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24 results on '"Perot, Gaëlle"'

3. Genomic and transcriptomic comparison of post-radiation versus sporadic sarcomas

Author

Lesluyes, Tom, Baud, Jessica, Pérot, Gaëlle, Charon-Barra, Céline, You, Axel, Valo, Isabelle, Bazille, Céline, Mishellany, Florence, Leroux, Agnès, Renard-Oldrini, Sophie, Terrier, Philippe, Le Cesne, Axel, Laé, Marick, Piperno-Neumann, Sophie, Bonvalot, Sylvie, Neuville, Agnès, Collin, Françoise, Maingon, Philippe, Coindre, Jean-Michel, and Chibon, Frédéric

Published
2019
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4. Uterine and vaginal sarcomas resembling fibrosarcoma: a clinicopathological and molecular analysis of 13 cases showing common NTRK-rearrangements and the description of a COL1A1-PDGFB fusion novel to uterine neoplasms

Author

Croce, Sabrina, Hostein, Isabelle, Longacre, Teri A., Mills, Anne M., Pérot, Gaëlle, Devouassoux-Shisheboran, Mojgan, Velasco, Valérie, Floquet, Anne, Guyon, Frédéric, Chakiba, Camille, Querleu, Denis, Khalifa, Emmanuel, Mayeur, Laetitia, Rebier, Flora, Leguellec, Sophie, Soubeyran, Isabelle, and McCluggage, W.Glenn

Published
2019
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5. Alternative PDGFD rearrangements in dermatofibrosarcomas protuberans without PDGFB fusions

Author

Dadone-Montaudié, Bérengère, Alberti, Laurent, Duc, Adeline, Delespaul, Lucile, Lesluyes, Tom, Pérot, Gaëlle, Lançon, Agnès, Paindavoine, Sandrine, Di Mauro, Ilaria, Blay, Jean-Yves, de la Fouchardière, Arnaud, Chibon, Frédéric, Karanian, Marie, MacGrogan, Gaëtan, Kubiniek, Valérie, Keslair, Frédérique, Cardot-Leccia, Nathalie, Michot, Audrey, Perrin, Virginie, Zekri, Yanis, Coindre, Jean-Michel, Tirode, Franck, Pedeutour, Florence, Ranchère-Vince, Dominique, Le Loarer, François, and Pissaloux, Daniel

Published
2018
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6. Analysis of the Peritumoral Tissue Unveils Cellular Changes Associated with a High Risk of Recurrence

Author

Michot, Audrey, primary, Lagarde, Pauline, additional, Lesluyes, Tom, additional, Darbo, Elodie, additional, Neuville, Agnès, additional, Baud, Jessica, additional, Perot, Gaëlle, additional, Bonomo, Iris, additional, Maire, Mathilde, additional, Michot, Maxime, additional, Coindre, Jean-Michel, additional, Le Loarer, François, additional, and Chibon, Frédéric, additional

Published
2023
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13. Chimeric EWSR1-FLI1 regulates the Ewing sarcoma susceptibility gene EGR2 via a GGAA microsatellite

Author

Grünewald, Thomas G P, Bernard, Virginie, Gilardi-Hebenstreit, Pascale, Raynal, Virginie, Surdez, Didier, Aynaud, Marie-Ming, Mirabeau, Olivier, Cidre-Aranaz, Florencia, Tirode, Franck, Zaidi, Sakina, Perot, Gaëlle, Jonker, Anneliene H, Lucchesi, Carlo, Le Deley, Marie-Cécile, Oberlin, Odile, Marec-Bérard, Perrine, Véron, Amélie S, Reynaud, Stephanie, Lapouble, Eve, Boeva, Valentina, Frio, Thomas Rio, Alonso, Javier, Bhatia, Smita, Pierron, Gaëlle, Cancel-Tassin, Geraldine, Cussenot, Olivier, Cox, David G, Morton, Lindsay M, Machiela, Mitchell J, Chanock, Stephen J, Charnay, Patrick, and Delattre, Olivier

Published
2015
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18. Developmental and cancer-associated plasticity of DNA replication preferentially targets GC-poor, lowly expressed and late-replicating regions

