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Dive into the research topics where Sonia Molina-Pinelo is active.

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Featured researches published by Sonia Molina-Pinelo.


Journal of Proteomics | 2013

Identification of proteomic signatures associated with lung cancer and COPD.

M.D. Pastor; A. Nogal; Sonia Molina-Pinelo; R. Meléndez; Ana Salinas; M. González De la Peña; J. Martín-Juan; J. Corral; R. Garcia-Carbonero; Amancio Carnero; Luis Paz-Ares

UNLABELLED Lung cancer (LC) and chronic obstructive pulmonary disease (COPD) commonly coexist in smokers, and the presence of COPD increases the risk of developing LC. The aim of this study was to identify distinct proteomic profiles able to discriminate these two pathological entities. Protein content was assessed in the bronchoalveolar lavage (BAL) of 60 patients classified in four groups: COPD, COPD and LC, LC without COPD, and control with neither COPD nor LC. Proteins were separated into spots by bidimensional polyacrylamide gel electrophoresis (2D-PAGE) and examined by matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF/TOF). A total of 40 proteins were differentially expressed in the LC and/or COPD groups as compared with the control group. Distinct protein profiles were identified and validated for each pathological entity (LC and COPD). The main networks involved were related to inflammatory signalling, free radical scavenging and oxidative stress response, and glycolysis and gluconeogenesis pathways. The most relevant signalling link between LC and COPD was through the NF-κB pathway. In conclusion, the protein profiles identified contribute to elucidate the underlying pathogenic pathways of both diseases, and provide new tools of potential use as biomarkers for the early diagnosis of LC. BIOLOGICAL SIGNIFICANCE Sequence coverage. The protein sequence coverage (95%) was estimated for specific proteins by the percentage of matching amino acids from the identified peptides having confidence greater than or equal to 95% divided by the total number of amino acids in the sequence. Ingenuity Pathways Analysis. Mapping of our proteins onto biological pathways and disease networks demonstrated that 22 proteins were linked to inflammatory signalling (p-value: 1.35 10(-08)-1.42 10(-02)), 15 proteins were associated with free radical scavenging and oxidative stress response (p-value: 4.93 10(-11)-1.27 10(-02)), and 9 proteins were related with glycolysis and gluconeogenesis pathways (p-value: 7.39 10(-09)-1.58 10(-02)).


Journal of Antimicrobial Chemotherapy | 2009

Premature immunosenescence in HIV-infected patients on highly active antiretroviral therapy with low-level CD4 T cell repopulation

Sonia Molina-Pinelo; Alejandro Vallejo; Laura Díaz; Natalia Soriano-Sarabia; Sara Ferrando-Martínez; Salvador Resino; María Ángeles Muñoz-Fernández; Manuel Leal

OBJECTIVES To analyse the role of thymic function and its association with cellular immunosenescence markers in patients with low-level CD4 T cell repopulation, despite complete HIV RNA replication control on highly active antiretroviral therapy (HAART). METHODS Cellular immunosenescence markers comparing patients with CD4 T cell counts <or=250 cells/mm(3) for >or=48 weeks (n = 11) and patients with a CD4 T cell count >or=500 cells/mm(3) (n = 11) were investigated. Both groups were also compared with 11 healthy volunteers of similar age. Naive CD4 T cell counts, beta- and delta-T cell rearrangement excision circles, recent thymic emigrants, replicative senescence marker, cell activation, and rate of apoptosis were analysed. The Mann-Whitney U-test was used to compare parameters between both low-level and high-level CD4 T cell repopulation groups, and healthy volunteers. RESULTS Our results showed a lower thymic activity in patients with low-level CD4 T cell repopulation, leading to a decline in CD4 T cell production. On the other hand, a higher activation along with a higher replicative senescence of CD4 T cells contributed to a higher rate of apoptotic CD4 T cells in this group of patients. CONCLUSIONS We propose a model with several different related mechanisms involved in premature immune senescence in HIV-infected patients with low-level CD4 repopulation on HAART. The understanding of such different mechanisms could help find effective strategies to prevent immune decay.


