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Relevant bibliographies by topics / RASopathie

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Journal articles
Dissertations / Theses
Book chapters
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Academic literature on the topic 'RASopathie'

Author: Grafiati

Published: 22 February 2023

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Journal articles on the topic "RASopathie"

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Davis, Amani Ali, Giulio Zuccoli, Mostafa M. Haredy, et al. "RASopathy in Patients With Isolated Sagittal Synostosis." Global Pediatric Health 6 (January 2019): 2333794X1984677. http://dx.doi.org/10.1177/2333794x19846774.

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RASopathy is caused by dysfunction in the MAPK pathway, and include syndromes like Noonan syndrome (NS), NS with multiple lentigines (formerly known as Leopard syndrome), cardiofaciocutaneous (CFC), Legius syndrome, capillary malformation–arteriovenous malformation, neurofibromatosis type 1, and Costello syndrome. When counted together, RASopathies affect 1/1000 live births, and are characterized by cardiovascular manifestations, short stature, developmental delay, renal, urogenital, skin/skeletal abnormalities, and dysmorphic appearance. NS—one of the most common RASopathies—occurs in 1/1000

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Kratz, Christian P., and Martin Zenker. "Inherited Disorders of the Ras-MAPK Pathway." Blood 132, Supplement 1 (2018): SCI—41—SCI—41. http://dx.doi.org/10.1182/blood-2018-99-109379.

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Abstract RASopathies are a group of rare congenital diseases in which dysregulated signaling through the RAS-MAPK signaling cases is the critical pathogenetic mechanism. This definition excludes postnatally acquired conditions (e.g. RAS-MAPK driven neoplasms) and PIK3-AKT pathway related disorders as well as conditions with only ancillary RAS pathway involvement (e.g. KAT6B-, RAP1A/B-related disorders). The definition, however, includes the following categories: (1) Noonan syndrome and related disorders, specifically Noonan syndrome (NS), NS with multiple lentigines, NS-like disorder with loos

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Slack, Jonathan C., Marie-Anne Bründler, Caitlin A. Chang, Renee Perrier, Lucie Lafay-Cousin, and Kyle C. Kurek. "Bilateral Nephroblastic Tumors and a Complex Renal Vascular Anomaly in a Patient With a Mosaic RASopathy: Novel Histopathologic Features and Molecular Insights." Pediatric and Developmental Pathology 24, no. 3 (2021): 235–40. http://dx.doi.org/10.1177/1093526620986502.

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Mosaic RASopathies are an emerging group of disorders characterized by mosaic or post-zygotic activating mutations in genes of the RAS/MAPKinase signaling pathway. The phenotype is highly variable, ranging from limited or localized forms to cases with a syndromic presentation with extensive or multiorgan involvement, and also overlaps with other mosaic disorders. While there are several reports of malignancies in patients with mosaic RASopathies, specifically rhabdomyosarcoma and transitional urothelial carcinoma, the lifetime risk and molecular mechanisms that lead to the development of malig

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Tajan, Mylène, Romain Paccoud, Sophie Branka, Thomas Edouard, and Armelle Yart. "The RASopathy Family: Consequences of Germline Activation of the RAS/MAPK Pathway." Endocrine Reviews 39, no. 5 (2018): 676–700. http://dx.doi.org/10.1210/er.2017-00232.

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Abstract Noonan syndrome [NS; Mendelian Inheritance in Men (MIM) #163950] and related syndromes [Noonan syndrome with multiple lentigines (formerly called LEOPARD syndrome; MIM #151100), Noonan-like syndrome with loose anagen hair (MIM #607721), Costello syndrome (MIM #218040), cardio-facio-cutaneous syndrome (MIM #115150), type I neurofibromatosis (MIM #162200), and Legius syndrome (MIM #611431)] are a group of related genetic disorders associated with distinctive facial features, cardiopathies, growth and skeletal abnormalities, developmental delay/mental retardation, and tumor predispositio

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Motta, Marialetizia, Lena Sagi-Dain, Oliver H. F. Krumbach, et al. "Activating MRAS mutations cause Noonan syndrome associated with hypertrophic cardiomyopathy." Human Molecular Genetics 29, no. 11 (2019): 1772–83. http://dx.doi.org/10.1093/hmg/ddz108.