Author

Wu, Xia, primary, Kabalane, Hadi, additional, Kahli, Malik, additional, Petryk, Nataliya, additional, Laperrousaz, Bastien, additional, Jaszczyszyn, Yan, additional, Drillon, Guenola, additional, Nicolini, Frank-Emmanuel, additional, Perot, Gaëlle, additional, Robert, Aude, additional, Fund, Cédric, additional, Chibon, Frédéric, additional, Xia, Ruohong, additional, Wiels, Joëlle, additional, Argoul, Françoise, additional, Maguer-Satta, Véronique, additional, Arneodo, Alain, additional, Audit, Benjamin, additional, and Hyrien, Olivier, additional

Published
2018
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19. Secretory Breast Carcinoma

Author

Del Castillo, Marie, primary, Chibon, Frédéric, additional, Arnould, Laurent, additional, Croce, Sabrina, additional, Ribeiro, Agnès, additional, Perot, Gaëlle, additional, Hostein, Isabelle, additional, Geha, Sameh, additional, Bozon, Catherine, additional, Garnier, Agnès, additional, Lae, Marick, additional, Vincent-Salomon, Anne, additional, and MacGrogan, Gaëtan, additional

Published
2015
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21. Secretory Breast Carcinoma.

Author

Castillo, Marie Del, Chibon, Frédéric, Arnould, Laurent, Croce, Sabrina, Ribeiro, Agnès, Perot, Gaëlle, Hostein, Isabelle, Geha, Sameh, Bozon, Catherine, Garnier, Agnès, Lae, Marick, Vincent-Salomon, Anne, and MacGrogan, Gaëtan

Published
2015
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22. Chimeric EWSR1-FLI1 regulates the Ewing sarcoma susceptibility gene EGR2 via a GGAA microsatellite.

Author

Raynal, Virginie, Surdez, Didier, Delattre, Olivier, Frio, Thomas Rio, Perot, Gaëlle, Lapouble, Eve, Oberlin, Odile, Reynaud, Stephanie, Grünewald, Thomas G P, Mirabeau, Olivier, Jonker, Anneliene H, Machiela, Mitchell J, Chanock, Stephen J, Alonso, Javier, Le Deley, Marie-Cécile, Véron, Amélie S, Pierron, Gaëlle, Aynaud, Marie-Ming, Gilardi-Hebenstreit, Pascale, and Cidre-Aranaz, Florencia

Subjects
EWING'S sarcoma, GENETICS of disease susceptibility, MICROSATELLITE repeats, MESENCHYMAL stem cells, POLYMERASE chain reaction
Abstract

Deciphering the ways in which somatic mutations and germline susceptibility variants cooperate to promote cancer is challenging. Ewing sarcoma is characterized by fusions between EWSR1 and members of the ETS gene family, usually EWSR1-FLI1, leading to the generation of oncogenic transcription factors that bind DNA at GGAA motifs. A recent genome-wide association study identified susceptibility variants near EGR2. Here we found that EGR2 knockdown inhibited proliferation, clonogenicity and spheroidal growth in vitro and induced regression of Ewing sarcoma xenografts. Targeted germline deep sequencing of the EGR2 locus in affected subjects and controls identified 291 Ewing-associated SNPs. At rs79965208, the A risk allele connected adjacent GGAA repeats by converting an interspaced GGAT motif into a GGAA motif, thereby increasing the number of consecutive GGAA motifs and thus the EWSR1-FLI1-dependent enhancer activity of this sequence, with epigenetic characteristics of an active regulatory element. EWSR1-FLI1 preferentially bound to the A risk allele, which increased global and allele-specific EGR2 expression. Collectively, our findings establish cooperation between a dominant oncogene and a susceptibility variant that regulates a major driver of Ewing sarcomagenesis. [ABSTRACT FROM AUTHOR]

Published
2015
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23. Are Peripheral Purely Undifferentiated Pleomorphic Sarcomas With MDM2Amplification Dedifferentiated Liposarcomas

Author

Le Guellec, Sophie, Chibon, Frédéric, Ouali, Monia, Perot, Gaëlle, Decouvelaere, Anne-Valérie, Robin, Yves-Marie, Larousserie, Frédérique, Terrier, Philippe, Coindre, Jean-Michel, and Neuville, Agnès

