Search

Your search keyword '"Real, Francisco X."' showing total 26 results
Start Over Author "Real, Francisco X." Journal international journal of cancer
26 results on '"Real, Francisco X."'

3. Plasma protein biomarkers for early detection of pancreatic ductal adenocarcinoma

Author

Yu, Jingru, primary, Ploner, Alexander, additional, Kordes, Maximilian, additional, Löhr, Matthias, additional, Nilsson, Magnus, additional, Maturana, Maria Evangelina Lopez, additional, Estudillo, Lidia, additional, Renz, Harald, additional, Carrato, Alfredo, additional, Molero, Xavier, additional, Real, Francisco X, additional, Malats, Núria, additional, and Ye, Weimin, additional

Published
2021
Full Text
View/download PDF

9. Asthma status is associated with decreased risk of aggressive urothelial bladder cancer

Author

Rava, Marta, primary, Czachorowski, Maciej J., additional, Silverman, Debra, additional, Márquez, Mirari, additional, Kishore, Sirish, additional, Tardón, Adonina, additional, Serra, Consol, additional, García-Closas, Montse, additional, Garcia-Closas, Reina, additional, Carrato, Alfredo, additional, Rothman, Nathaniel, additional, Real, Francisco X., additional, Kogevinas, Manolis, additional, and Malats, Núria, additional

Published
2017
Full Text
View/download PDF

10. The human PKP2/plakophilin-2 gene is induced by Wnt/ßcatenin in normal and colon cancer-associated fibroblasts.

Author

Niell, Núria, Larriba, María Jesús, Ferrer-Mayorga, Gemma, Sánchez-Pérez, Isabel, Cantero, Ramón, Real, Francisco X., del Peso, Luis, Muñoz, Alberto, and González-Sancho, José Manuel

Abstract

Colorectal cancer results from the malignant transformation of colonic epithelial cells. Stromal fibroblasts are the main component of the tumour microenvironment, and play an important role in the progression of this and other neoplasias. Wnt/ßcatenin signalling is essential for colon homeostasis, but aberrant, constitutive activation of this pathway is a hallmark of colorectal cancer. Here we present the first transcriptomic study on the effect of a Wnt factor on human colonic myofibroblasts. Wnt3A regulates the expression of 1,136 genes, of which 662 are upregulated and 474 are downregulated in CCD-18Co cells. A set of genes encoding inhibitors of the Wnt/ß-catenin pathway stand out among those induced by Wnt3A, which suggests that there is a feedback inhibitory mechanism. We also show that the PKP2 gene encoding the desmosomal protein Plakophilin-2 is a novel direct transcriptional target of Wnt/ß-catenin in normal and colon cancer-associated fibroblasts. PKP2 is induced by ß - catenin / TCF through three binding sites in the gene promoter and one additional binding site located in an enhancer 20 kb upstream from the transcription start site. Moreover, Plakophilin-2 antagonizes Wnt/ß-catenin transcriptional activity in HEK-293T cells, which suggests that it may act as an intracellular inhibitor of the Wnt/ß-catenin pathway. Our results demonstrate that stromal fibroblasts respond to canonical Wnt signalling and that Plakophilin-2 plays a role in the feedback control of this effect suggesting that the response to Wnt factors in the stroma may modulate Wnt activity in the tumour cells. [ABSTRACT FROM AUTHOR]

Published
2018
Full Text
View/download PDF

11. TGFB1andTGFBR1polymorphic variants in relationship to bladder cancer risk and prognosis

Author

Castillejo, Adela, primary, Rothman, Nathaniel, additional, Murta-Nascimento, Cristiane, additional, Malats, Núria, additional, García-Closas, Montserrat, additional, Gómez-Martínez, Angeles, additional, Lloreta, Josep, additional, Tardón, Adonina, additional, Serra, Consol, additional, García-Closas, Reina, additional, Chanock, Stephen, additional, Silverman, Debra T., additional, Dosemeci, Mustafa, additional, Kogevinas, Manolis, additional, Carrato, Alfredo, additional, Soto, José Luis, additional, and Real, Francisco X., additional

Published
2009
Full Text
View/download PDF

12. Polymorphisms in one-carbon metabolism and trans-sulfuration pathway genes and susceptibility to bladder cancer

Author

Moore, Lee E., primary, Malats, Núria, additional, Rothman, Nathaniel, additional, Real, Francisco X., additional, Kogevinas, Manolis, additional, Karami, Sara, additional, García-Closas, Reina, additional, Silverman, Debra, additional, Chanock, Stephen, additional, Welch, Robert, additional, Tardón, Adonina, additional, Serra, Consol, additional, Carrato, Alfredo, additional, Dosemeci, Mustafa, additional, and García-Closas, Montserrat, additional

Published
2007
Full Text
View/download PDF

24. <TOGGLE>In vitro</TOGGLE> analysis of the role of DCC in mucus-secreting intestinal differentiation<FNR HREF="fn1"></FNR><FN ID="fn1">M. Fabre and M. Martin made equivalent contributions to this work. </FN>

Author

Fabre, Myriam, Martin, Mercè, Ulloa, Fausto, and Real, Francisco X.