European Respiratory Journal | 2014

MicroRNA clusters: dysregulation in lung adenocarcinoma and COPD

Sonia Molina-Pinelo; M. Dolores Pastor; Rocío Suárez; Beatriz Romero-Romero; Miriam González De la Peña; Ana Salinas; R. Garcia-Carbonero; María José De Miguel; Francisco Rodríguez-Panadero; Amancio Carnero; Luis Paz-Ares

Lung adenocarcinoma and chronic obstructive pulmonary disease (COPD) are pulmonary diseases that share common aetiological factors (tobacco smoking) and probable dysregulated pathways. MicroRNAs (miRNAs) play an essential role in regulating numerous physiological and pathological processes. The purpose of this study was to assess global miRNA expression patterns in patients with COPD and/or adenocarcinoma to elucidate distinct regulatory networks involved in the pathogenesis of these two smoking-related diseases. Expression of 381 miRNAs was quantified by TaqMan Human MicroRNA A Array v2.0 in bronchoalveolar lavage fluid samples from 87 patients classified into four groups: COPD, adenocarcinoma, adenocarcinoma with COPD, and control (neither COPD nor adenocarcinoma). 11 differentially expressed miRNAs were randomly selected for validation in an independent cohort of 40 patients. Distinct miRNA expression profiles were identified and validated for each pathological group, involving 66 differentially expressed miRNAs. Four miRNA clusters (the mir-17-92 cluster and its paralogues, mir-106a-363 and mir-106b-25; and the miR-192-194 cluster) were upregulated in patients with adenocarcinoma and one miRNA cluster (miR-132-212) was upregulated in patients with COPD. These results contribute to unravelling miRNA-controlled networks involved in the pathogenesis of adenocarcinoma and COPD, and provide new tools of potential use as biomarkers for diagnosis and/or therapeutic purposes. MicroRNA expression profiles in bronchoalveolar lavage fluid enable discrimination of adenocarcinoma from COPD http://ow.ly/tPaVC


Clinical Therapeutics | 2016

Current Challenges in Cancer Treatment.

Jon Zugazagoitia; Cristiano Guedes; Santiago Ponce; Irene Ferrer; Sonia Molina-Pinelo; Luis Paz-Ares

PURPOSE In this review, we highlight the current concepts and discuss some of the current challenges and future prospects in cancer therapy. We frequently use the example of lung cancer. METHODS We conducted a nonsystematic PubMed search, selecting the most comprehensive and relevant research articles, clinical trials, translational papers, and review articles on precision oncology and immuno-oncology. Papers were prioritized and selected based on their originality and potential clinical applicability. FINDINGS Two major revolutions have changed cancer treatment paradigms in the past few years: targeting actionable alterations in oncogene-driven cancers and immuno-oncology. Important challenges are still ongoing in both fields of cancer therapy. On the one hand, druggable genomic alterations are diverse and represent only small subsets of patients in certain tumor types, which limits testing their clinical impact in biomarker-driven clinical trials. Next-generation sequencing technologies are increasingly being implemented for molecular prescreening in clinical research, but issues regarding clinical interpretation of large genomic data make their wide clinical use difficult. Further, dealing with tumor heterogeneity and acquired resistance is probably the main limitation for the success of precision oncology. On the other hand, long-term survival benefits with immune checkpoint inhibitors (anti-programmed death cell protein-1/programmed death cell ligand-1[PD-1/L1] and anti-cytotoxic T lymphocyte antigen-4 monoclonal antibodies) are restricted to a minority of patients, and no predictive markers are yet robustly validated that could help us recognize these subsets and optimize treatment delivery and selection. To achieve long-term survival benefits, drug combinations targeting several molecular alterations or cancer hallmarks might be needed. This will probably be one of the most challenging but promising precision cancer treatment strategies in the future. IMPLICATIONS Targeting single molecular abnormalities or cancer pathways has achieved good clinical responses that have modestly affected survival in some cancers. However, this approach to cancer treatment is still reductionist, and many challenges need to be met to improve treatment outcomes with our patients.


PLOS ONE | 2014

MicroRNA-dependent regulation of transcription in non-small cell lung cancer

Sonia Molina-Pinelo; Gabriel Gutiérrez; Maria Dolores Pastor; Marta Hergueta; Gema Moreno-Bueno; R. Garcia-Carbonero; Ana Nogal; Rocío Suárez; Ana Salinas; Francisco Pozo-Rodríguez; Fernando López-Ríos; María Teresa Agulló-Ortuño; Irene Ferrer; Asunción Perpiñá; José Palacios; Amancio Carnero; Luis Paz-Ares

Squamous cell lung cancer (SCC) and adenocarcinoma are the most common histological subtypes of non-small cell lung cancer (NSCLC), and have been traditionally managed in the clinic as a single entity. Increasing evidence, however, illustrates the biological diversity of these two histological subgroups of lung cancer, and supports the need to improve our understanding of the molecular basis beyond the different phenotypes if we aim to develop more specific and individualized targeted therapy. The purpose of this study was to identify microRNA (miRNA)-dependent transcriptional regulation differences between SCC and adenocarcinoma histological lung cancer subtypes. In this work, paired miRNA (667 miRNAs by TaqMan Low Density Arrays (TLDA)) and mRNA profiling (Whole Genome 44 K array G112A, Agilent) was performed in tumor samples of 44 NSCLC patients. Nine miRNAs and 56 mRNAs were found to be differentially expressed in SCC versus adenocarcinoma samples. Eleven of these 56 mRNA were predicted as targets of the miRNAs identified to be differently expressed in these two histological conditions. Of them, 6 miRNAs (miR-149, miR-205, miR-375, miR-378, miR-422a and miR-708) and 9 target genes (CEACAM6, CGN, CLDN3, ABCC3, MLPH, ACSL5, TMEM45B, MUC1) were validated by quantitative PCR in an independent cohort of 41 lung cancer patients. Furthermore, the inverse correlation between mRNAs and microRNAs expression was also validated. These results suggest miRNA-dependent transcriptional regulation differences play an important role in determining key hallmarks of NSCLC, and may provide new biomarkers for personalized treatment strategies.


