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  1. Home
  2. Browse by Author

Browsing by Author "Morales, Fernanda"

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    Current folate status in Chilean women of childbearing age: findings from the 2016-2017 National Health Survey
    (2019) Busso, Dolores; Echeverria, Guadalupe; Morales, Fernanda; Farias, Marcelo; Margozzini, Paula
    Introduction: Mandatory folic acid (FA) fortification is an effective policy to ensure adequate preconceptional serum folate (SF) levels in women and to reduce the incidence of neural tube defects (NTD). In Chile, FA fortification of wheat flour started in 2000 and significantly reduced NTD prevalence. In 2010, 1:2 Chileans over 65 years old had supraphysiological SF levels. In 2012, FA fortification was reduced from 2.2 to 1.8 mg FA/kg flour. Considering the epidemiological transition in Chile over the last decades and the adjustment of the FA fortification policy in 2012, this study was aimed at describing the current SF levels in women of reproductive age in our country. Methods: 225 women (15-49 years) who participated in the Chilean National Health Survey (NHS) 2016-17 were included in this analysis. NHS 2016-17 used stratified multistage sampling. SF levels were determined by electrochemiluminescence immunoassay, and defined as deficient (≤4.4 ng/ml), normal (4.41 to 20 ng/ml) and supraphysiological [three subcategories: high (20.01 to 25.6 ng/ml), very high (25.61 to 29 ng/ml) and highest (>29 ng/ml)]. Multiple logistic regression analyses were performed using SPSS software (version 17.0). Results: The proportions of women in each decade of life were representative of the national proportions. More than 99% of the women came from urban areas, and near 91% had medium or high educational level. Only 32% of the women declared being current smokers, and 88% declared they were sedentary. Almost 70% of subjects were either overweight or obese, reflecting the current nutritional status of the Chilean population. The SF mean ± SE, median and range were 14.20 ± 0.39, 13.52 and 2.10 - 32.22 ng/ml, respectively. Folate deficiency was present in 0.9% of the women studied, while 7% had supraphysiological levels of the vitamin (3.7% high, 1.6% very high and 1.7% highest levels). Multivariate analyses using linear regression did not show that age, educational level, marital status, parity, smoker/non-smoker or nutritional status had significant effects on FS levels. Conclusion: Folate deficiency in women of reproductive age living in the Metropolitan Region is almost inexistent according to the NHS 2016- 17, showing that most Chilean women are protected from NTD due to folate deficiency. Supraphysiological SF levels were found in 7% of the studied population, lower than the 50% determined in elderly subjects in 2010. Specific policies to reduce the proportion of Chileans at high risk of SF deficiency or excess, in combination with surveillance of FA fortification in flour mills, may help to avoid potential unintended effects of FA fortification in this country. Funding: Chilean Ministry of Health and Pontificia Universidad Católica de Chile.
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    Fibroblast growth factor receptor signaling in estrogen receptor-positive breast cancer: mechanisms and role in endocrine resistance
    (2024) Marin, Arnaldo; Morales, Fernanda; Walbaum García, Benjamín Vicente
    Fibroblast 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.
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    Folate status in women of childbearing age in the Urban Metropolitan Region of Chile: results from the National Health Survey 2016-2017
    (CAMBRIDGE UNIV PRESS, 2021) Busso, Dolores; Echeverria, Guadalupe; Passi Solar, Alvaro; Morales, Fernanda; Farias, Marcelo; Margozzini, Paula
    Objective: To analyse serum folate levels in women of childbearing age in the Metropolitan Region (MR) of Chile.
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    Immune-related IncRNA LINC00944 responds to variations in ADAR1 levels and it is associated with breast cancer prognosis
    (2021) de Santiago, Pamela R.; Blanco, Alejandro; Morales, Fernanda; Marcelain, Katherine; Harismendy, Olivier; Herrera, Marcela Sjoberg; Armisen, Ricardo
    Aims: Breast cancer is one of the leading causes of woman deaths worldwide, being a major public health problem. It has been reported that the expression of the RNA-editing enzyme Adenosine Deaminase Acting on RNAs 1 (ADAR1) is upregulated in breast cancer, predicting poor prognosis in patients. A few reports in literature examine ADAR1 and long non-coding RNAs (lncRNAs) interplay in cancer and suggest key roles in cancer-related pathways. This study aimed to investigate whether ADAR1 could alter the expression levels of lncRNAs and explore how those changes are related to breast cancer biology.
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    Increase in ADAR1p110 activates the canonical Wnt signaling pathway associated with aggressive phenotype in triple negative breast cancer cells
    (2022) Morales, Fernanda; Perez, Paola; Tapia, Julio C.; Lobos-Gonzalez, Lorena; Manuel Herranz, Jose; Guevara, Francisca; Rojas de Santiago, Pamela; Palacios, Esteban; Andaur, Rodrigo; Sagredo, Eduardo A.; Marcelain, Katherine; Armisen, Ricardo
    Triple-negative breast cancer (TNBC) represents a challenge in the search for new therapeutic targets. TNBCs are aggressive and generate resistance to chemotherapy. Tumors of TNBC patients with poor prognosis present a high level of adenosine deaminase acting on RNA1 (ADAR1). We explore the connection of ADAR1 with the canonical Wnt signaling pathway and the effect of modulation of its expression in TNBC. Expression data from cell line sequencing (DepMap) and TCGA samples were downloaded and analyzed. We lentivirally generated an MDA-MB-231 breast cancer cell line that overexpress (OE) ADAR1p110 or an ADAR knockdown. Abundance of different proteins related to Wnt/beta-catenin pathway and activity of nuclear beta-catenin were analyzed by Western blot and luciferase TOP/FOP reporter assay, respectively. Cell invasion was analyzed by matrigel assay. In mice, we study the behavior of tumors generated from ADAR1p110 (OE) cells and tumor vascularization immunostaining were analyzed. ADAR1 connects to the canonical Wnt pathway in TNBC. ADAR1p110 overexpression decreased GSK-3 beta, while increasing active beta-catenin. It also increased the activity of nuclear beta-catenin and increased its target levels. ADAR1 knockdown has the opposite effect. MDA-MB-231 ADAR1 (OE) cells showed increased capacity of invasion. Subsequently, we observed that tumors derived from ADAR1p110 (OE) cells showed increased invasion towards the epithelium, and increased levels of Survivin and CD-31 expressed in vascular endothelial cells. These results indicate that ADAR1 overexpression alters the expression of some key components of the canonical Wnt pathway, favoring invasion and neovascularization, possibly through activation of the beta-catenin, which suggests an unknown role of ADAR1p110 in aggressiveness of TNBC tumors.

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