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1.
Food Res Int ; 176: 113828, 2024 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-38163725

RESUMEN

Wines covered by PDO or PGI quality labels have specific sensory characteristics. According to EU regulations, product characteristics (including the sensory description) must be defined in the PDO technical specification and should be verified for their compliance. There exist internationally harmonized quantitative descriptive sensory methods applied to products such as virgin olive oil, with well-defined attributes described in the method itself. Currently, in the case of wine, there is no harmonized international sensory descriptive method that allows comparison of results between different PDOs or laboratories. In this work, a qualitative and quantitative olfactory profile for a broad variety of wines (11 PDO and 37 wine types) and their corresponding reference standards are proposed. The sensory profile obtained can be used both to verify compliance with the technical specifications of the product and to categorize wines by type or region, thus becoming a powerful tool for the wine sector.


Asunto(s)
Vino , Vino/análisis , Gusto , Olfato , Aceite de Oliva
2.
Nat Cell Biol ; 25(12): 1833-1847, 2023 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-37945904

RESUMEN

MAF amplification increases the risk of breast cancer (BCa) metastasis through mechanisms that are still poorly understood yet have important clinical implications. Oestrogen-receptor-positive (ER+) BCa requires oestrogen for both growth and metastasis, albeit by ill-known mechanisms. Here we integrate proteomics, transcriptomics, epigenomics, chromatin accessibility and functional assays from human and syngeneic mouse BCa models to show that MAF directly interacts with oestrogen receptor alpha (ERα), thereby promoting a unique chromatin landscape that favours metastatic spread. We identify metastasis-promoting genes that are de novo licensed following oestrogen exposure in a MAF-dependent manner. The histone demethylase KDM1A is key to the epigenomic remodelling that facilitates the expression of the pro-metastatic MAF/oestrogen-driven gene expression program, and loss of KDM1A activity prevents this metastasis. We have thus determined that the molecular basis underlying MAF/oestrogen-mediated metastasis requires genetic, epigenetic and hormone signals from the systemic environment, which influence the ability of BCa cells to metastasize.


Asunto(s)
Neoplasias de la Mama , Epigénesis Genética , Receptor alfa de Estrógeno , Amplificación de Genes , Proteínas Proto-Oncogénicas c-maf , Animales , Femenino , Humanos , Ratones , Neoplasias de la Mama/genética , Neoplasias de la Mama/patología , Línea Celular Tumoral , Cromatina , Receptor alfa de Estrógeno/genética , Receptor alfa de Estrógeno/metabolismo , Estrógenos , Histona Demetilasas/genética , Histona Demetilasas/metabolismo , Proteínas Proto-Oncogénicas c-maf/genética
3.
Foods ; 11(19)2022 Sep 22.
Artículo en Inglés | MEDLINE | ID: mdl-36230046

RESUMEN

Producers of PDO (Protected Designation of Origin) wines must submit to the EU authorities' technical specifications that include the specific sensory description of each product typology, to be subsequently checked by the competent authority in each country. Unfortunately, there is no consensual and standardized approach for the development of sensory control methods for PDO wines. The aim of this work was to develop a sensory profile for the taste and mouthfeel descriptors that allows the characterization of wines from 11 existing PDOs in Catalonia (Spain), and with the purpose of advancing the process of harmonization of the official sensory analysis of wines. This paper includes the selection process of tasters, the procedure used for the definition and grouping of descriptors, and the development of references for the selected attributes. The use of this analytical tool should allow PDO/PGI product certification and control authorities to verify compliance with their specifications (descriptive and quantitative) based on objectively evaluated results.

