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Relevant bibliographies by topics / Gene oncosuppresseur

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Academic literature on the topic 'Gene oncosuppresseur'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Gene oncosuppresseur"

1

Vizioli, M. G., M. Sensi, C. Miranda, L. Cleris, F. Formelli, M. C. Anania, M. A. Pierotti, and A. Greco. "IGFBP7: an oncosuppressor gene in thyroid carcinogenesis." Oncogene 29, no. 26 (May 3, 2010): 3835–44. http://dx.doi.org/10.1038/onc.2010.136.

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Zucchini, C., M. Concu, F. Martini, C. Morelli, N. Salfi, P. Carinci, M. Tognon, and E. Caramelli. "FHIT Oncosuppressor Gene Expression Profile in Human Anal Cancers." International Journal of Biological Markers 22, no. 1 (January 2007): 39–42. http://dx.doi.org/10.1177/172460080702200106.

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The FHIT gene, a member of the histidine triad gene family, is a tumor suppressor gene exhibiting deletions in the majority of human cancers. Aberrant transcripts of this gene have been found in about 50% of esophageal, stomach and colon carcinomas. Little is known about the molecular mechanisms involved in malignant transformation of the lining cells of the anus. In this study FHIT gene expression was investigated in this particular kind of human cancer. FHIT expression was comparatively analyzed at the mRNA level, by RT-PCR, in squamous anal cancers, normal anal tissue and peripheral blood samples. cDNA analyses showed variability in FHIT transcripts, without apparent effects on the predicted amino acid sequence. These different FHIT mRNAs could represent transcripts from an alternative splicing event. Our data indicate that the FHIT mRNA detected in anal cancers and in normal samples is heterogeneous. Immunohistochemical data suggest that the Fhit protein is expressed only in a fraction of the tumor cells, while it is strongly expressed in the epithelial cells of glands of the normal anal mucosa. The absence or poor expression of the Fhit protein in anal cancers suggests a role for this tumor suppressor gene product, as a risk factor, in the onset of this human cancer, as reported before for other human gastrointestinal tumors.

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Zucchini, C., M. Concu, F. Martini, C. Morelli, N. Salfi, P. Carinci, M. Tognon, and E. Caramelli. "FHIT oncosuppressor gene expression profile in human anal cancers." International Journal of Biological Markers 22, no. 1 (2007): 39–42. http://dx.doi.org/10.5301/jbm.2008.3425.

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Lecomte, Fabienne, Bénédicte Champagne, Jean-François Dasnoy, Josiane Szpirer, and Claude Szpirer. "The mammalianRPS6 gene, homolog of theDrosophila air8 tumor suppressor gene: Is it an oncosuppressor gene?" Somatic Cell and Molecular Genetics 21, no. 6 (November 1995): 443–50. http://dx.doi.org/10.1007/bf02310210.

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Thivakaran, Aniththa, Lacramioara Botezatu, Judith Maria Hoenes, Yahya Saleh Al-Matary, Nadine Olberding, Judith Schütte, Renata Köster, Bertram Opalka, Ulrich Dührsen, and Cyrus Khandanpour. "GFI1b As a Novel Oncosuppressor in AML." Blood 128, no. 22 (December 2, 2016): 2717. http://dx.doi.org/10.1182/blood.v128.22.2717.2717.

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Abstract The proper differentiation of hematopoietic stem cells (HSCs) is regulated by a concert of different so called transcription factors (TFs). A disturbed function of these TFs can be the basis of malignant diseases such as acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS). Growth Factor Independence 1b (Gfi1b) is a repressing transcription factor, with a key role in maintaining the quiescence of HSCs and the proper emergence and maturation of erythrocytes and platelets. Here we show that low expression of GFI1B in blast cells is associated with an inferior prognosis of AML and MDS patients. Using three different mice models of human AML (Nup98-HoxD13, MLL-AF9 and expression of a mutated K-Ras), we could show that reduced expression of Gfi1b accelerates AML development in mice and the latency is even more shortened when Gfi1b is conditionally deleted. Using a limiting dilution assay of transplantation of different number of Gfi1b-wildtype and Gfi1b-deficient cells, we could show that loss of Gfi1b significantly enhanced stemness of leukemic cells. Since Gfii1b is involved in epigenetic regulation of gene expression, we analyzed effect of loss of Gfi1b on an epigenetic level by analyzing the whole genome using Chip-Seq. We found that loss of Gfi1b leads to genome wide increased level of H3K9 acetylation of genes and hence expression of these genes involved in leukemia development. On a molecular level, we found that loss of Gfi1b not only increases the levels of reactive oxygen species (ROS), but also induces gene expression changes of key AML-pathways such as the p38/ AKT pathways. These results demonstrate that Gfi1b functions as an oncosuppressor in MDS/AML development. Disclosures Dührsen: Roche: Honoraria, Research Funding; Amgen: Honoraria, Research Funding; Alexion Pharmaceuticals: Honoraria, Research Funding. Khandanpour:Max-Eder: Research Funding; Hospital of Essen university: Research Funding.

