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Relevant bibliographies by topics / Ras Proto-oncogene proteins B-raf

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Academic literature on the topic 'Ras Proto-oncogene proteins B-raf'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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Journal articles on the topic "Ras Proto-oncogene proteins B-raf"

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Zebisch, Armin, Philipp B. Staber, Katja Fischereder, et al. "Two Novel Activating Germline Mutations of the C-RAF Proto-Oncogene Predisposing to Solid Tumors and Therapy-Related Acute Myeloid Leukemia." Blood 104, no. 11 (2004): 3370. http://dx.doi.org/10.1182/blood.v104.11.3370.3370.

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Abstract Constitutive activation of the RAS-RAF-MEK-ERK signaling cascade plays an important role in the pathogenesis of AML. We were interested whether abnormalities of the serine-threonine kinases A -, B, - and C -RAF occur in AML and whether they might be causative for activation of this pathway. Expression of these genes was assessed by real-time quantitative (rtq) PCR in 102 patient samples of AML, three AML cell lines and normal CD34+ cells of seven individuals. Results were correlated with the phosphorylation status of ERK 1/2, as measured by immunoblot analysis. 45/82 (54,9%) of AML ca

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Nelson, Andrew C., Thomas J. Turbyville, Srisathiyanarayanan Dharmaiah, et al. "RAS internal tandem duplication disrupts GTPase-activating protein (GAP) binding to activate oncogenic signaling." Journal of Biological Chemistry 295, no. 28 (2020): 9335–48. http://dx.doi.org/10.1074/jbc.ra119.011080.

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The oncogene RAS is one of the most widely studied proteins in cancer biology, and mutant active RAS is a driver in many types of solid tumors and hematological malignancies. Yet the biological effects of different RAS mutations and the tissue-specific clinical implications are complex and nuanced. Here, we identified an internal tandem duplication (ITD) in the switch II domain of NRAS from a patient with extremely aggressive colorectal carcinoma. Results of whole-exome DNA sequencing of primary and metastatic tumors indicated that this mutation was present in all analyzed metastases and exclu

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Wiechmann, Svenja, Pierre Maisonneuve, Britta M. Grebbin, et al. "Conformation-specific inhibitors of activated Ras GTPases reveal limited Ras dependency of patient-derived cancer organoids." Journal of Biological Chemistry 295, no. 14 (2020): 4526–40. http://dx.doi.org/10.1074/jbc.ra119.011025.

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The small GTPases H, K, and NRAS are molecular switches indispensable for proper regulation of cellular proliferation and growth. Several mutations in the genes encoding members of this protein family are associated with cancer and result in aberrant activation of signaling processes caused by a deregulated recruitment of downstream effector proteins. In this study, we engineered variants of the Ras-binding domain (RBD) of the C-Raf proto-oncogene, Ser/Thr kinase (CRAF). These variants bound with high affinity with the effector-binding site of Ras in an active conformation. Structural characte

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Bellio, Helene, Jean David Fumet, and Francois Ghiringhelli. "Targeting BRAF and RAS in Colorectal Cancer." Cancers 13, no. 9 (2021): 2201. http://dx.doi.org/10.3390/cancers13092201.

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Colorectal cancer (CRC) is still one of the most frequent forms of cancer in the world in terms of incidence. Around 40% of CRC patients carry a mutation of the Kirsten rat sarcoma (KRAS) gene, while 10% have a mutation in the B-Raf proto-oncogene serine/threonine kinase (BRAF) gene. These mutations are responsible for dysregulation of the mitogen-associated protein kinase (MAPK) pathway, leading to the proliferation, differentiation, angiogenesis, and resistance to apoptosis of cells. Activation of the MAPK pathway results in adaptive therapeutic resistance, rendering EGFR inhibitors ineffect

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Gaudi, Sudeep, and Jane L. Messina. "Molecular Bases of Cutaneous and Uveal Melanomas." Pathology Research International 2011 (August 18, 2011): 1–8. http://dx.doi.org/10.4061/2011/159421.