4.
Cancer Res ; 80(21): 4668-4680, 2020 11 01.
Artículo en Inglés | MEDLINE | ID: mdl-32816905

RESUMEN

Carcinoma development in colorectal cancer is driven by genetic alterations in numerous signaling pathways. Alterations in the RAS-ERK1/2 pathway are associated with the shortest overall survival for patients after diagnosis of colorectal cancer metastatic disease, yet how RAS-ERK signaling regulates colorectal cancer metastasis remains unknown. In this study, we used an unbiased screening approach based on selection of highly liver metastatic colorectal cancer cells in vivo to determine genes associated with metastasis. From this, an ERK1/2-controlled metastatic gene set (EMGS) was defined. EMGS was associated with increased recurrence and reduced survival in patients with colorectal cancer tumors. Higher levels of EMGS expression were detected in the colorectal cancer subsets consensus molecular subtype (CMS)1 and CMS4. ANGPT2 and CXCR4, two genes within the EMGS, were subjected to gain-of-function and loss-of-function studies in several colorectal cancer cell lines and then tested in clinical samples. The RAS-ERK1/2 axis controlled expression of the cytokine ANGPT2 and the cytokine receptor CXCR4 in colorectal cancer cells, which facilitated development of liver but not lung metastases, suggesting that ANGPT2 and CXCR4 are important for metastatic outgrowth in the liver. CXCR4 controlled the expression of cytokines IL10 and CXCL1, providing evidence for a causal role of IL10 in supporting liver colonization. In summary, these studies demonstrate that amplification of ERK1/2 signaling in KRAS-mutated colorectal cancer cells affects the cytokine milieu of the tumors, possibly affecting tumor-stroma interactions and favoring liver metastasis formation. SIGNIFICANCE: These findings identify amplified ERK1/2 signaling in KRAS-mutated colorectal cancer cells as a driver of tumor-stroma interactions that favor formation of metastases in the liver.


Asunto(s)
Angiopoyetina 2/biosíntesis , Neoplasias del Colon/patología , Sistema de Señalización de MAP Quinasas/fisiología , Invasividad Neoplásica/patología , Receptores CXCR4/biosíntesis , Animales , Neoplasias del Colon/genética , Regulación Neoplásica de la Expresión Génica/fisiología , Xenoinjertos , Humanos , Neoplasias Hepáticas/secundario , Ratones , Invasividad Neoplásica/genética , Regulación hacia Arriba
5.
J Assoc Res Otolaryngol ; 20(6): 553-563, 2019 12.
Artículo en Inglés | MEDLINE | ID: mdl-31297642

RESUMEN

The tail-lift reflex and the air-righting reflex are anti-gravity reflexes in rats that depend on vestibular function. To obtain objective and quantitative measures of performance, we recorded these reflexes with slow-motion video in two experiments. In the first experiment, vestibular dysfunction was elicited by acute exposure to 0 (control), 400, 600, or 1000 mg/kg of 3,3'-iminodipropionitrile (IDPN), which causes dose-dependent hair cell degeneration. In the second, rats were exposed to sub-chronic IDPN in the drinking water for 0 (control), 4, or 8 weeks; this causes reversible or irreversible loss of vestibular function depending on exposure time. In the tail-lift test, we obtained the minimum angle defined during the lift and descent maneuver by the nose, the back of the neck, and the base of the tail. In the air-righting test, we obtained the time to right the head. We also obtained vestibular dysfunction ratings (VDRs) using a previously validated behavioral test battery. Each measure, VDR, tail-lift angle, and air-righting time demonstrated dose-dependent loss of vestibular function after acute IDPN and time-dependent loss of vestibular function after sub-chronic IDPN. All measures showed high correlations between each other, and maximal correlation coefficients were found between VDRs and tail-lift angles. In scanning electron microscopy evaluation of the vestibular sensory epithelia, the utricle and the saccule showed diverse pathological outcomes, suggesting that they have a different role in these reflexes. We conclude that these anti-gravity reflexes provide useful objective and quantitative measures of vestibular function in rats that are open to further development.


