers are the RAS/RAF/MEK &amp; PI3K/Akt/mTOR pathways. Systemic therapy in thyroid cancer involves the use of tyrosine kinase inhibitors targeting the above mentioned pathways
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Jinga, Dan-Corneliu, and Maria-Ruxandra Jinga. "Immunotherapy of Metastatic Melanoma." In Melanoma - Standard of Care, Challenges, and Updates in Clinical Research [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105585.

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Immunotherapy is part of the new treatments that significantly improved the prognostic of metastatic melanoma patients. The article reviews briefly the old immunotherapeutic approaches e.g., interferon-ᾳ2 and interleukin-2, and focuses on immune checkpoint inhibitors such as anti-CTLA-4 inhibitors and anti-PD-1 inhibitors in monotherapy or in combination (dual immune blockade). We detailed the results from CheckMate and KEYNOTTE clinical trials that lead to US Food and Drug Administration and European Medicines Agency approvals of the new agents for the treatment of advanced melanoma. The chap
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Tartaglia, Marco, and Bruce D. Gelb. "RAS Signaling Defects and Noonan Syndrome." In Inborn Errors Of Development. Oxford University PressNew York, NY, 2008. http://dx.doi.org/10.1093/oso/9780195306910.003.0063.

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Abstract Moonan syndrome (OMIM 163950) is a pleomorphic disorder affecting the cardiovascular, craniofacial, skeletal, hematopoietic, lymphatic, and central nervous systems. It can result from mutations in the PTPN11 gene, which encodes the protein tyrosine phosphatase (PTP), Src homology 2 (SHP-2), or the KRAS gene, which encodes a RAS GTPase. The disorder is generally transmitted as an autosomal dominant trait, although many cases result from de novo mutations. Defects in the PTPN11 gene, which resides at chromosomal band 12q24.1, account for approximately 50% of cases. The more than 60 muta
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Tizro, Parastou, Rami Abdulbaki, Anita Aggarwal, Aaron Auerbach, and Victor E. Nava. "Splenic B-Cell Lymphoma/Leukemia, Unclassifiable." In Lymphoma [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101418.

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Splenic B-cell lymphoma/leukemia, which is unclassifiable, includes low-grade B-cell lymphoproliferative disorders that do not fit into any other splenic lymphoid neoplasm based on current WHO classification. Presently, two provisional entities, splenic diffuse red pulp small B-cell lymphoma (SDRPL) and hairy-cell leukemia variant (HCL-v), are the most recognizable members of this group. SDRPL is an uncommon malignancy representing less than 1% of all non-Hodgkin lymphomas. Frequent clinical manifestations include splenomegaly and lymphocytosis. SDRPL is currently considered a diagnosis of exc
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Conference papers on the topic "BRAF/RAS wild type"

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Poulikakos, Poulikos I., Chao Zhang, Eric W. Joseph, et al. "Abstract LB-190: RAF inhibitors transactivate RAF dimers and ERK signaling in a wild-type BRAF-dependent manner." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-190.

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Capparelli, Claudia, Nadège Gaborit, Yosef Yarden, and Andrew Aplin. "Abstract C44: Targeting neuregulin1-ErbB3 signaling in wild-type BRAF/NRAS melanoma." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c44.

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Popovici, Vlad, Eva Budinska, Sabine Tejpar, et al. "Abstract 4722: A BRAF-mutated gene expression signature identifies BRAF wild type colon cancer patients with poor prognosis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4722.

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Ming, Zizhen, Su Yin Lim, Richard F. Kefford, and Helen Rizos. "Abstract 765: Multiple signalling pathways are active in BRAF/NRAS wild type melanomas." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-765.

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Banjin, Maja, Amina Jalovčić, and Velda Smajlbegović. "CILJANA TERAPIJA I METASTATSKI MELANOM." In Okrugli sto s međunarodnim učešćem "Melanom". Akademija nauka i umjetnosti Bosne i Hercegovine, 2018. http://dx.doi.org/10.5644/pi2019.180.02.

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Melanom je globalni zdravstveni problem s kontinuiranim porastom u incidence. Rezultati tretmana metastatskog melanoma su, do skorašnjih napredovanja u terapijama, bili slabi, s medijanom ukupnog preživljavanja (OS) od 7,5 mjeseci i petogodišnjom stopom preživljavanja 6%. U kliničkim istraživanjima za metastatski melanom, selektivni inhibitori BRAF gena, vemurafenib i dabrafenib, pokazali su značajnu antitumorsku aktivnost i poboljšanje u OS i PFS kada se porede s dakarbazinom. Međutim, skoro će svaki pacijent tretiran BRAF inhibitorima imati progresiju bolesti, a tumori pokazuju reaktivacije
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Zhang, Yanping, Guangyong Peng, and Eddy C. Hsueh. "Abstract 375: Combination of MEK and PI3K inhibition in BRAF wild-type and mutant melanoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-375.

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Fragomeni, Roberto A. Salas, Hye-Won Chung, Sharon Shacham, Michael Kauffman, and James C. Cusack. "Abstract 1914: Potent anticancer activity against both BRAF-mutant and BRAF wild-type melanoma cell lines using a novel CRM1 nuclear export inhibitor." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1914.

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Rosenbaum, Sheera, Claudia Capparelli, Lisa D. Berman-Booty, et al. "Abstract A52: Extracellular matrix regulation of ErbB3 in a subset of wild-type BRAF/NRAS melanoma." In Abstracts: AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; September 14-17, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.pi3k14-a52.

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Haendler, Bernard, Kathy A. Gelato, Laura Schöckel, et al. "Abstract 4703: The BET inhibitor BAY 1238097 shows efficacy in BRAF wild-type and mutant melanoma models." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4703.

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Essner, Richard, Ke Wei Gong, David Kaufman, et al. "Abstract A26: Protein phosphatase 4 (PP4) as a potential therapeutic target gene for BRAF wild type melanoma." In Abstracts: AACR Special Conference on Advances in Melanoma: From Biology to Therapy; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.mel2014-a26.

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