Abstract

The deleted in colorectal cancer (DCC) gene was initially described as a colon cancer-associated tumor suppressor gene and subsequently proposed to be involved in goblet cell differentiation, but its precise role in normal intestine physiology and in cancer remains to be established. We have analyzed DCC mRNA expression in a panel of human colorectal cancer cell lines with a variety of differentiation phenotypes by reverse transcription-polymerase chain reaction (RT-PCR) and have shown that (1) most cell lines showed lower levels of DCC mRNA than normal colonic tissue; (2) only 1 cell line lacked detectable levels of DCC mRNA expression; (3) a discrepancy was found between the detectability of RT-PCR products corresponding to the extracellular and intracellular domains of DCC; and (4) there was no association between the presence of DCC transcripts and the differentiation phenotype. Specifically, DCC was not exclusively associated with the mucus-secreting phenotype, as determined by Alcian blue staining and Northern blotting with mucin gene probes. This was further supported by immunohistochemical results on DCC product and mucins in normal colon: DCC was detected in both goblet and absorptive cells. The introduction of full-length DCC cDNA in undifferentiated HT-29 cells did not have any effect on their differentiation phenotype, as shown by morphological studies and analysis of markers for this process in colon, such as mucins, dipeptidylpeptidase IV, villin and sucrase-isomaltase. There were no effects on cell proliferation in vitro. Our results indicate that DCC is not selectively involved in the mucosecretory differentiation pathway and that it is neither sufficient nor essential for normal intestinal differentiation. Int. J. Cancer 81:799–807, 1999. © 1999 Wiley-Liss, Inc.

Published
1999
Full Text
View/download PDF

25. MUC6 expression in breast tissues and cultured cells: Abnormal expression in tumors and regulation by steroid hormones

Author

Bolòs, Carme de, Gumà, Mónica, Barranco, Carlos, Garrido, Marta, Kim, Young S., and Real, Francisco X.

Abstract

Neoplastic transformation of epithelial cells is commonly associated with alterations in the expression of mucin genes. The mechanisms involved in this process are largely unknown. MUC6, isolated from a stomach cDNA library, is mainly expressed in stomach antral glands, as detected by using in situ hybridization and immunohistochemistry. We examined MUC6 expression in normal and pathological breast tissues using immunohistochemistry with MUC6-specific antibodies and in cultured breast cancer cells using immunocytochemistry and Northern blotting. MUC6 was generally not detected in normal breast (1/11) but was detected in fibrocystic disease without atypia (7/17, 41%), in atypical fibrocystic disease (11/11, 100%) and in carcinoma (57/60, 95%). To study the mechanisms involved in mucin gene up-regulation in breast cancer, we examined baseline, growth-related and steroid-induced levels of MUC1, MUC3 and MUC6 in 4 breast cancer cell lines, 2 of which express estrogen receptors. MUC6 levels were up-regulated at post-confluence in 2/4 cell lines, whereas no changes were detected for the other mucin genes examined. MUC6 and MUC3 were constitutively expressed, and steroid-induced, in BT-474 and MCF-7 cells, respectively. As a control, pS2 was induced in both cell lines. Our results indicate that (1) MUC6 is overexpressed in breast cancer and in benign breast disease, (2) in vitro, MUC6 and MUC3 are up-regulated by steroids and (3) abnormal expression of MUC6 in breast cancers may, in part, be explained by hormonal changes associated with tumor development. Int. J. Cancer 77:193–199, 1998.© 1998 Wiley-Liss, Inc.

Published
1998
Full Text
View/download PDF

26. Pancreatic cancer and autoimmune diseases: An association sustained by computational and epidemiological case-control approaches.

Author

Gomez-Rubio P, Piñero J, Molina-Montes E, Gutiérrez-Sacristán A, Marquez M, Rava M, Michalski CW, Farré A, Molero X, Löhr M, Perea J, Greenhalf W, O'Rorke M, Tardón A, Gress T, Barberá VM, Crnogorac-Jurcevic T, Muñoz-Bellvís L, Domínguez-Muñoz E, Balsells J, Costello E, Yu J, Iglesias M, Ilzarbe L, Kleeff J, Kong B, Mora J, Murray L, O'Driscoll D, Poves I, Lawlor RT, Ye W, Hidalgo M, Scarpa A, Sharp L, Carrato A, Real FX, Furlong LI, and Malats N

Subjects
Case-Control Studies, Computational Biology methods, Europe epidemiology, Female, Gene Ontology, Genetic Predisposition to Disease, Humans, Logistic Models, Male, Odds Ratio, Risk Factors, Autoimmune Diseases epidemiology, Autoimmune Diseases genetics, Pancreatic Neoplasms epidemiology, Pancreatic Neoplasms genetics
Abstract

Deciphering the underlying genetic basis behind pancreatic cancer (PC) and its associated multimorbidities will enhance our knowledge toward PC control. The study investigated the common genetic background of PC and different morbidities through a computational approach and further evaluated the less explored association between PC and autoimmune diseases (AIDs) through an epidemiological analysis. Gene-disease associations (GDAs) of 26 morbidities of interest and PC were obtained using the DisGeNET public discovery platform. The association between AIDs and PC pointed by the computational analysis was confirmed through multivariable logistic regression models in the PanGen European case-control study population of 1,705 PC cases and 1,084 controls. Fifteen morbidities shared at least one gene with PC in the DisGeNET database. Based on common genes, several AIDs were genetically associated with PC pointing to a potential link between them. An epidemiologic analysis confirmed that having any of the nine AIDs studied was significantly associated with a reduced risk of PC (Odds Ratio (OR) = 0.74, 95% confidence interval (CI) 0.58-0.93) which decreased in subjects having ≥2 AIDs (OR = 0.39, 95%CI 0.21-0.73). In independent analyses, polymyalgia rheumatica, and rheumatoid arthritis were significantly associated with low PC risk (OR = 0.40, 95%CI 0.19-0.89, and OR = 0.73, 95%CI 0.53-1.00, respectively). Several inflammatory-related morbidities shared a common genetic component with PC based on public databases. These molecular links could shed light into the molecular mechanisms underlying PC development and simultaneously generate novel hypotheses. In our study, we report sound findings pointing to an association between AIDs and a reduced risk of PC., (© 2018 UICC.)

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results