Asunto(s)
Gravitación , Reflejo/fisiología , Vestíbulo del Laberinto/fisiología , Animales , Relación Dosis-Respuesta a Droga , Masculino , Nitrilos/toxicidad , Ratas , Ratas Long-Evans , Vestíbulo del Laberinto/efectos de los fármacos , Vestíbulo del Laberinto/patología
7.
Nat Cell Biol ; 20(2): 211-221, 2018 02.
Artículo en Inglés | MEDLINE | ID: mdl-29358704

RESUMEN

For many patients with breast cancer, symptomatic bone metastases appear after years of latency. How micrometastatic lesions remain dormant and undetectable before initiating colonization is unclear. Here, we describe a mechanism involved in bone metastatic latency of oestrogen receptor-positive (ER+) breast cancer. Using an in vivo genome-wide short hairpin RNA screening, we identified the kinase MSK1 as an important regulator of metastatic dormancy in breast cancer. In patients with ER+ breast cancer, low MSK1 expression associates with early metastasis. We show that MSK1 downregulation impairs the differentiation of breast cancer cells, increasing their bone homing and growth capacities. MSK1 controls the expression of genes required for luminal cell differentiation, including the GATA3 and FOXA1 transcription factors, by modulating their promoter chromatin status. Our results indicate that MSK1 prevents metastatic progression of ER+ breast cancer, suggesting that stratifying patients with breast cancer as high or low risk for early relapse based on MSK1 expression could improve prognosis.


Asunto(s)
Neoplasias de la Mama/genética , Factor de Transcripción GATA3/genética , Factor Nuclear 3-alfa del Hepatocito/genética , Proteínas Quinasas S6 Ribosómicas 90-kDa/genética , Adulto , Anciano , Animales , Biomarcadores de Tumor/genética , Neoplasias Óseas/genética , Neoplasias Óseas/patología , Neoplasias Óseas/secundario , Neoplasias de la Mama/patología , Diferenciación Celular/genética , Cromatina/genética , Femenino , Regulación Neoplásica de la Expresión Génica , Genoma Humano/genética , Humanos , Ratones , Persona de Mediana Edad , Metástasis de la Neoplasia , Pronóstico , ARN Interferente Pequeño/genética , Receptores de Estrógenos/genética , Ensayos Antitumor por Modelo de Xenoinjerto
9.
Nat Cell Biol ; 18(6): 645-656, 2016 06.
Artículo en Inglés | MEDLINE | ID: mdl-27214280

RESUMEN

Cellular transformation and cancer progression is accompanied by changes in the metabolic landscape. Master co-regulators of metabolism orchestrate the modulation of multiple metabolic pathways through transcriptional programs, and hence constitute a probabilistically parsimonious mechanism for general metabolic rewiring. Here we show that the transcriptional co-activator peroxisome proliferator-activated receptor gamma co-activator 1α (PGC1α) suppresses prostate cancer progression and metastasis. A metabolic co-regulator data mining analysis unveiled that PGC1α is downregulated in prostate cancer and associated with disease progression. Using genetically engineered mouse models and xenografts, we demonstrated that PGC1α opposes prostate cancer progression and metastasis. Mechanistically, the use of integrative metabolomics and transcriptomics revealed that PGC1α activates an oestrogen-related receptor alpha (ERRα)-dependent transcriptional program to elicit a catabolic state and metastasis suppression. Importantly, a signature based on the PGC1α-ERRα pathway exhibited prognostic potential in prostate cancer, thus uncovering the relevance of monitoring and manipulating this pathway for prostate cancer stratification and treatment.