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Intensive research in recent years has begun to unlock the mysteries surrounding the molecular pathogenesis of melanoma, the deadliest of skin cancers. The high-penetrance, low-frequency susceptibility gene CDKN2A produces tumor suppressor proteins that function in concert with p53 and retinoblastoma protein to thwart melanomagenesis. Aberrant CDKN2A gene products have been implicated in a great many cases of familial cutaneous melanoma. Sporadic cases, on the other hand, often involve constitutive signal transduction along the mitogen-activated protein kinase (MAPK) pathway, with particular f

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Aashiq, Mohamed, Deborah A. Silverman, Shorook Na’ara, Hideaki Takahashi, and Moran Amit. "Radioiodine-Refractory Thyroid Cancer: Molecular Basis of Redifferentiation Therapies, Management, and Novel Therapies." Cancers 11, no. 9 (2019): 1382. http://dx.doi.org/10.3390/cancers11091382.

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Recurrent, metastatic disease represents the most frequent cause of death for patients with thyroid cancer, and radioactive iodine (RAI) remains a mainstay of therapy for these patients. Unfortunately, many thyroid cancer patients have tumors that no longer trap iodine, and hence are refractory to RAI, heralding a poor prognosis. RAI-refractory (RAI-R) cancer cells result from the loss of thyroid differentiation features, such as iodide uptake and organification. This loss of differentiation features correlates with the degree of mitogen-activated protein kinase (MAPK) activation, which is hig

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Acosta, Andres Martin, and ShriHari S. Kadkol. "Mitogen-Activated Protein Kinase Signaling Pathway in Cutaneous Melanoma: An Updated Review." Archives of Pathology & Laboratory Medicine 140, no. 11 (2016): 1290–96. http://dx.doi.org/10.5858/arpa.2015-0475-rs.

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The mitogen-activated protein kinase (MAPK) signaling pathway is a cascade of protein kinases that act in a sequential and predominantly linear fashion, albeit displaying some cross talk with other signaling cascades. Mutations in proteins integral to the MAPK signaling pathway are present in more than 50% of cutaneous melanomas. The most frequently mutated protein is v-raf murine sarcoma viral oncogene homolog B (BRAF), followed by neuroblastoma Ras viral oncogene homolog (NRAS). Recently, the development of targeted drugs for the treatment of BRAF-mutant melanoma has led to the widespread im

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Sloane, B. F., K. Moin, M. Sameni, L. R. Tait, J. Rozhin, and G. Ziegler. "Membrane association of cathepsin B can be induced by transfection of human breast epithelial cells with c-Ha-ras oncogene." Journal of Cell Science 107, no. 2 (1994): 373–84. http://dx.doi.org/10.1242/jcs.107.2.373.

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Alterations in trafficking and increases in expression of the lysosomal proteases cathepsins B, D and L have been observed in transformed cells and malignant tumors, including human breast carcinoma. ras and the related rab proteins participate in the vesicular transport processes required for normal trafficking of lysosomal enzymes. In addition, transfection of murine fibroblasts with the ras oncogene has been shown to increase the expression of cathepsins L and B. As human cancers are primarily epithelial in origin, we have investigated whether there are alterations in the trafficking and ex

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Czarnecka, Anna M., Ewa Bartnik, Michał Fiedorowicz, and Piotr Rutkowski. "Targeted Therapy in Melanoma and Mechanisms of Resistance." International Journal of Molecular Sciences 21, no. 13 (2020): 4576. http://dx.doi.org/10.3390/ijms21134576.

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The common mutation BRAFV600 in primary melanomas activates the mitogen-activated protein kinase/extracellular-signal-regulated kinase (MAPK/ERK) pathway and the introduction of proto-oncogene B-Raf (BRAF) and mitogen-activated protein kinase kinase (MEK) inhibitors (BRAFi and MEKi) was a breakthrough in the treatment of these cancers. However, 15–20% of tumors harbor primary resistance to this therapy, and moreover, patients develop acquired resistance to treatment. Understanding the molecular phenomena behind resistance to BRAFi/MEKis is indispensable in order to develop novel targeted thera

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Okuda, Keiko, Yoshiaki Sonoda, and James D. Griffin. "A New Model to Evaluate Signaling of Raf in Hematopoietic Cells." Blood 104, no. 11 (2004): 1533. http://dx.doi.org/10.1182/blood.v104.11.1533.1533.

