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Mühlmann, Gilbert, Dietmar Öfner, Matthias Zitt, Hannes M. Müller, Hans Maier, Patrizia Moser, Kurt W. Schmid, Marion Zitt, and Albert Amberger. "14-3-3 Sigma And p53 Expression in Gastric Cancer and Its Clinical Applications." Disease Markers 29, no. 1 (2010): 21–29. http://dx.doi.org/10.1155/2010/470314.
14-3-3 sigma (σ) induces G2 arrest enabling the repair of damaged DNA. The function of 14-3-3 σ is frequently lost in tumor cells, indicating a potential tumor suppressor function. The purpose of this study was to evaluate the prognostic value of 14-3-3 σ expression in human gastric cancer. 14-3-3 σ expression was analyzed by immunohistochemistry in 157 tumor samples of patients, who underwent resection for gastric cancer. Since 14-3-3 σ is involved in the p53 network, p53 expression was detected in parallel and correlated with 14-3-3 σ. 14-3-3 σ was found to be overexpressed in 75 (47.8%) of 157 cases, the overexpression rate of p53 protein was 27.4%. 14-3-3 σ overexpression was statistically significantly associated with pT-stage (p=0.041) pN-stage (p=0.015) and UICC-stage (p=0.019) and showed a borderline significance with Lauren classification (p=0.057). Univariate survival calculations revealed a coexistent 14-3-3 σ and p53 overexpression as a significant predictor of disease-free survival. Multivariate analysis did not unfold 14-3-3 as an independent prognostic factor for disease-free survival and overall survival. Concomitant 14-3-3 σ and p53 overexpression in tumor cells of patients with gastric cancer identifies a population of patients with relatively unfavorable prognosis.
ABSTRACT The 14-3-3σ (sigma) protein, a negative regulator of the cell cycle, is a human mammary epithelium-specific marker that is downregulated in transformed mammary carcinoma cells. It has also been identified as a p53-inducible gene product involved in cell cycle checkpoint control after DNA damage. Although 14-3-3σ is linked to p53-regulated cell cycle checkpoint control, detailed mechanisms of how cell cycle regulation occurs remain unclear. Decreased expression of 14-3-3σ was recently reported in several types of carcinomas, further suggesting that the negative regulatory role of 14-3-3σ in the cell cycle is compromised during tumorigenesis. However, this possible tumor-suppressive role of 14-3-3σ has not yet been characterized. Here, we studied the link between 14-3-3σ activities and p53 regulation. We found that 14-3-3σ interacted with p53 in response to the DNA-damaging agent adriamycin. Importantly, 14-3-3σ expression led to stabilized expression of p53. In studying the molecular mechanism of this increased stabilization of p53, we found that 14-3-3σ antagonized the biological functions of Mdm2 by blocking Mdm2-mediated p53 ubiquitination and nuclear export. In addition, we found that 14-3-3σ facilitated the oligomerization of p53 and enhanced p53's transcriptional activity. As a target gene of p53, 14-3-3σ appears to have a positive feedback effect on p53 activity. Significantly, we also showed that overexpression of 14-3-3σ inhibited oncogene-activated tumorigenicity in a tetracycline-regulated 14-3-3σ system. These results defined an important p53 regulatory loop and suggested that 14-3-3σ expression can be considered for therapeutic intervention in cancers.
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CHEN, DE-YU, DONG-FANG DAI, YE HUA, and WEN-QING QI. "p53 suppresses 14-3-3γ by stimulating proteasome-mediated 14-3-3γ protein degradation." International Journal of Oncology 46, no. 2 (November 7, 2014): 818–24. http://dx.doi.org/10.3892/ijo.2014.2740.
Doveston, Richard G., Ave Kuusk, Sebastian A. Andrei, Seppe Leysen, Qing Cao, Maria P. Castaldi, Adam Hendricks, et al. "Small-molecule stabilization of the p53 - 14-3-3 protein-protein interaction." FEBS Letters 591, no. 16 (August 2017): 2449–57. http://dx.doi.org/10.1002/1873-3468.12723.