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Abstract The RASopathies are a group of genetic syndromes caused by upregulated RAS signaling. Noonan syndrome (NS), the most common entity among the RASopathies, is characterized mainly by short stature, cardiac anomalies and distinctive facial features. Mutations in multiple RAS-MAPK pathway-related genes have been associated with NS and related phenotypes. We describe two unrelated patients presenting with hypertrophic cardiomyopathy (HCM) and dysmorphic features suggestive of NS. One of them died in the neonatal period because of cardiac failure. Targeted sequencing revealed de novo MRAS v

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Mission, P., A. Foy, and E. Pierpont. "C-56 Predictors of Social Outcomes for Individuals with RASopathies: A Systematic Literature Review with Implications for Assessment, Intervention and Education." Archives of Clinical Neuropsychology 34, no. 6 (2019): 1085. http://dx.doi.org/10.1093/arclin/acz034.218.

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Abstract Objective This review sought to provide a better understanding of the factors that contribute to social functioning outcomes in individuals with these RASopathies (i.e., genetic syndromes caused by disruption to the RAS-MAPK cellular signaling pathway). Data Selection A systematic literature search in the PubMed electronic database yielded 462 articles on social functioning in individuals with RASopathies. An additional five articles were identified through hand searches. Two researchers reviewed each article abstract, resulting in 58 full-text articles to be assessed for eligibility.

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Ando, Yoshihito, Mikio Sawada, Tadataka Kawakami, Mitsuya Morita, and Yoko Aoki. "A Patient with Noonan Syndrome with a KRAS Mutation Who Presented Severe Nerve Root Hypertrophy." Case Reports in Neurology 13, no. 1 (2021): 108–18. http://dx.doi.org/10.1159/000512265.

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We report a 45-year-old female with clinical features resembling Noonan syndrome (NS) who presented with significant nerve root hypertrophy. She was initially diagnosed with Charcot-Marie-Tooth disease because her gait disturbance gradually deteriorated and nerve conduction velocity was reduced. However, she did not carry a <i>PMP22</i> gene mutation. RASopathies are a group of phenotypically overlapping developmental syndromes caused by germline mutations that encode components of the Ras/MAPK signaling pathway. These disorders include NS, cardiofaciocutaneous (CFC) syndrome, and

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Vallejos, Carla, Víctor Bolanos-Garcia, Diana Ponce, et al. "Co-occurrence of Noonan and Cardiofaciocutaneous Syndrome Features in a Patient with KRAS Variant." Journal of Pediatric Genetics 07, no. 04 (2018): 158–63. http://dx.doi.org/10.1055/s-0038-1653977.

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AbstractWe report the case of a 3-year-old girl, who is the third child of nonconsanguineous parents, with short stature, hypertrophic cardiomyopathy, and mild dysmorphic features; all suggestive of Noonan syndrome. In addition, the patient presents with feeding difficulties, deep palmar and plantar creases, sparse hair, and delayed psychomotor and language development, all characteristics frequently observed in cardiofaciocutaneous syndrome. Molecular analysis of the Ras/ MAPK pathway genes using high-resolution melting curve analysis and gene sequencing revealed a de novo KRAS amino acid sub

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Gross, Andrea M., Megan Frone, Karen W. Gripp, et al. "Advancing RAS/RASopathy therapies: An NCI‐sponsored intramural and extramural collaboration for the study of RASopathies." American Journal of Medical Genetics Part A 182, no. 4 (2020): 866–76. http://dx.doi.org/10.1002/ajmg.a.61485.

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Zenker, Martin, and Kerstin Kutsche. "RASopathien." medizinische genetik 28, no. 1 (2016): 15–38. http://dx.doi.org/10.1007/s11825-016-0080-8.

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Dissertations / Theses on the topic "RASopathie"

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PAULAT, NICOLE SUZANNE. "DEVELOPING CURATED RESOURCES FOR RASOPATHIES RESEARCH." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/613385.

