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218 results on '"Fernández-Piqueras J"'

20. Hypermethylation of the cell cycle inhibitor p15INK4b 3′-untranslated region interferes with its transcriptional regulation in primary lymphomas

Author

Fernández Piqueras J, Marcos Malumbres, Javier Santos, Angel Pellicer, and Pérez de Castro I

Subjects
Cancer Research, Lymphoma, Transcription, Genetic, Molecular Sequence Data, Cell Cycle Proteins, Mice, Inbred Strains, Biology, medicine.disease_cause, Genomic Imprinting, Mice, Epigenetics of physical exercise, Genetics, medicine, Animals, 3' Untranslated Regions, Molecular Biology, Cyclin-Dependent Kinase Inhibitor p16, Cyclin-Dependent Kinase Inhibitor p15, DNA Primers, Regulation of gene expression, Base Sequence, Three prime untranslated region, Tumor Suppressor Proteins, Promoter, Thymus Neoplasms, Methylation, DNA Methylation, Molecular biology, Cyclin-Dependent Kinases, Gene Expression Regulation, Neoplastic, CpG site, DNA methylation, Cancer research, Carrier Proteins, Carcinogenesis
Abstract

The cyclin-dependent kinase inhibitor p15INK4b has been shown to be involved in human and rodent tumors and seems to act as a tumor suppressor gene in hematological malignancies. Alterations of this gene in tumors include mainly homozygous deletions and hypermethylation of the CpG island in the promoter region. In this work, we describe a new area sensitive to methylation in the 3' untranslated region (UTR) of the murine p15INK4b gene. This region shows different levels of methylation depending on the tissues, being relatively highly methylated in brain and gut, and weakly methylated in liver, spleen or thymus. DNA methylation and expression is similar in both maternal and paternal alleles indicating no imprinting effect. Although methylation of the p15INK4b 3'-UTR is low in normal thymus, increased levels (up to 100%) of specific methylation in this region are found in up to 30% of radiation- or carcinogen-induced thymic lymphomas, correlating with decreased gene expression. Hypermethylation of the p15INK4b 3'-UTR frequently occurs in tumors with loss of heterozygosity (LOH) but without methylation of the promoter CpG island or intragenic mutations. Furthermore, in vitro CpG methylation of the 3'-UTR produces reduced levels of a luciferase reporter in cultured cells. Methylation of two CpG sites in a 120 bp region is sufficient to interfere with transcription of the reporter gene. These data suggest that although the levels of p15INK4b in normal tissues can be mainly determined by promoter regulatory elements, strong hypermethylation of the 3'-UTR can interfere with transcription. Thus, hypermethylation of the 3'-UTR may explain the lack of p15INK4b gene expression in a subset of tumors with no promoter methylation and could be a new alternative mechanism for tumor suppressor gene inactivation in tumorigenesis.

Published
1999
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24. Contribution of JAK2 mutations to T-cell lymphoblastic lymphoma development

Author

Roncero, A M, primary, López-Nieva, P, additional, Cobos-Fernández, M A, additional, Villa-Morales, M, additional, González-Sánchez, L, additional, López-Lorenzo, J L, additional, Llamas, P, additional, Ayuso, C, additional, Rodríguez-Pinilla, S M, additional, Arriba, M C, additional, Piris, M A, additional, Fernández-Navarro, P, additional, Fernández, A F, additional, Fraga, M F, additional, Santos, J, additional, and Fernández-Piqueras, J, additional

Published
2015
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25. FAS system deregulation in T-cell lymphoblastic lymphoma

Author

Villa-Morales, M, primary, Cobos, M A, additional, González-Gugel, E, additional, Álvarez-Iglesias, V, additional, Martínez, B, additional, Piris, M A, additional, Carracedo, A, additional, Benítez, J, additional, and Fernández-Piqueras, J, additional

Published
2014
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26. Instability of the D4Mit12 microsatellite marker in C57BL/6J x BALB/cJF1 hybrid mice is independent of the tumor phenotype