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de Biase, Dario, Giorgia Acquaviva, Michela Visani, Viviana Sanza, Chiara M. Argento, Antonio De Leo, Thais Maloberti, Annalisa Pession, and Giovanni Tallini. "Molecular Diagnostic of Solid Tumor Using a Next Generation Sequencing Custom-Designed Multi-Gene Panel." Diagnostics 10, no. 4 (April 23, 2020): 250. http://dx.doi.org/10.3390/diagnostics10040250.

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Next generation sequencing (NGS) allows parallel sequencing of multiple genes at a very high depth of coverage. The need to analyze a variety of targets for diagnostic/prognostic/predictive purposes requires multi-gene characterization. Multi-gene panels are becoming standard approaches for the molecular analysis of solid lesions. We report a custom-designed 128 multi-gene panel engineered to cover the relevant targets in 22 oncogene/oncosuppressor genes for the analysis of the solid tumors most frequently subjected to routine genotyping. A total of 1695 solid tumors were analyzed for panel validation. The analytical sensitivity is 5%. Analytical validation: (i) Accuracy: sequencing results obtained using the multi-gene panel are concordant using two different NGS platforms and single-gene approach sequencing (100% of 83 cases); (ii) Precision: consistent results are obtained in the samples analyzed twice with the same platform (100% of 20 cases). Clinical validation: the frequency of mutations identified in different tumor types is consistent with the published literature. This custom-designed multi-gene panel allows to analyze with high sensitivity and throughput 22 oncogenes/oncosuppressor genes involved in diagnostic/prognostic/predictive characterization of central nervous system tumors, non-small-cell lung carcinomas, colorectal carcinomas, thyroid nodules, pancreatic lesions, melanoma, oral squamous carcinomas and gastrointestinal stromal tumors.

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Manara, Maria Cristina, Ghislaine Bernard, Pier-Luigi Lollini, Patrizia Nanni, Monia Zuntini, Lorena Landuzzi, Stefania Benini, et al. "CD99 Acts as an Oncosuppressor in Osteosarcoma." Molecular Biology of the Cell 17, no. 4 (April 2006): 1910–21. http://dx.doi.org/10.1091/mbc.e05-10-0971.

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CD99 was recently reported to be under control of the osteoblast-specific transcription factor Cbfa1 (RUNX2) in osteoblasts, suggesting a role in the phato-physiology of these cells. No extensive information is available on the role(s) of this molecule in malignant phenotype, and osteosarcoma, in particular, has never been studied. We report that in 11 different cell lines and 17 clinical samples CD99 expression is either undetectable or very low. Being expressed in the normal counterpart, we tested the hypothesis that CD99 down-regulation may have a role in osteosarcoma development and progression. CD99-forced expression in two osteosarcoma cell lines significantly reduced resistance to anoikis, inhibited growth in anchorage independence as well as cell migration, and led to abrogation of tumorigenic and metastatic ability. Therefore, the molecule acts as a potent suppressor of malignancy in osteosarcoma. CD99 gene transfection induces caveolin-1 up-regulation and the two molecules were found to colocalize on the cell surface. Treatment with antisense oligonucleotides to caveolin-1 abrogates the effects of CD99 on migration. The findings point to an antioncogenic role for CD99 in osteosarcoma, likely through the regulation of caveolin-1 and inhibition of c-Src kinase activity.

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Manera, S., S. Bonfiglio, A. Malusà, C. Denis, M. Boussaha, V. Russo, F. Roperto, et al. "Comparative Mapping and Genomic Annotation of the Bovine Oncosuppressor Gene WWOX." Cytogenetic and Genome Research 126, no. 1-2 (2009): 186–93. http://dx.doi.org/10.1159/000245919.

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Hui-Ying, Xue, Zhang Da-Hong, Ji Li-Juan, and Lu Xiao-Jie. "Anticancer Opportunity Created by Loss of Tumor Suppressor Genes." Technology in Cancer Research & Treatment 15, no. 6 (July 9, 2016): 729–31. http://dx.doi.org/10.1177/1533034615604798.

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Deletion of oncosuppressors occurs frequently in the cancer genome. A great deal of effort has been made to therapeutically restore the lost function of oncosuppressors, with little clinically translatable success, however. Reassuringly, besides the disappointing restoration endeavors, oncosuppressor loss can be therapeutically exploited in several other ways, such as the “synthetic lethality” strategies and the “therapeutic vulnerability” created by codeletion of neighboring genes. The study by Liu et al showed that codeletion of p53 and a neighboring essential gene POLR2A rendered colon cancer cells highly sensitive to further inhibition of POLR2A both in vitro and in vivo. In recent years, several studies have reported similar phenomenon in a wide range of cancer types. In this focus article, we will introduce several kinds of anticancer opportunities created by the loss of oncosuppressors and discuss their mechanisms. Given the frequency of oncosuppressor loss in cancer, its therapeutic exploitation rather merits further investigation and may open a new window for oncotherapy.