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Abstract The Raf/MEK/ERK pathway is thought to be critical in mediating cell survival and proliferation by cytokine receptors. However, the exact contribution of Raf is complex and not well understood. A better understanding of Raf signaling is important because of the recent observation that B-Raf is frequently mutated in various human cancers. We have generated a new model system that activates Raf directly by linking the extracytoplasmic and transmembrane domains of the erythropoietin receptor (EPOR) with the catalytic domain of Raf (CR3). This synthetic oncogene in which dimerization can b

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Dissertations / Theses on the topic "Ras Proto-oncogene proteins B-raf"

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Iritani, Brian Masao. "Control of B lymphocyte development by Ras and Raf /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/8322.

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Omholt, Katarina. "Activating proto-oncogene mutations in human cutaneous melanoma /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-191-1/.

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Estrozi, Bruna. "Avaliação anatomoclínica e molecular do melanoma cutâneo em pacientes jovens (idade 18-30 anos)." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-01042015-144721/.

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A incidência do melanoma cutâneo em pacientes adultos jovens tem aumentado consideravelmente nos últimos anos. Há, contudo, carência de conhecimentos clinicopatológicos e moleculares sobre os melanomas que ocorrem nessa faixa etária. O presente estudo teve por objetivo avaliar 132 casos de melanoma cutâneo primário em pacientes com idade entre 18 e 30 anos, com ênfase no estudo das características clínicas, histopatológicas e avaliação molecular das mutações nos genes BRAF, NRAS e KIT. Em relação aos achados clínicos e histopatológicos, houve predomínio de indivíduos do sexo feminino (61,4%),

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Appleman, Victoria A. "Mechanisms of KRAS-Mediated Pancreatic Tumor Formation and Progression: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/600.

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Pancreatic cancer is the 4th leading cause of cancer related death in the United States with a median survival time of less than 6 months. Pancreatic ductal adenocarcinoma (PDAC) accounts for greater than 85% of all pancreatic cancers, and is marked by early and frequent mutation of the KRAS oncogene, with activating KRAS mutations present in over 90% of PDAC. To date, though, targeting activated KRAS for cancer treatment has been very difficult, and targeted therapies are currently being sought for the downstream effectors of activated KRAS. Activation of KRAS stimulates multiple signaling pa

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Dutenhefner, Simone Elisa. "Pesquisa da mutação T1799A do gene BRAF e a presença de metástases linfáticas no carcinoma papilífero da tireoide." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5132/tde-24012012-163817/.

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Muitos pacientes submetidos à tireoidectomia por Carcinoma Papilífero da Tireoide (CPT) têm doença linfonodal subclínica no momento da cirurgia. A mutação BRAF T17799A (V600E) é um evento comum no CPT e alguns estudos demonstram correlação entre a mutação e características de maior agressividade tumoral, incluindo a presença de metástases linfonodais. O esvaziamento eletivo do compartimento central ganha aceitação, uma vez que alguns estudos evidenciam que a presença de metástases linfonodais aumenta o risco de recidiva e mortalidade. Devido ao grande potencial de complicações do esvaziamento

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Borysova, Meghan E. K. "Novel roles for B-Raf in mitosis and cancer." [Tampa, Fla] : University of South Florida, 2009. http://purl.fcla.edu/usf/dc/et/SFE0002899.

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Freitas, Isabella Nicacio de. "Caracterização imuno-histoquímica e molecular dos pacientes com suspeita clínica de Síndrome de Lynch." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5168/tde-09022015-095440/.

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Suspeita-se da Síndrome de Lynch (SL) a partir da história pessoal e familial do indivíduo. Posteriormente, os dados histopatológicos, imuno-histoquímicos e moleculares podem ser utilizados para aprimorar o diagnóstico da doença. Entretanto, um grande desafio no diagnóstico da Síndrome de Lynch é a baixa acurácia dos critérios clínicos utilizados. OBJETIVOS: Avaliar a frequência de SL em pacientes submetidos a tratamento cirúrgico por câncer colorretal e com história familial de câncer. Avaliar quais dos critérios clínicos e/ou moleculares seriam mais informativos no diagnóstico desta Síndrome

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Urcia, Roby Joseph. "The modulation of tumour suppressor MST2 and proto-oncogene Raf-1 kinases by the scaffold protein CNK1." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/4183/.