Abstract In human carcinogenesis, given the plethora of pathways associated with 14-3-3σ and their complex interactions, the causality of 14-3-3σ deregulation remains elusive, with both tumour suppressive and oncogenic roles. To study mechanisms driving/inhibiting skin carcinogenesis, stage-specific expression of endogenous 14-3-3σ (stratifin) was analysed in skin carcinogenesis driven by activated rasHa/fos expression (HK1.ras/fos) and ablation of phosphatase and tensin homolog (PTEN)-mediated Akt regulation (K14.creP/Δ5PTENflx) and via conditional RU486-inducible 14-3-3σ knockout (K14.creP-Δ14-3-3). Consistent with 14-3-3σ roles in the commitment of keratinocytes to differentiate, bigenic HK1.fos/Δ5PTENflx hyperplasia expressed 14-3-3σ in basal layers and paralleled keratin K1 expression which appeared alongside elevated p53/p21 to increase keratinocyte differentiation leading to a keratoacanthoma (KA) aetiology. Trigenic HK1.ras/fos-Δ5PTENflx hyperplasia/papillomas also displayed increased basal-layer 14-3-3σ, suggesting attempts to protect basal layer p53 tumour suppressor gene function, given that 14-3-3σ acts as a chaperone protein to remove/relocate MDM2 for degradation, thus maintaining p53 levels. With time, HK1.ras/fos-Δ5PTENflx papillomas exhibited reduced p53 and increased p-MDM2166 activity in basal layers, which coincided with malignant conversion. Surprisingly, despite this p53 loss, 14-3-3σ expression persisted in well-differentiated squamous cell carcinomas (wdSCC) and, alongside elevated p21, appeared to limit further malignant progression via inhibiting p-Akt1473 expression. To further assess causality, 14-3-3σ functions were ablated in this model via an RU486-inducible cre/loxP system expressed from a keratin 14 (K14) promoter (K14.creP-Δ14-3-3σ). In bigenic HK1.fos-Δ14-3-3σ, preliminary data suggest loss of 14-3-3σ functions resulted in increased hyperplasia and keratosis similar to that observed in bigenic HK1.fos/Δ5PTENflx hyperplasia. Functional 14-3-3σ ablation in HK1.ras.fos/Δ5PTENflx/Δ14-3-3σflx genotypes apparently failed to accelerate papillomatogenesis, suggesting elements of redundancy in terms of tumour promotion; however, loss of 14-3-3σ facilitated increased p-MDM2166 and p53 loss, resulting in malignant conversion with progression to aggressive SCC. Collectively, these data suggest that 14-3-3σ/stratifin exerts suppressive roles in papillomatogenesis via MDM2/p53-dependent mechanisms, while persistent expression in wdSCCs suggests p53-independent scenarios that may involve p21-mediated Akt1 inhibition. However, if ablated, this limit of early-stage malignant progression is lost and 14-3-3σ loss leads to rapid progression to aggressive, p21-negative SCCs exhibiting uniform p-Akt1473activation.
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Yang, Wensheng, David T. Dicker, Jiandong Chen, and Wafik S. El-Deiry. "CARPs enhance p53 turnover by degrading 14-3-3σ and stabilizing MDM2." Cell Cycle 7, no. 5 (March 2008): 670–82. http://dx.doi.org/10.4161/cc.7.5.5701.
Rajagopalan, Sridharan, Robert S. Sade, Fiona M. Townsley, and Alan R. Fersht. "Mechanistic differences in the transcriptional activation of p53 by 14-3-3 isoforms." Nucleic Acids Research 38, no. 3 (November 20, 2009): 893–906. http://dx.doi.org/10.1093/nar/gkp1041.
Schumacher, Benjamin, Justine Mondry, Philipp Thiel, Michael Weyand, and Christian Ottmann. "Structure of the p53 C-terminus bound to 14-3-3: Implications for stabilization of the p53 tetramer." FEBS Letters 584, no. 8 (March 3, 2010): 1443–48. http://dx.doi.org/10.1016/j.febslet.2010.02.065.
Waterman, Matthew J. F., Elena S. Stavridi, Jennifer L. F. Waterman, and Thanos D. Halazonetis. "ATM-dependent activation of p53 involves dephosphorylation and association with 14-3-3 proteins." Nature Genetics 19, no. 2 (June 1998): 175–78. http://dx.doi.org/10.1038/542.
Dissertations / Theses on the topic "P53, 14-3-3":
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LeBron, Cynthia. "Regulation of MDMX nuclear import and degradation by Chk2 and 14-3-3." [Tampa, Fla.] : University of South Florida, 2007. http://purl.fcla.edu/usf/dc/et/SFE0001992.
Radhakrishnan, Vijayababu, Charles Putnam, Wenqing Qi, and Jesse Martinez. "P53 suppresses expression of the 14-3-3gamma oncogene." BioMed Central, 2011. http://hdl.handle.net/10150/610345.