Asunto(s)
Mitocondrias/metabolismo , Coactivador 1-alfa del Receptor Activado por Proliferadores de Peroxisomas gamma/metabolismo , Neoplasias de la Próstata/metabolismo , Animales , Modelos Animales de Enfermedad , Metabolismo Energético/fisiología , Proteínas de Choque Térmico/metabolismo , Humanos , Masculino , Ratones , Metástasis de la Neoplasia/patología , Neoplasias de la Próstata/patología , Receptores de Estrógenos/metabolismo , Receptor Relacionado con Estrógeno ERRalfa
10.
J Natl Cancer Inst ; 107(12): djv256, 2015 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-26376684

RESUMEN

BACKGROUND: There are currently no biomarkers for early breast cancer patient populations at risk of bone metastasis. Identification of mediators of bone metastasis could be of clinical interest. METHODS: A de novo unbiased screening approach based on selection of highly bone metastatic breast cancer cells in vivo was used to determine copy number aberrations (CNAs) associated with bone metastasis. The CNAs associated with bone metastasis were examined in independent primary breast cancer datasets with annotated clinical follow-up. The MAF gene encoded within the CNA associated with bone metastasis was subjected to gain and loss of function validation in breast cancer cells (MCF7, T47D, ZR-75, and 4T1), its downstream mechanism validated, and tested in clinical samples. A multivariable Cox cause-specific hazard model with competing events (death) was used to test the association between 16q23 or MAF and bone metastasis. All statistical tests were two-sided. RESULTS: 16q23 gain CNA encoding the transcription factor MAF mediates breast cancer bone metastasis through the control of PTHrP. 16q23 gain (hazard ratio (HR) for bone metastasis = 14.5, 95% confidence interval (CI) = 6.4 to 32.9, P < .001) as well as MAF overexpression (HR for bone metastasis = 2.5, 95% CI = 1.7 to 3.8, P < .001) in primary breast tumors were specifically associated with risk of metastasis to bone but not to other organs. CONCLUSIONS: These results suggest that MAF is a mediator of breast cancer bone metastasis. 16q23 gain or MAF protein overexpression in tumors may help to select patients at risk of bone relapse.


Asunto(s)
Biomarcadores de Tumor/metabolismo , Neoplasias Óseas/metabolismo , Neoplasias Óseas/secundario , Neoplasias de la Mama/metabolismo , Neoplasias de la Mama/patología , Variaciones en el Número de Copia de ADN , Proteínas Proto-Oncogénicas c-maf/metabolismo , Animales , Línea Celular Tumoral , Femenino , Regulación Neoplásica de la Expresión Génica , Xenoinjertos , Humanos , Inmunohistoquímica , Hibridación Fluorescente in Situ , Incidencia , Ratones , Ratones Endogámicos BALB C , Oportunidad Relativa , Valor Predictivo de las Pruebas , Pronóstico , Modelos de Riesgos Proporcionales , Regulación hacia Arriba
11.
Nat Cell Biol ; 16(7): 685-94, 2014 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-24880666

RESUMEN

The mechanisms that allow colon cancer cells to form liver and lung metastases, and whether KRAS mutation influences where and when metastasis occurs, are unknown. We provide clinical and molecular evidence showing that different MAPK signalling pathways are implicated in this process. Whereas ERK2 activation provides colon cancer cells with the ability to seed and colonize the liver, reduced p38 MAPK signalling endows cancer cells with the ability to form lung metastasis from previously established liver lesions. Downregulation of p38 MAPK signalling results in increased expression of the cytokine PTHLH, which contributes to colon cancer cell extravasation to the lung by inducing caspase-independent death in endothelial cells of the lung microvasculature. The concerted acquisition of metastatic traits in the colon cancer cells together with the sequential colonization of liver and lung highlights the importance of metastatic lesions as a platform for further dissemination.


Asunto(s)
Neoplasias del Colon/patología , Neoplasias Hepáticas/secundario , Neoplasias Pulmonares/secundario , Metástasis de la Neoplasia , Proteína Relacionada con la Hormona Paratiroidea/metabolismo , Transducción de Señal , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismo , Animales , Células Cultivadas , Neoplasias del Colon/fisiopatología , Modelos Animales de Enfermedad , Células Endoteliales/metabolismo , Humanos , Ratones , Mutación , Proteína Relacionada con la Hormona Paratiroidea/genética , Proteínas Quinasas p38 Activadas por Mitógenos/genética , Proteínas ras/genética , Proteínas ras/metabolismo
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