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1.
EJNMMI Res ; 8(1): 4, 2018 Jan 18.
Artigo em Inglês | MEDLINE | ID: mdl-29349517

RESUMO

BACKGROUND: Building a universal genomic signature predicting the intensity of FDG uptake in diverse metastatic tumors may allow us to understand better the biological processes underlying this phenomenon and their requirements of glucose uptake. METHODS: A balanced training set (n = 71) of metastatic tumors including some of the most frequent histologies, with matched PET/CT quantification measurements and whole human genome gene expression microarrays, was used to build the signature. Selection of microarray features was carried out exclusively on the basis of their strong association with FDG uptake (as measured by SUVmean35) by means of univariate linear regression. A thorough bioinformatics study of these genes was performed, and multivariable models were built by fitting several state of the art regression techniques to the training set for comparison. RESULTS: The 909 probes with the strongest association with the SUVmean35 (comprising 742 identifiable genes and 62 probes not matched to a symbol) were used to build the signature. Partial least squares using three components (PLS-3) was the best performing model in the training dataset cross-validation (root mean square error, RMSE = 0.443) and was validated further in an independent validation dataset (n = 13) obtaining a performance within the 95% CI of that obtained in the training dataset (RMSE = 0.645). Significantly overrepresented biological processes correlating with the SUVmean35 were identified beyond glycolysis, such as ribosome biogenesis and DNA replication (correlating with a higher SUVmean35) and cytoskeleton reorganization and autophagy (correlating with a lower SUVmean35). CONCLUSIONS: PLS-3 is a signature predicting accurately the intensity of FDG uptake in diverse metastatic tumors. FDG-PET might help in the design of specific targeted therapies directed to counteract the identified malignant biological processes more likely activated in a tumor as inferred from the SUVmean35 and also from its variations in response to antineoplastic treatments.

3.
Rev. esp. patol ; 39(2): 128-131, abr.-jun. 2006. ilus
Artigo em Es | IBECS | ID: ibc-049679

RESUMO

La Miocarditis de Células Gigantes (MCG) es una miocardiopatíapoco frecuente, de posible causa inmunológica,con evolución fatal por fallo cardíaco congestivo, cuya principalterapia es el tratamiento inmunosupresor o el trasplante.El diagnóstico definitivo es histopatológico. El caso quese describe corresponde a una mujer de 59 años, que mostróun cuadro clínico de infarto agudo de miocardio, conimágenes de coronariografía normales, realizándose el diagnóstico«post-mortem» en la autopsia


Giant Cell Myocarditis is a rare myocardiopathy, withuncertain immunology basis, fatal evolution and congestiveheart failure. Its main treatment is immunosuppressive therapyor cardiac transplantation. The diagnosis is definitivelyhistopathological. The reported case corresponds to a 59years old woman, showing clinical findings of acute myocardiuminfarct but normal coronariography. The definitivediagnosis was made in the autopsy


Assuntos
Feminino , Pessoa de Meia-Idade , Humanos , Miocardite/patologia , Arterite de Células Gigantes/patologia , Infarto do Miocárdio/etiologia , Autopsia
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