Abstract

Dedifferentiated liposarcoma (DDLPS) has been defined as a tumor composed of well-differentiated liposarcoma associated with a nonlipogenic undifferentiated sarcoma and is genetically characterized by a 12q13-15 amplicon with MDM2amplification. Some peripheral (extremities, trunk wall, headneck) undifferentiated pleomorphic sarcomas (UPS) without areas of well-differentiated liposarcoma present an MDM2amplification. We addressed whether they are true DDLPS or not. We compared the clinical data, histologic data, MDM2 status (immunohistochemistry IHC, fluorescence in situ hybridization FISH), genomic profile (array comparative genomic hybridization), and follow-up of 19 patients with peripheral UPS with MDM2amplification and 62 with peripheral conventional DDLPS retrieved from the French sarcoma network (RRePS) and the Conticabase (Connective Tissue Cancer Network database). For a control cohort, we described 153 patients from the Conticabase, with peripheral UPS without expression of MDM2 by IHC. By IHC, tumor cells were positive for MDM2 in 59 conventional DDLPS and in all UPS with MDM2amplification. FISH analysis andor quantitative polymerase chain reaction showed amplification of MDM2in 54 conventional DDLPS and in all UPS with MDM2amplification. The 2-year overall survival rates of UPS with MDM2amplification, conventional DDLPS, and UPS without expression of MDM2 were 93.3, 90.7, and 73.9, respectively. Such similarities in the clinical characteristics, morphology, genomic profile, and follow-up of peripheral UPS with MDM2amplification and peripheral conventional DDLPS strongly suggest that peripheral UPS with MDM2amplification are in fact DDLPS. Faced with histologic diagnosis of UPS, a systematic IHC evaluation of MDM2 allows a selection of cases for FISH analysis permitting the diagnosis of DDLPS.

Published
2014
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24. Secretory Breast Carcinoma: A Histopathologic and Genomic Spectrum Characterized by a Joint Specific ETV6-NTRK3 Gene Fusion.

Author

Del Castillo M, Chibon F, Arnould L, Croce S, Ribeiro A, Perot G, Hostein I, Geha S, Bozon C, Garnier A, Lae M, Vincent-Salomon A, and MacGrogan G

Subjects
Adolescent, Adult, Biomarkers, Tumor analysis, Biopsy, Breast Neoplasms chemistry, Breast Neoplasms classification, Breast Neoplasms therapy, Carcinoma chemistry, Carcinoma classification, Carcinoma therapy, Comparative Genomic Hybridization, Female, France, Gene Dosage, Gene Duplication, Gene Rearrangement, Genetic Predisposition to Disease, Humans, Immunohistochemistry, In Situ Hybridization, Fluorescence, Middle Aged, Mitosis, Necrosis, Neoplasm Grading, Phenotype, Reverse Transcriptase Polymerase Chain Reaction, Treatment Outcome, Biomarkers, Tumor genetics, Breast Neoplasms genetics, Breast Neoplasms pathology, Carcinoma genetics, Carcinoma pathology, Gene Fusion, Oncogene Proteins, Fusion genetics
Abstract

Secretory breast carcinoma (SBC) is a rare breast carcinoma with distinctive morphologic features and a recurrent specific chromosomal translocation t(12;15)(p13;q25), usually of low histologic grade and favorable prognosis. We describe the morphologic and genetic characteristics of 11 cases of SBC from 10 patients. Histologic and immunohistochemical analyses, fluorescence in situ hybridization using break-apart probes specific to ETV6 on 12p13, reverse transcription polymerase chain reaction with in-house probes specific to the ETV6-NTRK3 gene fusion, and DNA copy number variation by array comparative genomic hybridization analyses were performed on all cases. Seven cases were of low histologic grade, 3 were intermediate, and 1 had high-grade nuclear atypia, necrosis, and numerous mitoses. This patient had a fatal outcome. Five cases displayed low hormonal receptor expression, whereas the rest had basal-type immunoprofiles. All interpretable cases harbored an ETV6-NTRK3 gene fusion by reverse transcription polymerase chain reaction and/or an ETV6 rearrangement by fluorescence in situ hybridization, with duplication of the oncogenic derivative in 2 cases. Array comparative genomic hybridization analysis showed simplex genomic profiles. The 2 cases with ETV6-NTRK3 duplication included a gain of 12p starting from the ETV6 locus to the telomere, associated with a gain of the 15q from the centromere to NTRK3 in 1 case, and in the other a normal profile up to NTRK3 on 15q, and then a loss up to the telomere, suggesting loss of corresponding normal chromosome 15. These findings provide a novel insight into the morphologic and genetic spectrum of SBC, ranging from low-grade to high-grade histology, with occasional low hormonal receptor expression, simplex genomic profiles, and possible unfavorable course.

Published
2015
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