Author

Herranz M, Santos J, Pérez de Castro I, Barbara Melendez, and Fernández-Piqueras J

Subjects
Genetic Markers, Mice, Inbred C57BL, Mice, Mice, Inbred BALB C, Neoplasms, Radiation-Induced, Phenotype, Lymphoma, Animals, Hybridization, Genetic, Thymus Neoplasms, DNA, Satellite
Abstract

We examined the stability of different types of DNA microsatellite markers in gamma-radiation-induced thymic lymphomas as well as normal, nontumorous tissues of F1 hybrid mice derived from the parental strains C57BL/6J, RF/J, and BALB/cJ. Surprisingly, the D4Mit12 microsatellite showed genomic instability in a significant fraction of DNAs of the (C57BL/6J x BALB/cJ) F1 hybrids with independence of the tumor phenotype. This instability was not found in the reciprocal F1 DNAs, in DNAs of the parental strains, or in DNAs of (C57BL/6J x RF/J) F1 hybrid mice. These results suggest that the instability of the D4Mit 12 microsatellite is dependent on its repeat length, the genetic background of F1 hybrids, and the maternal origin of the C57BL/6J allele.

Published
1997

38. Tumorigenic activity of p21Waf1/Cip1 in thymic lymphoma.

Author

de la Cueva, E., García-Cao, I., Herranz, M., López, P., García-Palencia, P., Flores, J. M., Serrano, M., Fernández-Piqueras, J., and Martín-Caballero, J.

Subjects
P53 antioncogene, CANCER genetics, ATAXIA telangiectasia, CEREBELLUM diseases, GENETIC disorders, LABORATORY mice
Abstract

The cell cycle inhibitor p21Waf1/Cip1 is among the most important mediators of the tumor suppressor p53. However, there is increasing evidence indicating that p21 could favor tumorigenesis in specific cell types. In particular, the absence of p21 delays the development of thymic lymphomas induced either by ataxia-telangiectasia mutated deficiency or by ionizing irradiation. Here, we extend these observations to the context of p53-deficient mice. The absence of p21 results in a significant extension of the lifespan of p53-null and p53-haploinsufficient mice, and this effect can be attributed exclusively to a decrease in the incidence of spontaneous thymic lymphomas. Specifically, despite the occurrence of a variety of tumor types in the context of p53 deficiency, the only tumors that were significantly impaired by the absence of p21 were thymic lymphomas. Moreover, the absence of p21 also delays the incidence of radiation-induced thymic lymphomas in p53-deficient mice. Interestingly, p21-deficient lymphomas have a higher apoptotic rate than p21-proficient lymphomas, and this could be on the basis of the delayed incidence of thymic lymphomas in the absence of p21. Together, our results indicate that p21 plays an oncogenic role restricted to thymic lymphomas that is mechanistically independent of p53 and associated to a lower tumor apoptotic rate.Oncogene (2006) 25, 4128–4132. doi:10.1038/sj.onc.1209432; published online 6 February 2006 [ABSTRACT FROM AUTHOR]

Published
2006
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43. A weak association between TH and DRD2 genes and bipolar affective disorder in a Spanish sample.

Author

Pérez de Castro, I, Santos, J, Torres, P, Visedo, G, Saiz-Ruiz, J, Llinares, C, and Fernández-Piqueras, J

Abstract

Genetic factors play an important role in the aetiology of bipolar affective disorder (BP). So far, results of linkage studies have been largely disappointing. We have searched for a possible association between polymorphic DNA markers of two candidate genes (tyrosine hydroxylase, TH; dopamine D2 receptor gene, DRD2) and BP in a population from central Spain. Our results are consistent with the existence of a weak association between these two genes and BP, in such a way that TH and DRD2 could be considered as minor genes contributing to susceptibility. [ABSTRACT FROM PUBLISHER]

Published
1995

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