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1.
J Feline Med Surg ; 26(4): 1098612X241234984, 2024 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-38682929

RESUMEN

OBJECTIVES: This study undertook a scoping review of research on blood fibroblast growth factor 23 (FGF-23) concentrations in healthy non-azotemic cats and cats with chronic kidney disease (CKD) to describe the volume and nature of existing literature, to determine whether published studies provide adequate evidence to support the use of FGF-23 as a biomarker in clinical practice and to identify any existing gaps in knowledge. METHODS: PRISMA Extension for Scoping Reviews guidelines were used to design and perform the scoping review. Online databases were used to identify observational and clinical studies of blood FGF-23 concentrations in healthy cats and cats with CKD published before December 2022. Study and population characteristics and descriptive data on FGF-23 concentrations were extracted. RESULTS: A total of 205 publications were reviewed; 17 were retained for inclusion. Most studies were retrospective. Most studies included cats with International Renal Interest Society stage 2-4 CKD, with some variation. Key concepts explored in the literature include FGF-23 concentrations by CKD stage, effect of dietary phosphate restriction on FGF-23 concentrations, relationship between FGF-23 concentrations and blood phosphorus, calcium and magnesium concentrations, and FGF-23 concentrations in cats with progressive CKD. FGF-23 concentrations tended to be higher in cats with CKD compared with healthy cats, with an overlap between healthy and CKD populations, and there was significant variation within stages of CKD. CONCLUSIONS AND RELEVANCE: FGF-23 is a biomarker of interest for the management and monitoring of phosphate overload in cats. Studies support several potential clinical applications for measuring FGF-23 concentration in practice; however, evidence is limited. Research on FGF-23 in cats with CKD would benefit from longitudinal, prospective studies that standardize CKD diagnosis and categorize cats by stage using current guidelines. Studies should include cats with early-stage, non-azotemic CKD and use commercially available assays so such results are comparable across studies.


Asunto(s)
Biomarcadores , Enfermedades de los Gatos , Factor-23 de Crecimiento de Fibroblastos , Factores de Crecimiento de Fibroblastos , Insuficiencia Renal Crónica , Gatos , Animales , Insuficiencia Renal Crónica/veterinaria , Insuficiencia Renal Crónica/sangre , Enfermedades de los Gatos/sangre , Factores de Crecimiento de Fibroblastos/sangre , Biomarcadores/sangre
2.
Clin. transl. oncol. (Print) ; 8(4): 231-241, abr. 2006. ilus, tab
Artículo en En | IBECS (España) | ID: ibc-047662

RESUMEN

No disponible


Molecular genetic evidence indicates that endometrialcarcinoma likely develops as the result of a multistepprocess of oncogene activation and tumor suppressorgene inactivation. These molecular alterations appearto be specific for Type I (endometrioid) and Type II(non endometrioid) cancers. Type I cancers are characterizedby mutation of PTEN, KRAS2, defects in DNAmismatch repair, as evidenced by the microsatelliteinstability phenotype, and a near diploid karyotype.Type II cancers often contain mutations of TP53 andHer-2/neu and are usually nondiploid. The clinicalvalue of many of these molecular markers is now beingtested and it may help to refine diagnosis and establishan accurate prognosis. Furthermore, some ofthese tumor biomarkers constitute the targets foremerging therapies. Transtuzumab against Her-2/neuand bevacizumab against VEGF overexpressing carcinomasare among the promising novel treatments.Additional translational research is needed to identifymolecular and genetic alterations with potential fortherapeutic interventions


Asunto(s)
Femenino , Humanos , Técnicas de Diagnóstico Molecular/tendencias , Biomarcadores de Tumor/análisis , Neoplasias Endometriales/diagnóstico , Receptores de Estradiol/análisis , Receptores de Progesterona/análisis , Genes Supresores de Tumor , Repeticiones de Microsatélite , Genes p53 , Ploidias , Neovascularización Patológica/patología , Receptor ErbB-2
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