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The RASopathies are a diverse set of genetic diseases that are caused by mutations to the RAS/MAPK signaling pathway, which is crucial in embryonic and early development. Biomedical model studies are important for developing understanding of mechanisms of the RAS/MAPK pathway and their individual effects on disease phenotype, however these studies are hindered by lack of standard nomenclature and functional annotations. We selected chicken as a comparative model, and analyzed a human RAS/MAPK pathway gene set to identify chicken orthologs. These orthologs were then assessed and standardized ge

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Bessis, Didier. "Étude prospective des manifestations dermatologiques des RASopathies." Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT089.

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Les RASopathies avec phénotype Noonan associent le syndrome de Noonan (SN), le syndrome cardio-facio-cutané (SCFC) et le syndrome de Costello (SC). Leurs manifestations dermatologiques restent peu étudiées.Objectifs Colliger les différentes manifestations dermatologiques des SN, SCFC et SC afin d’établir leur nature et leur prévalence, et définir d’éventuelles corrélations phénotype/génotype au sein de chacune de ces affections.Méthodes Les patients atteints d’un SN, SCFC et SC confirmé sur le plan moléculaire par la présence d’une mutation germinale pathogène étaient inclus dans une étude men

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Lißewski, Christina Antonia [Verfasser]. "The RASopathies : molecular genetics and genotype-phenotype correlations / Christina Antonia Lißewski." Magdeburg : Universitätsbibliothek, 2018. http://d-nb.info/1158660081/34.

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Titus-Mitchell, Haley E. M. S. "Signaling Pathways Controlling CNS Myelin Compaction in Gain-of-function Rasopathies." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1439296184.

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Lißewski, Christina [Verfasser]. "The RASopathies : molecular genetics and genotype-phenotype correlations / Christina Antonia Lißewski." Magdeburg : Universitätsbibliothek, 2018. http://d-nb.info/1158660081/34.

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Medina-Pérez, Paula Andrea. "Functional characterization of cancer- and RASopathies-associated SHP2 and BRAF mutations." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2016. http://dx.doi.org/10.18452/17420.

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Deregulierung des RAS/MAPK Signalwegs führen nicht nur zur Krebsentstehung, sondern sind auch mitverantwortlich für Entwicklungsstörungen, dieals Keimbahnmutationen in Schlüsselregulatoren des MAPK Signalwegs zurückzuführen sind, werden aufgrund überlappender Phänotypen unter dem Begriff RASopathien subsumiert. Obwohl die Inzidenz für solide Tumore bei diesen Patienten gering ist, wird ein Zusammenhang zum Auftreten verschiedener Leukämieformen deutlich. Im Rahmen dieser Arbeit wurden Mutationen zweier Schlüsselregulatoren des MAPK Signalwegs, PTPN11 und BRAF, hinsichtlich ihrer Fähigkeit zur

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Anastasaki, Korina. "MAPK pathway : a role in development, disease and behaviour." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5955.

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Mutations in the RAS-RAF-MEK-ERK (MAPK) pathway give rise to a range of developmental disorders collectively referred to as the RASopathies. De novo germline mutations in patients suffering from these syndromes promote similar phenotypes, which include heart abnormalities, characteristic facial features, cutaneous malformations, gastrointestinal malfunctions, failure to thrive and a spectrum of mental retardation. Although many RASopathies patients show a propensity to develop early-onset benign and malignant tumours, Cardio-faciocutaneous (CFC) syndrome patients do not seem to share this pred

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Tamburrino, Federica <1980&gt. "I disordini del pathway RAS-MAPK o Rasopatie: aspetti diagnostici, clinici e terapeutici." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2016. http://amsdottorato.unibo.it/7435/4/Tamburrino_Federica_Tesi.pdf.

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Le “RASopatie” includono un gruppo di patologie congenito-malformative a trasmissione autosomica-dominante causate da mutazioni eterozigoti germinali in geni che codificano per proteine del pathway RAS-MAPKinasi. Sono caratterizzate da dismorfismi faciali, iposomia, cardiopatia congenita, anomalie ectodermiche e scheletriche, coinvolgimento cognitivo e suscettibilità tumorale. La bassa statura è uno dei principali elementi distintivi sul quale si può agire sotto il profilo terapeutico, mediante somministrazione di Ormone della Crescita biosintetico (GH). In questo studio è stato analizzato l

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Tamburrino, Federica <1980&gt. "I disordini del pathway RAS-MAPK o Rasopatie: aspetti diagnostici, clinici e terapeutici." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2016. http://amsdottorato.unibo.it/7435/.