BACKGROUND:14-3-3 proteins are a family of highly conserved proteins that are involved in a wide range of cellular processes. Recent evidence indicates that some of these proteins have oncogenic activity and that they may promote tumorigenesis. We previously showed that one of the 14-3-3 family members, 14-3-3gamma, is over expressed in human lung cancers and that it can induce transformation of rodent cells in vitro.METHODS:qRTPCR and Western blot analysis were performed to examine 14-3-3gamma expression in non-small cell lung cancers (NSCLC). Gene copy number was analyzed by qPCR. P53 mutations were detected by direct sequencing and also by western blot. CHIP and yeast one hybrid assays were used to detect p53 binding to 14-3-3gamma promoter.RESULTS:Quantitative rtPCR results showed that the expression level of 14-3-3gamma was elevated in the majority of NSCLC that we examined which was also consistent with protein expression. Further analysis of the expression pattern of 14-3-3gamma in lung tumors showed a correlation with p53 mutations suggesting that p53 might suppress 14-3-3 gamma expression. Analysis of the gamma promoter sequence revealed the presence of a p53 consensus binding motif and in vitro assays demonstrated that wild-type p53 bound to this motif when activated by ionizing radiation. Deletion of the p53 binding motif eliminated p53's ability to suppress 14-3-3gamma expression.CONCLUSION:Increased expression of 14-3-3gamma in lung cancer coincides with loss of functional p53. Hence, we propose that 14-3-3gamma's oncogenic activities cooperate with loss of p53 to promote lung tumorigenesis.
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Seco, Martins Marques Neves João Filipe. "NMR study of 14-3-3 protein-protein interactions and modulation thereof by small molecules." Thesis, Lille, 2019. http://www.theses.fr/2019LIL1S108.
Les protéines 14-3-3 sont des protéines adaptatrices qui exercent leurs fonctions biologiques en modulant l’activité de centaines d’autres protéines. De part leur impressionnant interactome, les protéines 14-3-3 sont des acteurs qui influencent de nombreux événements cellulaires et, par conséquent, de maladies associées. La stabilisation ou l’inhibition sélective d’interactions protéine-protéine (IPP) de 14-3-3 sont considérées comme des approches prometteuses pour trouver des thérapies innovantes contre des maladies comme la maladie d’Alzheimer, certains cancers ou la maladie de Parkinson.Notre premier but afin de trouver des petites molécules capables de moduler ces cibles a été d’étudier au niveau moléculaire des IPP de 14-3-3. Dans ce but, nous avons utilisé la Résonance Magnétique Nucléaire (RMN) pour attribuer les déplacements chimiques des atomes du squelette de 14-3-3σ. Nous avons ensuite étudié l’interaction entre 14-3-3 et la protéine Tau phosphorylée. Nous avons découvert que Tau se lie strictement dans la cavité amphipathique de 14-3-3 et peut s’ancrer aux deux monomères du dimère de 14-3-3. Nous avons aussi étudié l’interaction 14-3-3/p53 et avons découvert, en utilisant la RMN, que l’affinité du peptide p53 envers 14-3-3 est liée à des interactions intramoléculaires au niveau du peptide. Nous nous sommes enfin focalisés sur l’optimisation d’expériences RMN visant le criblage et la caractérisation de l’activité des petites molécules qui se lient à 14-3-3 ou à des complexes de 14-3-3 avec des peptides phosphorylés. Nous avons aussi utilisé des peptides phospho-mimétiques pour inhiber l’interaction 14-3-3/Tau. D’autre part, nous avons criblé une bibliothèque de fragments contre 14-3-3σ et trouvé trois hits qui se lient à des régions différentes de la protéine. Des expériences RMN ont ensuite permis de caractériser l’activité de certaines petites molécules actives sur des complexes de 14-3-3 avec, par exemple des peptides de p53 ou p65, et nous avons aussi démontré la capacité de certains de ces composés à stabiliser les complexes 14-3-3 proteins are adapter proteins that exert their biological functions by modulating the activity of hundreds of proteins. This remarkable interactome makes 14-3-3 proteins influent actors in many cellular events and, by consequence, in several pathologies. The selective stabilization or inhibition of 14-3-3 protein-protein interactions (PPIs) are therefore seen as promising approaches for finding innovative therapies for a number of conditions like Alzheimer’s, cancer or Parkinson. Our first objective towards finding small molecule modulators of these targets was to obtain the molecular detail of 14-3-3 PPIs. To this end, using Nuclear Magnetic Resonance (NMR), we assigned the backbone chemical shifts of 14-3-3σ. We then studied the 14-3-3/phosphorylated Tau interaction and found that Tau binds strictly within the amphipathic binding grove of 14-3-3 and can anchor in both monomers of the 14-3-3 dimer. We also studied the 14-3-3/p53 interaction and showed by NMR, that intramolecular interactions within the peptide define a conformation that drives the affinity towards 14-3-3. 2019We then focused on the optimization of NMR assays for screening and characterization of the effect of small-molecules binding to 14-3-3 or 14-3-3 complexes with target’s phosphopeptides. We used, for example, phospho-mimetic peptides to inhibit the Tau/14-3-3 interaction. In a different strategy, we screened a fragment library against 14-3-3σ and found three hits binding to different regions of the protein. Using our NMR assays we further characterized small molecules binding 14-3-3 complexes with, for example, p53 and p65 peptides and demonstrated the stabilization capacity of some compounds
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Alleman, Cécile. "Accès synthétique au châssis [5-8-5] de la fusicoccine-A pour la synthèse d’analogues simplifiés en vue d'étudier les interactions protéine-protéine." Electronic Thesis or Diss., Université de Rennes (2023-....), 2023. http://www.theses.fr/2023URENS090.
