Browsing by Author "Marin, Arnaldo"
Now showing 1 - 3 of 3
Results Per Page
Sort Options
- ItemEndocarditis infecciosa por Listeria monocytogenes: revisión de la literatura a partir de un caso clínico(2013) Marin, Arnaldo; Lustig, Nicole; Cruz Urrutia, Ricardo Javier; Cordova, SamuelInfective endocarditis caused by Listeria monocytogenes is an extremely rare but usually aggressive disease. We have seen in recent years an increase in age of onset of this disease and a predilection for patients With valvular disease, especially prosthetic valve. The treatment of choice is ampicillin, which is combined with gentamicin for synergy. It is known that even with treatment the Mortality is very high and higher than in other types of bacterial endocarditis. With optimal therapy, that is medical-surgical, mortality has declined significantly in recent years. We presents a review of literature and a clinical ease of a patient with a febrile syndrome diagnosed as a infective endocarditis caused by L. monocytogenes treated Medically with successful Outcome to date.
- ItemFibroblast growth factor receptor signaling in estrogen receptor-positive breast cancer: mechanisms and role in endocrine resistance(2024) Marin, Arnaldo; Morales, Fernanda; Walbaum García, Benjamín VicenteFibroblast Growth Factor Receptors (FGFRs) play a significant role in Estrogen Receptor-positive (ER+) breast cancer by contributing to tumorigenesis and endocrine resistance. This review explores the structure, signaling pathways, and implications of FGFRs, particularly FGFR1, FGFR2, FGFR3, and FGFR4, in ER+ breast cancer. FGFR1 is frequently amplified, especially in aggressive Luminal B-like tumors, and its amplification is associated with poor prognosis and treatment resistance. The co-amplification of FGFR1 with oncogenes like EIF4EBP1 and NSD3 complicates its role as a standalone oncogenic driver. FGFR2 amplification, though less common, is critical in hormone receptor regulation, driving proliferation and treatment resistance. FGFR3 and FGFR4 also contribute to endocrine resistance through various mechanisms, including the activation of alternate signaling pathways like PI3K/AKT/mTOR and RAS/RAF/MEK/ERK. Endocrine resistance remains a major clinical challenge, with around 70% of breast cancers initially hormone receptor positive. Despite the success of CDK 4/6 inhibitors in combination with endocrine therapy (ET), resistance often develops, necessitating new treatment strategies. FGFR inhibitors have shown potential in preclinical studies, but clinical trials have yielded limited success due to off-target toxicities and lack of predictive biomarkers. Current clinical trials, including those evaluating FGFR inhibitors like erdafitinib, lucitanib, and dovitinib, have demonstrated mixed outcomes, underscoring the complexity of FGFR signaling in breast cancer. The interplay between FGFR and other signaling pathways highlights the need for comprehensive molecular profiling and personalized treatment approaches. Future research should focus on identifying robust biomarkers and developing combination therapies to enhance the efficacy of FGFR-targeted treatments. In conclusion, targeting FGFR signaling in ER+ breast cancer presents both challenges and opportunities. A deeper understanding of the molecular mechanisms and resistance pathways is crucial for the successful integration of FGFR inhibitors into clinical practice, aiming to improve outcomes for patients with endocrine-resistant breast cancer.
- ItemHipertensión arterial: el factor de riesgo más importante para grosor íntima-media carotídeo elevado y placa carotídea en adultos de Santiago(SOC MEDICA SANTIAGO, 2011) Acevedo, Monica; Tagle, Rodrigo; Kramer, Veronica; Arnaiz, Pilar; Marin, Arnaldo; Pino, Felipe; Godoy, Ivan; Berrios, Ximena; Navarrete, CarlosBackground: Carotid Ultima media thickness (CIMT) is a marker of cardiovascular damage that can be modified by traditional risk factors. Aim: To determine attributable risk factors for a high CIMT among healthy adults. Material and Methods: A sample of 1270 individuals (636 males and 634 females) aged 44 +/- 11 years, was studied. Blood pressure, weight, height, lipid profile and blood glucose were measured in all. CIMT and the presence of atherosclerotic plaques were determined by carotid ultrasound. Standard criteria were used to define hypertension, dyslipidemia and diabetes. Results: Mean CIMT in the sample studied was 0.62 +/- 0.01 mm and percentile 75 was 0.67. The most important risk factor for a CIMT over percentile 75 and the presence of atherosclerotic plaques was hypertension with attributable risks of 54 and 57%, respectively. Conclusions: In this sample, the main risk factor for a high CIMT was hypertension. (Rev Med Chile 2011; 139: 290-297).