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Le “RASopatie” includono un gruppo di patologie congenito-malformative a trasmissione autosomica-dominante causate da mutazioni eterozigoti germinali in geni che codificano per proteine del pathway RAS-MAPKinasi. Sono caratterizzate da dismorfismi faciali, iposomia, cardiopatia congenita, anomalie ectodermiche e scheletriche, coinvolgimento cognitivo e suscettibilità tumorale. La bassa statura è uno dei principali elementi distintivi sul quale si può agire sotto il profilo terapeutico, mediante somministrazione di Ormone della Crescita biosintetico (GH). In questo studio è stato analizzato l

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Brand, Kristina [Verfasser], and Kerstin [Akademischer Betreuer] Kutsche. "Funktionelle Charakterisierung von humanen CBL- und RRAS-Proteinvarianten für ein besseres Verständnis der Pathophysiologie bei RASopathien / Kristina Brand. Betreuer: Kerstin Kutsche." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2015. http://d-nb.info/106893168X/34.

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Book chapters on the topic "RASopathie"

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Hernández-Porras, Isabel, and Carmen Guerra. "Modeling RASopathies with Genetically Modified Mouse Models." In Methods in Molecular Biology. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6424-6_28.

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Chao, Mwe Mwe, Martin Zenker, and Christian Peter Kratz. "Cancer Risk and Spectrum in Individuals with RASopathies." In Multidisciplinary Approach to Neurofibromatosis Type 1. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-92450-2_17.

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Tidyman, William E., and Katherine A. Rauen. "The RASopathies: Syndromes of Ras/MAPK Pathway Dysregulation." In Neurofibromatosis Type 1. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-32864-0_32.

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Lee, Yong-Seok, and Alcino J. Silva. "Molecular and Cellular Approaches to Cognitive Impairments Associated with NF1 and Other Rasopathies." In Neurofibromatosis Type 1. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-32864-0_37.

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Vincent, Lisa M., Karen W. Gripp, and Heather Mason-Suares. "RASopathies." In Clinical DNA Variant Interpretation. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-820519-8.00011-9.

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Maccora, Ilaria, Matteo Della Monica, Giovanna Traficante, Gianpaolo De Filippo, and Stefano Stagi. "Learning Disability in RASopathies." In Learning Disabilities - An International Perspective. InTech, 2017. http://dx.doi.org/10.5772/intechopen.69571.

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Tidyman, William E., and Katherine A. Rauen. "Cardio-Facio-Cutaneous Syndrome and Other RASopathies." In Treatment of Neurodevelopmental Disorders. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199937806.003.0007.

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Longo, Jody Fromm, and Steven L. Carroll. "The RASopathies: Biology, genetics and therapeutic options." In Advances in Cancer Research. Elsevier, 2022. http://dx.doi.org/10.1016/bs.acr.2021.07.007.

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Clark, Robin D., and Cynthia J. Curry. "Macrocephaly and Megalencephaly." In Genetic Consultations in the Newborn, edited by Robin D. Clark and Cynthia J. Curry. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199990993.003.0014.

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This chapter reviews isolated and syndromic causes of macrocephaly and megalencephaly. The two terms are usually but not always interchangeable. The differential diagnosis of macrocephaly includes familial macrocephaly, chromosome duplications and deletions, metabolic disorders and complex somatic mosaic conditions including CLOVES, MCAP and MPPH. Single gene disorders with macrocephaly include those in the Noonan syndrome spectrum (RASopathies). Syndromes with hemimegalencephaly, including linear nevus sebaceous and tuberous sclerosis are briefly reviewed. Many syndromes with macrocephaly have associated overgrowth and are covered in the Overgrowth chapter as well, including Weaver, Sotos and Malan syndromes. A clinical case presentation features an infant with basal cell nevus syndrome.