Les interactions protéine – protéine (IPP) sont essentielles à la régulation des phénomènes cellulaires. Elles impliquent deux partenaires : une protéine adaptatrice et une protéine effectrice, cette dernière étant régulée positivement ou négativement. Bien que l’inhibition des IPPs constitue une approche thérapeutique solide, la stabilisation reste encore peu étudiée, mais pourrait mener à de nouvelles modalités prometteuses. Ce projet se concentre sur la famille de protéines adaptatrices 14-3-3 qui interagit avec plus de 200 partenaires. Parmi eux, la protéine p53 est l’objet de multiples recherches dû à sa fonction régulatrice clé de nombreux processus biologiques (réparation de l’ADN, apoptose). Ces fonctions majeures sont cependant altérées dans la moitié des cancers, favorisant ainsi le développement tumoral. Des études préliminaires ont montré que la stabilisation de l’interaction entre p53 et 14-3-3 à l’aide d’une colle moléculaire permettait de restaurer l’activité antitumorale de p53. Parmi ces colles moléculaires, la fusicoccine-A (FC-A) se localise dans la vallée formée par 14-3-3 et permet d’augmenter la stabilisation du complexe protéique. Dans ce contexte, ce projet se concentre sur l’accès à des analogues simplifiés de la FC-A à travers la synthèse de squelettes tricycliques afin d’élargir la librairie de colles moléculaires. Des analogues [6-8-5] à partir d’un substrat aromatique sont envisagés, ainsi que des analogues [5-8-5] à partir d’un dérivé cyclopentane, plus proches de la structure cible. Différentes stratégies de synthèse ont été explorées afin d’accéder à ces analogues In biological media, protein-protein interactions (PPI) are of huge importance, as they allow the regulation of many cellular events. PPI classically involve two partners: an adapter protein and its effector protein(s) regulated either in a positive or a negative manner. Inhibition of PPI has thus been considered as a solid therapeutic approach. On the other hand, stabilization of PPI remains scarcely investigated, but may lead to new promising approaches. This project focuses on the 14-3-3 family adapter protein which interacts with more than 200 protein partners. Among them, p53 protein is subjected to a lot of studies as this tumor suppressor protein regulates multiple biological processes (DNA repair, apoptosis). However, those major functions appear to be silenced in most cancer cases, thus allowing tumor cells proliferation. Some studies have shown that stabilization of the 14-3-3/p53 pair with the help of a molecular glue permitted to restore tumor suppressor activity of p53. Among the examined molecular glues, the fusicoccin-A (FC-A) natural product is shown to lodge in the valley formed by 14-3-3 and increases stabilization of the 14-3-3/p53 interaction. In this context, to enlarge the p53/14-3-3 molecular glue library, this project focuses on the access to simplified FC-A analogs through the synthesis of tricyclic scaffold. [6-8-5] analogs from an aromatic substrate are envisaged, as well as [5-8-5] analogs from a cyclopentane derivative, closer to the target structure. Various strategies have been explored in order to access these analogs
Book chapters on the topic "P53, 14-3-3":
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Galat, Andrzej, and Sylvie Riviere. "Genes and the cellular localization of PPlases." In Peptidyl–Prolyl Cis/Trans lsomerases, 32–35. Oxford University PressOxford, 1998. http://dx.doi.org/10.1093/oso/9780198502883.003.0003.