International Journal of Molecular Sciences | 2013

Identification of Oxidative Stress Related Proteins as Biomarkers for Lung Cancer and Chronic Obstructive Pulmonary Disease in Bronchoalveolar Lavage

Maria Dolores Pastor; Ana Nogal; Sonia Molina-Pinelo; Ricardo Melendez; Beatriz Romero-Romero; Maria Dolores Mediano; José Luis López-Campos; R. Garcia-Carbonero; Amparo Sanchez-Gastaldo; Amancio Carnero; Luis Paz-Ares

Lung cancer (LC) and chronic obstructive pulmonary disease (COPD) commonly coexist in smokers, and the presence of COPD increases the risk of developing LC. Cigarette smoke causes oxidative stress and an inflammatory response in lung cells, which in turn may be involved in COPD and lung cancer development. The aim of this study was to identify differential proteomic profiles related to oxidative stress response that were potentially involved in these two pathological entities. Protein content was assessed in the bronchoalveolar lavage (BAL) of 60 patients classified in four groups: COPD, COPD and LC, LC, and control (neither COPD nor LC). Proteins were separated into spots by two dimensional polyacrylamide gel electrophoresis (2D-PAGE) and examined by matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF/TOF). A total of 16 oxidative stress regulatory proteins were differentially expressed in BAL samples from LC and/or COPD patients as compared with the control group. A distinct proteomic reactive oxygen species (ROS) protein signature emerged that characterized lung cancer and COPD. In conclusion, our findings highlight the role of the oxidative stress response proteins in the pathogenic pathways of both diseases, and provide new candidate biomarkers and predictive tools for LC and COPD diagnosis.


Journal of Clinical Immunology | 2006

Thymic function-related markers within the thymus and peripheral blood: Are they comparable?

María Victoria Arellano; Antonio Ordoñez; Ezequiel Ruiz-Mateos; Santiago R. Leal-Noval; Sonia Molina-Pinelo; Ana Hernández; Alejandro Vallejo; Rafael Hinojosa; Manuel Leal

The thymus involutes with age and its functionality has traditionally been assumed to be limited early in life. However, some studies have demonstrated that thymic function persists in adults. In humans, since it is difficult to obtain thymic samples from healthy individuals, indirect parameters have been used to study the thymic function. The aim of this study was to compare thymic function parameters within both the thymus and peripheral blood mononuclear cells from thirty-three patients who underwent cardiac surgery, as well as to relate these parameters with aging. The proportion of peripheral naïve T cells and intrathymic T cell differentiation stages, as well as peripheral and intrathymic TREC levels were analysed. We demonstrated that thymopoyesis persists in the healthy elderly since all T cell differentiation stages were found within the thymus. Among the studied parameters, peripheral TREC levels are found to be a good thymic function marker since they correlated with age. In healthy individuals, peripheral TREC levels are a good reflect of thymic function as demonstrated by their correlation with intrathymic TREC values.


The Journal of Pathology | 2011

Down-regulation of spinophilin in lung tumours contributes to tumourigenesis.

Sonia Molina-Pinelo; Irene Ferrer; Carmen Blanco-Aparicio; Sandra Peregrino; Maria Dolores Pastor; Juan Alvarez-Vega; Rocío Suárez; Mar Verge; Juan J. Marin; Javier Hernández-Losa; Santiago Ramón y Cajal; Luis Paz-Ares; Amancio Carnero