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An emerging concept in the regulation of signal transduction specificity is the mediation of scaffold proteins embedded in the circuitry of signalling pathways. The multidomainbased architecture of scaffold proteins facilitates the assembly and modulation of protein complexes to regulate cellular signals to bring about an exacting biological output. The work presented in this thesis aimed to investigate the mechanisms of the protein scaffold CNK1 (connector enhancer of Ras 1) in the pro-apoptotic MST2 pathway and the prooncogenic Raf-1 signalling pathways. Here, by using several molecular, bio

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PAPIN, CATHERINE. "Etude biochimique et fonctionnelle des isoformes de l'oncoproteine b-raf (doctorat : bases fondamentales de l'oncogenese)." Paris 11, 1998. http://www.theses.fr/1998PA11T026.

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Benisty, Hannah 1986. "Post-transcriptional determinants of RAS protein abundance." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/668206.

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The RAS oncogenes KRAS, NRAS and HRAS are mutated in one third of human cancers where they exhibit different mutation patterns. A potential factor contributing to this mutation bias is the variation of RAS expression levels. Here, I investigate some of the determinants of RAS protein abundance. First, I examine whether codon bias among RAS genes and within other cancer gene families plays a role in cell context-specific expression. I further describe a tRNA expression program that favors oncogene translation in proliferating cells. Second, I investigate why oncogenic RAS mutants exhibit a hi

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Books on the topic "Ras Proto-oncogene proteins B-raf"

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Sullivan, Ryan J. BRAF Targets in Melanoma: Biological Mechanisms, Resistance, and Drug Discovery. Humana, 2014.

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Sullivan, Ryan J. BRAF Targets in Melanoma: Biological Mechanisms, Resistance, and Drug Discovery. Humana, 2016.

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Book chapters on the topic "Ras Proto-oncogene proteins B-raf"

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Marshall, M. S., M. D. Schaber, U. S. Vogel, et al. "The ras Oncogene Protein." In Molecular Mechanisms of Hormone Action. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-75022-9_10.

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Teruya, Kiichiro, Sanetaka Shirahata, Takahiro Yano, et al. "RAS Oncogene Enhances the Various Recombinant Protein Productivities of BHK-21 Cells Regulated by the CMV Promoter." In Animal Cell Technology: Developments Towards the 21st Century. Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0437-1_15.

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Agnantis, N. J., A. Pintzas, A. Kakkanas, P. Markoulatos, and D. A. Spandidos. "Expression of the ras Oncogene p 21 Protein in Human Breast Tumors and in Several Benign Conditions Using the Y13 259 Monoclonal Antibody." In Fundamental Problems in Breast Cancer. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2049-4_36.

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Kerr, David J., Daniel Haller, and Jaap Verweij. "Principles of chemotherapy." In Oxford Textbook of Cancer Biology, edited by Francesco Pezzella, Mahvash Tavassoli, and David J. Kerr. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0028.

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Systemic cancer treatment stems initially from empirically discovered DNA synthesis inhibitors, which either deplete the cell of nucleotides, induce cross-link, or cause DNA single and double strand breaks or impair the cellular machinery of DNA repair, using mechanistically diverse drugs. A period of enlightenment followed, with anticancer drug development driven by an increased understanding of enzymes and pathways involved in cell signalling, control of angiogenesis, and epigenetics. This provided a parallel path towards precision cancer medicine where specific drugs can be targeted to patients with particular mutations. These include point mutations in RAS, which are used to exclude colorectal cancer patients from being treated with epidermal growth factor inhibitors; chromosomal translocations encoding fusion proteins which are cancer specific and serve as novel drug targets (e.g. BCR/ABL and imatinib, or EML4-ALK fusion oncogene and crizotinib). More recently, there has been a reanimation of immune approaches to cancer therapy with the clinical introduction of immune checkpoint inhibitors, designer T cells, and patient-specific antitumour vaccines. What next? It may be that next-generation sequencing provides an endless stream of so-called actionable mutations that permits tailored application of mutation-specific drugs, but so far there is little evidence of clinical benefit from such therapies.

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Conference papers on the topic "Ras Proto-oncogene proteins B-raf"

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Pirogova, Elena, Vuk Vojisavljevic, and Irena Cosic. "Prediction of protein active and/or binding site using time-frequency analysis: Application to ras oncogene proteins." In 2012 ISSNIP Biosignals and Biorobotics Conference: Biosignals and Robotics for Better and Safer Living (BRC). IEEE, 2012. http://dx.doi.org/10.1109/brc.2012.6222173.

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