Abstract The gene PPIA encoding hCyP-A has been mapped to chromosome 7 in the region 7p11.2-p13 and there are 14 other CyP-A-related pseudogenes, on chromosomes 3, 7, 10, 14 and 18 [297, 353]. The gene PPIB coding for hCyP-B is on chromosome 15 [342]. The gene PPID encoding hCyP-40 is on chromosome 4 and consists of ten exons and nine introns. The exon organization of the genes encoding the CPLDs of hCyP-40 and hCyP-A are very different, suggesting that these two genes diverged early in evolution [355]. Zoo blots show that the PPID gene is highly conserved among different species. Fluorescence in situ hybridization to human metaphase chromosomes allowed the identification of another gene (PPIL1) encoding a cyclophilin of 166 amino acid residues. The gene was mapped to chromosome 2 in the region p23.3-p23.1. The protein seems to be expressed in many tissues [341].
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Taber, Douglass. "The Toste Synthesis of ( + )-Fawcettimine." In Organic Synthesis. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199764549.003.0091.
The tetracyclic Lycopodium alkaloid fawcettimine 3 and its derivatives are of interest as inhibitors of acetylcholine esterase. F. Dean Toste of the University of California, Berkeley recently reported (Angew. Chem. Int. Ed. 2007, 46, 7671) the first enantioselective synthesis of 3. The key to the synthesis was the rapid assembly of the enantiomerically-enriched hydrindane 2. The preparation of 2 began with the enantioselective Robinson annulation of the β-keto ester 4 with crotonaldehyde 5, mediated by the organocatalyst 6. In this protocol, originally developed by Karl Anker Jørgensen, the single stereogenic center was established by conjugate addition, presumably to the chiral iminium salt generated by the condensation of 5 with 6. Subsequent aldol (or more likely Mannich) cyclization followed by elimination gave 7. Hydrolysis and decarboxylation by heating with p-TsOH converted 7 to 1. This procedure was robust enough to allow preparation of a ten gram batch of 1. This Jørgensen annulation is the current method of choice for the enantioselective preparation of 2,5-dialkyl cyclohexenones. Conjugate addition of the propargyl anion equivalent 8 to 1 proceeded with the expected > 95:5 axial diastereoselectivity, to give the silyl enol ether 9. Exposure of the derived iodide 10 to catalytic [Ph3 PAu]Cl and AgBF4 induced smooth cyclization to the cis hydrindane 2. Before constructing the nine-membered ring amine of fawcettimine 3, it was first necessary to protect the ketone as the ketal. Pd-mediated coupling of the alkenyl iodide with the organoborane derived from 11 then proceeded smoothly, as did the subsequent hydroboration of the terminal alkene. Neither the mesylate nor the tosylate derived from 12 could be induced to cyclize. In contrast, intramolecular displacement of the iodide proceeded well, to give 13. Hydroboration followed by oxidation then gave 15, which on deprotection cyclized to (+)-fawcettimine 3. Several aspects of this synthesis are attractive. While the stereochemical outcome of the hydroboration of 14 could not necessarily be predicted with confidence, in fact it did not matter, as the stereogenic center adjacent to the ketone could be epimerized under the trifluoroacetic acid deprotection conditions, and only the desired diastereomer would be able to add in an intramolecular fashion to the cyclohexanone.
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Ito, M., H. Hiroi, T. Urano, M. Momoeda, Y. Hosokawa, R. Tsutumi, M. Koizumi, T. Yano, S. Inoue, and Y. Taketani. "A Progesterone Responsive Gene, 14-3-3 Tau, Upregulates the Transcriptional Activity of Progesterone Receptor B (PR-B) in Uterine Endometrium." In Posters I, P3–14—P3–14. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part3.p1.p3-14.
Cheng, Theresa M., Vinod Ganju, Steve R. Ritland, Gobinda Sarkar, and Robert B. Jenkins. "[14] Analysis of p53 mutations in human gliomas by RNA single-strand conformational polymorphism." In Methods in Neurosciences, 210–24. Elsevier, 1995. http://dx.doi.org/10.1016/s1043-9471(06)80092-3.
Danilov, Alexey V., Amitabh Srivastava, Elena V. Feofanova, Leigh Ann Humphries, James Direnzo, and Murray Korc. "Abstract 3076:p53 homologue p63 trans-activates epidermal growth factor (EGF) receptor and 14-3-3α and thus promotes tumorigenesis and chemoresistance in pancreatic cancer." 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.am2012-3076.
Xu, Jia, Sunil Acharya, Ozgur Sahin, Lin Zhang, Frank J. Lowery, Aysegul A. Sahin, Xiang H. f. Zhang, Mien-Chie Hung, and Dihua Yu. "Abstract LB-202: 14-3-3ζ turns TGF-β's function from tumor suppressor to metastasis promoter in breast cancer by contextual changes of Smad partners from p53 to Gli2." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-lb-202.