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Corbetta, S., V. Vaira, V. Guarnieri, A. Scillitani, C. Eller-Vainicher, S. Ferrero, L. Vicentini, et al. "Differential expression of microRNAs in human parathyroid carcinomas compared with normal parathyroid tissue." Endocrine-Related Cancer 17, no. 1 (March 2010): 135–46. http://dx.doi.org/10.1677/erc-09-0134.

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Parathyroid carcinoma (PaC) is a rare cause of primary hyperparathyroidism. Though the loss of the oncosuppressor CDC73/HRPT2 gene product, parafibromin, has been involved in the hyperparathyroidism–jaw tumor syndrome and in a consistent set of sporadic PaCs, parathyroid carcinogenesis remains obscure. MicroRNAs are a new class of small, non-coding RNAs implicated in development of cancer, since their deregulation can induce aberrant expression of several target genes. The aim of the present study was to identify differentially expressed microRNAs in parathyroid cancers compared with normal tissues. We performed a TaqMan low-density array profiling of four parathyroid cancers harboring CDC73 inactivating mutations and negative for parafibromin immunostaining. Their microRNA profiling was compared with that of two normal parathyroid biopsies. Out of 362 human microRNAs assayed, 279 (77%) were successfully amplified. Fourteen and three microRNAs were significantly down- and over-expressed in parathyroid cancers respectively. Of these, miR-296 and miR-139 were down-regulated, and miR-503 and miR-222 were over-expressed with a null false discovery rate. Carcinomas could be discriminated from parathyroid adenomas by a computed score based on the expression levels of miR-296, miR-222, and miR-503 as miR-139 was similarly down-regulated in both cancers and adenomas. Finally, miR-296 and miR-222 levels negatively correlated with mRNA levels of the hepatocyte growth factor receptor-regulated tyrosine kinase substrate and p27/kip1 levels respectively. These results suggest the existence of an altered microRNA expression pattern in PaCs together with a potential role of miR-296 as novel oncosuppressor gene in these neoplasia.

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Dissertations / Theses on the topic "Gene oncosuppresseur"

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Ponchel, Frédérique. "Etude comparative des activites biologiques des formes sauvage et mutees de la proteine p53 sur le modele du carcinome hepatocellulaire." Paris 11, 1994. http://www.theses.fr/1994PA11T041.

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Saffroy, Raphael. "Instabilite genomique et alterations de p53 dans le carcinome hepatocellulaire." Paris 5, 2000. http://www.theses.fr/2000PA05N117.

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Dereure, Olivier. "Étude des gènes suppresseurs de tumeurs et gouvernant l'apoptose dans les lymphomes cutanés T épidermotropes." Montpellier 1, 2000. http://www.theses.fr/2000MON1T028.

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Brault, Estelle. "Etude structurale et fonctionnelle de la schwannomine, produit du gene suppresseur de tumeur impliquee dans la neurofibromatose de type 2." Paris 5, 2001. http://www.theses.fr/2001PA05N081.

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Rondeau, Gaëlle. "Clonage positionnel d'un gene suppresseur de tumeur implique dans les leucemies lymphoides chroniques de type b et situe en 13q14. 3 (doctorat : genetique moleculaire)." Nantes, 1999. http://www.theses.fr/1999NANT04VS.

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Quittau-Prévostel, Corinne. "Mutant D294G de la PKC[alpha] tumorigénèse humaine : la PKC[alpha], un nouveau suppresseur de tumeur." Montpellier 1, 1997. http://www.theses.fr/1997MON1T005.

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Thieblemont, Catherine. "Contribution à l'analyse des anomalies génétiques impliquées dans la lymphomagénèse." Lyon 1, 2000. http://www.theses.fr/2000LYO1T051.

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Jonveaux, Philippe. "Les mutations du gène suppresseur de tumeur TP 53 dans les hémopathies malignes." Bordeaux 2, 1991. http://www.theses.fr/1991BOR2M147.

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Le, Morvan Valérie. "Etude du gène candidat suppresseur de tumeur codant pour la protéine de jonction serrée ZO-2." Bordeaux 2, 1999. http://www.theses.fr/1999BOR28649.

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HUANG, ZHEN-GUO, and 黃鎮國. "P53 oncosuppressor gene in nasopharyngeal carcinoma." Thesis, 1992. http://ndltd.ncl.edu.tw/handle/68705393833144168890.

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Book chapters on the topic "Gene oncosuppresseur"

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Hooper, Martin L. "Analysis of Oncosuppressor Gene Function in the Mouse by Gene Targeting." In Gene Technology, 263–81. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61122-3_19.

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Conference papers on the topic "Gene oncosuppresseur"

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Wiesinger, A., R. Blanco, J. León, and MD Delgado. "PO-104 Role of the oncosuppressor CTCF in the erythroid cell differentiation and regulation of erythroid genes." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.145.

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