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Clark, Robin D., and Cynthia J. Curry. "Overgrowth." In Genetic Consultations in the Newborn, edited by Robin D. Clark and Cynthia J. Curry. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199990993.003.0003.

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This chapter reviews information on disorders that cause large birth weight, macrosomia, and/or segmental overgrowth. The most common of these conditions is seen in infants of diabetic mothers. Abnormal dosage of growth regulating genes make chromosomal microarray abnormalities a relatively common cause of overgrowth. Particularly notable is the distinctive Pallister Killian syndrome (12p tetrasomy). Other common overgrowth syndromes include Beckwith-Wiedemann syndrome, Sotos, Malan, and Weaver syndromes. The RASopathy syndromes including Noonan syndrome* and Costello syndrome are also often large at birth. Segmental overgrowth syndromes including Proteus and Klippel Trenaunay as well as PIK3CA related overgrowth (PROS) are discussed as well as their somatic mosaic origin in affected tissues. Clinical guidelines for evaluation and surveillance are outlined. The clinical case presentation features an infant with Sotos syndrome.

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Conference papers on the topic "RASopathie"

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Siemer, J., B. Schlehe, and J. Kohlhase. "Molekulargenetischer RASopathie-Panel als wichtige Differenzialdiagnose bei erhöhter Nackentransparenz im Erst-Trimester-Screening – zwei Fallberichte." In Interdisziplinärer Kongress | Ultraschall 2019 – 43. Dreiländertreffen DEGUM | ÖGUM | SGUM. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695896.

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Sfecci, Alicia, Alain Dupuy, Monica Dinulescu, et al. "Abstract 3407: Side effects of BRAF inhibitors mimic RASopathies." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3407.

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Jung, Nikolai, and Volker Mall. "Impaired Synaptic Plasticity in Humans with RASopathies – An Update." In Abstracts of the 45th Annual Meeting of the Society for Neuropediatrics. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1698245.

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Wolf, C. M., M. Zenker, G. Norrish, et al. "AKT/mTOR and MAPK Inhibition Improves Childhood RASopathic Cardiomyopathy." In The 54th Annual Meeting of the German Society for Pediatric Cardiology (DGPK). Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1742990.

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Krisna, Made Ananda, and Yulia Ariani Aswin. "Alteration of the Signal Transduction Pathway in RASopathies as a Basis of Targeted Therapeutic Drug Development." In 1’s t Jenderal Soedirman International Medical Conference (JIMC) in conjunction with the Annual Scientific Meeting (Temilnas) Consortium of Biomedical Science Indonesia (KIBI ). SCITEPRESS - Science and Technology Publications, 2020. http://dx.doi.org/10.5220/0010492003180329.

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Spencer-Smith, Russell, Elizabeth M. Terrell, Constance Agamasu, et al. "Abstract A31: Germline RASopathy mutations provide functional insights into the Raf cysteine-rich domain (CRD)." In Abstracts: AACR Special Conference on Targeting RAS-Driven Cancers; December 9-12, 2018; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.ras18-a31.

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Rosa, Salvatore La, Pamela Knight, Patrice Pancza, Kimberly Scobie, and Annette Bakker. "Abstract A32: Gaps and opportunities for RASopathies: Use of new tools to make the right choice in target and compound selection." In Abstracts: AACR Special Conference on RAS Oncogenes: From Biology to Therapy; February 24-27, 2014; Lake Buena Vista, FL. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1557-3125.rasonc14-a32.

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Minso, J., C. T. Mauriello, and G. Syverson. "Severe Presentation in a Child with Systemic Lupus Erythematosus, and Somatic Mutation of NRAS Gene Without Documented Rasopathy." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1963.

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Sherekar, Mukul, Sae-Won Han, Simon Messing, et al. "Abstract 1768: Biochemical and structural analysis of the Neurofibromin (NF1) protein and a potential role for protein destabilization in Rasopathy diseases." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1768.

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Sherekar, Mukul, Sae-Won Han, Simon Messing, et al. "Abstract 1768: Biochemical and structural analysis of the Neurofibromin (NF1) protein and a potential role for protein destabilization in Rasopathy diseases." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1768.

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