Rodrigues, Antonio Rony da S. P., and Edinalda Maria Cavalcante. "ESTUDO GENÉTICO DO CÂNCER DE TIREOIDE – UMA REVISÃO." In I SIMPÓSIO MARANHENSE DE GENÉTICA E GENÔMICA EM SAÚDE. Doity - Plataforma de Eventos, 2022. http://dx.doi.org/10.55664/simaggens2022.005.
INTRODUÇÃO: O câncer de tireoide é um dos agravos mais comuns ao sistema endócrino, com o maior aumento anual de incidência em diferentes países, principalmente devido à melhoria das tecnologias de diagnóstico, sendo mais proeminente em regiões com acesso aos cuidados de saúde amplamente disponíveis. Alguns eventos moleculares são descritos tanto na carciogênese da tireoide quanto na evolução do tumor glandular. Dados do Atlas do câncer no Genoma Humano dividiu os carcinomas papilíferos de tireoide nas categorias BRAF e RAS, com base nos resultados do exoma do sequenciamento de DNA, RNA e perfil proteômico, e padrões de metilação. OBJETIVOS: Observar nos estudos da literatura os marcadores genéticos relacionados ao câncer de tireóide. MÉTODOS MÉTODOS: Para alcançar os objetivos propostos neste estudo, o método eleito foi a Revisão Integrativa que inclui a análise de pesquisas relevantes que dão suporte para a tomada de decisão, permitindo a incorporação desses achados na prática clínica. A partir de então, foi feita uma busca, ocorrida entre fevereiro e março de 2022, em 5 bases de dados: LILACS (Literatura Latino-Americana e do Caribe em Ciências da Saúde) e SciELO (Scientific Electronic Library Online), PubMed (Central: PMC- National Library of Medicine National Institutes of Health), ScienceDirect e IBECS (Índice Bibliográfico Espanhol em Ciências da Saúde). A pesquisa por artigos foi feita através dos termos em língua inglesa: “thyroid cancer”, “risk markers” e “thyroid cancer genetics” junto ao operador booleano AND. Os resultados obtidos foram comparados, estabelecendo-se concordância quanto a formulação da amostra final. Os achados foram apresentados a partir do método de “nuvem de palavras”, utilizando o software wordle. Nuvem de palavras é uma forma de facilitar a demonstração de quais são as palavras mais frequentes quando pesquisado por determinado assunto ou tema. RESULTADOS E DISCUSSÃO: Na etapa de seleção subsequente os artigos foram lidos na íntegra onde 213 artigos foram excluídos por não se apresentarem dentro do objeto estudo, e incluídos 14 trabalhos na versão final da revisão. A análise proteica demostrou projeção da estrutura molecular e homologia proteica dos seguintes marcadores moleculares de câncer de tireoide: proto-oncogene receptor tirosina quinase (RET); proto-oncogene do receptor de tirosina quinase neurotrófico 1 (NTRK1); homólogo de fosfatase tensina (PTEN); gene da proteína tumoral p53 (TP53); fosfoinositida 3-quinase/treonina proteína quinase (PI3K/AKT); catenina beta 1 (CTNNB1); gama de receptor ativado por proliferador de peroxissoma de caixa pareada 8 (PAX8-PPARG); oncogene viral de sarcoma de rato (RAS); proto-oncogene B-raf, serina/treonina quinase (BRAF); e receptor do hormônio estimulante da tireóide (TSHR). Experimentos utilizando o tipo de array identificaram três genes diferencialmente expressos, cuja expressão foi analisada por RT-PCR em 10 amostras de cada tipo de tecido. Dois deles foram capazes de diferenciar carcinomas papilíferos de tecido normal e bócio com 89% de precisão para o tumor maligno e 80% para os tecidos não malignos. Conclusão: Após a análise dos resultados desta RI, foi possível observar alguns marcadores de risco para câncer de tireóide. Desse modo, o presente trabalho contribui para o aprofundamento e desenvolvimento de novas reflexões dos estudos sobre marcadores genéticos canceriginos
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Trejo, Leonard J., and Gregory W. Lewis. "Individual differences in classification of transient, isoluminant, chromatic signals: a behavioral and electrophysiological analysis." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1989. http://dx.doi.org/10.1364/oam.1989.fk1.