The scaffold protein spinophilin (Spn, PPP1R9B) is one of the regulatory subunits of phosphatase‐1a (PP1), targeting it to distinct subcellular locations and to its target. Loss of Spn reduces PPP1CA levels, thereby maintaining higher levels of phosphorylated pRb. This effect contributes to an increase in p53 activity. However, in the absence of p53, reduced levels of Spn increase the tumourigenic properties of cells. In addition, Spn knockout mice have a reduced lifespan, an increased number of tumours and increased cellular proliferation in some tissues, such as the mammary ducts. In addition, the combined loss of Spn and p53 activity leads to an increase in mammary carcinomas, confirming the functional relationship between p53 and Spn. In this paper, we report that Spn is absent in 20% and reduced in another 37% of human lung tumours. Spn reduction correlates with malignant grade. Furthermore, the loss of Spn also correlates with p53 mutations. Analysis of miRNAs in a series of lung tumours showed that miRNA106a* targeting Spn is over‐expressed in some patients, correlating with decreased Spn levels. Proof‐of‐concept experiments over‐expressing miRNA106a* or Spn shRNA in lung tumour cells showed increased tumourigenicity. In conclusion, our data showed that miRNA106a* over‐expression found in lung tumours might contribute to tumourigenesis through Spn down‐regulation in the absence of p53. Copyright


Journal of Viral Hepatitis | 2009

HCV RNA in peripheral blood cell subsets in HCV–HIV coinfected patients at the end of PegIFN/RBV treatment is associated with virologic relapse

B. de Felipe; Manuel Leal; Natalia Soriano-Sarabia; A. Gutiérrez; Luis F. López-Cortés; Sonia Molina-Pinelo; Alejandro Vallejo

Summary.  Extrahepatic replication may have important implications for the treatment of hepatitis C virus (HCV). Our aim was to analyse the association between the presence of positive/negative strand HCV RNA in different peripheral blood cell subsets at the end of PegIFN/RBV treatment, and treatment response in HIV‐coinfected patients. Thirty‐four HCV–HIV coinfected patients who concluded 48 weeks of PegIFN/RBV treatment were included in the present study. Positive/negative strand HCV RNA was detected by amplification of the 5′ untranslated region (5′ UTR) using high‐temperature RT‐PCR in immunomagnetic‐isolated cell subsets. Twenty‐three patients (67.6%) had sustained virologic response (SVR) while 11 patients (32.4%) relapsed. The frequency of positive/negative strand HCV RNA in any cell subsets was significantly lower in patients with SVR (8.6%) compared to relapsers (63.6%) (P = 0.002). Baseline HCV viral load was statistically higher among patients who relapsed (P = 0.008), while patients with SVR had very early virologic response more frequently (P = 0.003). Multivariate analysis showed, among these three variables, that only the presence of positive/negative strand HCV RNA was independently associated with relapse [P = 0.024; OR 14 (14–137)]. In conclusion, the presence of positive/negative strand HCV RNA at the end of treatment is associated with relapse among HCV–HIV coinfected patients and might have important implications in the clinical practice.


Journal of Acquired Immune Deficiency Syndromes | 2006

Thymic volume predicts CD4 T-cell decline in HIV-infected adults under prolonged treatment interruption.

Sonia Molina-Pinelo; Jorge Vivancos; Beatriz De Felipe; Natalia Soriano-Sarabia; Angela Valladares; Rafael de la Rosa; Alejandro Vallejo; Manuel Leal

Objective: To analyze the predictive capacity of thymic volume in CD4 T-cell loss after treatment interruption in HIV-infected patients with high nadir CD4 count. Methods: Thirty-nine HIV-infected patients with CD4 counts greater than or equal to 500 cells/&mgr;L, nadir CD4 counts greater than or equal to 250 cells/&mgr;L, and plasma viral loads less than 50 copies/mL for at least the past 12 months began a treatment interruption program. The event of interest for this study was the decrease of CD4 count below 350 cells/&mgr;L. Kaplan-Meier curves were used for all time-to-event analyses, and log-rank tests were used for comparison between groups in the univariate analysis. All variables with statistical association with CD4 T-cell loss were analyzed using multivariate Cox proportional hazards regression models. Results: Twenty-three percent of the patients had a decrease in CD4 count to less than 350 cells/&mgr;L. In the univariate analysis, only thymic volume was statistically significant with this event (P = 0.02). Nadir CD4 count nearly reached statistical significance. However, age, sex, HCV coinfection, CD4 count, T-cell receptor excision circle-bearing cells, and early viral load rebound did not show statistical differences. Thymic volume and CD4 T-cell loss were independently associated using Cox proportional hazards regression model (P = 0.04; relative risk, 0.76; 95% confidence interval, 0.59-0.99). Conclusions: In this study, we demonstrate for the first time that thymic volume predicts CD4 T-cell loss in patients with nadir CD4 count greater than or equal to 250 cells/&mgr;L under treatment interruption.

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Luis Paz-Ares

Complutense University of Madrid

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Irene Ferrer

Spanish National Research Council

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Maria Dolores Pastor

Spanish National Research Council

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Ana Salinas

Spanish National Research Council

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Rocío Suárez

Spanish National Research Council

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R. Garcia-Carbonero

Spanish National Research Council

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Purificacion Estevez-Garcia

Spanish National Research Council

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