Individual differences in classification of transient, isoluminant, chromatic signals were studied in 39 male subjects (age 29 ± 2.9 yr). Chromatic contrast was constrained to either R-G or B-Y axes of opponent color theory. Subjects binocularly and centrally fixated a light grey (D6500, 10.3 ft-L), 14° by 9.7° background. Stimuli uniformly replaced the central 7° by 6.5° of the background for 10.8 ms and had either low or high contrast with respect to it. Achromatic stimuli were also presented. Recorded data included two-alternative forced choice responses (based on stimulus hue) and event-related brain potentials (ERP). Five fifty-trial blocks were presented in the order: black/white (high con trast), R/Y (low contrast), B/Y (low), R/G (high), B/Y (high). Across subjects, corresponding mean percentages of correctly classified stimuli were (mean/sd): 92 ± 7, 72 ± 23, 26 ± 3, 91 ± 11, 71 ± 29. Across blocks, correlations of mean percent correct vs variables CIELUV ΔE, MacAdam's AS, N1-amplitude and P3-amplitude were 0.09, 0.45, 0.86, and 0.97.
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Papapetrou, Georghios Dorou, Chia Pei Chuen, Mohd Nur Adzizie Mahamad, Ros Aliza Md Rabi, and Yong Han Seah. "FDP Simulation Studies for Green Fields Cluster Development in Less than 30 Days Utilizing Cloud Technologies." In ADIPEC. SPE, 2022. http://dx.doi.org/10.2118/211415-ms.
Abstract BD Cluster green fields development located offshore Sabah, Malaysia, consists of three multi-stacked turbidite fields, namely A, B and C, encompassing thick and thin bed sands. Due to the lack of existing infrastructure in close proximity, a wellhead platform (WHP) will be installed on top of Field A. Fields B and C will be developed with a respective 8 and 7km subsea tie back to this WHP. Gas will be exported from the WHP to Facility-1 situated 5km away, whereas oil from a single thin oil rim reservoir in Field A will be exported to Facility-2 50km away. The challenges faced by the Reservoir Engineering (RE) Team was delivering an extensive number of dynamic simulations while adhering to the Field Development Planning (FDP) submission deadline: 1) uncertainty analysis and probabilistic modelling for 9 models, 2) construction of coupled reservoir models 3) screening alternative oil and gas export routes, and 4) optimizing capex phasing by determining the optimum startup sequence of the fields. Delivering the FDP work on time with the limited software licenses and computing infrastructure available on-premise appeared to be a "bridge too far". The limitations were addressed by PETRONAS LiveFDP digital transformation initiative commenced in 2019, through deployment of digital cloud technologies and solutions with scalable High-Performance Computing (HPC) environment. A total of 9 geological models were delivered to REs for dynamic simulation studies. Probabilistic modelling was then employed to obtain the dynamic P10, P50 and P90 models for each field. The Reservoir Coupling facility and Extended Network option were used in the numerical simulator to couple the standalone models in order to honor the overall facility constraints and incorporate the pipeline effects. Utilizing the coupled network model, multiple studies including condensate banking, determining optimum field sequencing and export route scenario were performed. The FDP subsurface development simulation runs were completed within 1 month using HPC cloud solutions and workflows compared to 9 months if using on-premise infrastructure. It provided the necessary tools to allow the team: 1) accurately assess the impact of condensate banking on well productivity, 2) executed over 1200 cases for probabilistic modelling for the 9 models in 24 hours of simulation time, 3) reduced the number of wells derived from a previous study from 14 to 9 yielding a saving of ~US$115 million, 4) ~US$50 million savings as a result of capex phasing by optimizing the field start up sequence, and 5) US$130 million savings by establishing the lowest cost oil and gas export route scenario.
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Pratt, Sheila Alhana, Valeria Sanabria, Ana Soskin, Aurora Rocio Rizzi, and Marcos Cabrera. "ADENOID CYSTIC CARCINOMA OF THE BREAST." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1014.
Introduction: Adenoid cystic adenoid carcinoma (ACC) of the breast is a rare variant that occurs in large series only in less than 1% of the patients. It has favorable prognosis and morphological resemblance to tumors originating in the salivary glands. Histopathological diagnosis is based on a mixture of proliferating glands, which correspond to the adenoid component and the replication of the basal membrane in the form of cylinders established by the pseudoglandular component. It usually occurs in adult women. Its form of clinical presentation is a painless breast nodule, located in the retroareolar region, without compromise of skin or nipple secretion, of small size and circumscribed limits. Treatment of ACC is not protocolized, although it is accepted that conservative surgery is applicable in most cases. Our goal is to publicize the clinical case of a patient treated in our service and to show some clinical and histopathological aspects of this same rare pathology. Case report: 63-year-old patient, with no history of cancer in the family, menarche at 16 years of age, three full births, 24 months of lactation, menopause at 46 years of age, no hormone replacement therapy. Hypertensive and diabetic, a right breast nodule was self-detected six months before; slow and painless growth that then fistulizes the skin and is accompanied by serohematic secretion of a gelatinous consistency. On physical examination, a 7 cm nodule is felt in lower quadrants, showing elastic consistency and poorly defined edges. No adenopathies in the armpits or neck. Sectional biopsy performed in another service. Pathological anatomy: differential diagnosis between Cystic Hypersecretory Carcinoma and Cystic Secretory Hyperplasia. With the diagnosis of ACC of the right breast, T2N0Mx stage IIa. Mammography: breasts type b, at the junction of lower quadrants of the right breast, dense delimited mass measuring 5x4 cm, no retraction or skin edema. BIRADS V. Ecograph: A mass located in H6 to 3 cm of the nipple with well delimited edges, with heterogeneous characteristics with liquid and solid areas of 5.71 cm x 4.06 cm. BIRADS V. Extensive resection and sentinel node biopsy is performed. Histopathological result revealed ACC G1 of 5.5 cm with no associated in situ carcinoma. No vascular plungers or perineural invasion are observed. Free surgical limits. pT3 Nx.Mx. Immunohistochemistry: RE-; RP-; HER2-;ki67 <14%. Our case showed a neoplastic proliferation consisting of two types of cavity formation; true glandular lights (adenoid component) and pseudo lumens that produce basal membrane material (cylinder component) with eosinophilic basal membrane material, the adenoid component with basophilic mucin and surrounded by myoepithelial cells. Three negative lymph nodes metastasis. Radiation therapy was decided as an adjuvant treatment.
Reports on the topic "P53, 14-3-3":
1
Halzonetis, Thanos. Interaction of p53 with 14-3-3. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada405400.
Halazonetis, Thanos. Interaction of p53 with 14-3-3. Fort Belvoir, VA: Defense Technical Information Center, May 2000. http://dx.doi.org/10.21236/ada390713.
Dorman, Eleanor, Zara Markovic-Obiago, Julie Phillips, Richard Szydlo, and Darren K. Patten. Wellbeing in UK Frontline Healthcare Workers During Peaks One and Three of the COVID-19 Pandemic: A Retrospective Cross-Sectional Analysis. Science Repository, December 2022. http://dx.doi.org/10.31487/j.ejgm.2022.01.01.
Background: COVID-19 had a huge impact on the wellbeing of healthcare workers (HCWs). This is well documented during the first peak of the pandemic. With cases in the UK rising for a third peak, hospitalisations and deaths surpassing the first, there is very little known about the mental health of HCWs during this time. Methods: Using a questionnaire, data was collected from patient-facing staff at Barking, Havering, and Redbridge University Trust to quantify and compare the period prevalence of symptoms of depression, anxiety, and PTSD during the first peak (P1: March-May 2020) and third peak (P3: December 2020-Feburary 2021) of the COVID-19 pandemic as well as wellbeing service use, demographics of responders and what they found most difficult during the peaks. Results: Of 158 responders, only 22·4% felt they had enough access to wellbeing services during P1 and 21·5% in P3. Of those who used wellbeing services 34·4% found them useful in P1 and 34·6% in P3. 70·3% of responders felt that not enough was done for staff wellbeing. The median anxiety score decreased from P1 (10(range 5-17)) to P3 (8(range 4-16)) p=0·031. Under 30-year-olds’ depression and PTSD scores increased from P1 to P3 (depression: P1 7(1-11), P3 8(3-14), p=0·048, PTSD: P1 4(0-7) peak 3 5(2-9), p=0·037). Several groups showed a decrease in anxiety scores from P1 to P3 including; over 30-year-olds (P1 10(5-17), P3 7(3-15) p=0·002), BME responders (P1 8(3·75-15) P3 6·5(1-12) p=0·006), AHP (P1 14(7-19), P3 11(5-19) p=0·005), ITU workers (P1 15(8-18·25) P3 12(5·75-18·25) p=0·004), and those who were redeployed (P1 8(5-18·25), P3 5(2-14·75), p=0·032). Conclusion: We have observed changes in mental health symptoms within the study population as the peaks of the pandemic continue. With the majority of responders reporting they felt not enough had been done for their wellbeing support - and of those who used the wellbeing services only around 1/3 felt they were useful - we hope that this paper can help inform wellbeing provision and identify groups at higher risk of developing mental health symptoms.
