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12 results on '"Esther Oliva"'

1. P1692: UNMET NEEDS IN PATIENTS WITH 'LOW RISK' POLYCYTHEMIA VERA (PV): SYMPTOM BURDEN AND QUALITY OF LIFE

Author

Tatiana Nikitina, Ekena Andreevskaya, Elena Babich, Natalia Bulieva, Olga Vinogradova, Elena Volodicheva, Sergey Voloshin, Natalia Glonina, Sergey Dubov, Natalya Esefieva, Elena Zinina, Maria Ivanova, Tatyana Klitochenko, Anna Kopylova, Alexander Kulagin, Galina Kuchma, Olga LI, Elza Lomaia, Anna Lyamkina, Anait Melikyan, Vladimir Melnichenko, Svetlana Menshakova, Natalia Minaeva, Tatiana Mitina, Elena Morozova, Oksana Ochirova, Alexey Polyakov, Tatiana Pospelova, Andrey Proydakov, Oleg Rukavitsyn, Guzel’ Safuanova, Irina Soubortseva, Mikhail Fominykh, Maria Frolova, Tatiana Shelekhova, Dmitriy Sherstnev, Tatiana Shneider, Vasiliy Shuvaev, Natalia Porfirieva, Esther Oliva, Sam Salek, and Tatyana Ionova

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Published
2023
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3. PB2672: EXPLORING UNMET NEEDS OF PATIENTS WITH MYELODYSPLASTIC NEOPLASMS AND CAREGIVERS IN A NATIONAL ITALIAN SURVEY

Author

Elena Crisà, Annamaria Nosari, Daniela Cilloni, Sam Salek, Tatyana Ionova, Matteo Giovanni Della Porta, Maria Teresa Voso, Luca Maurillo, Carlo Finelli, Valeria Santini, Enrico Balleari, Federica Pilo, Giuseppe Palumbo, Alfredo Molteni, Marta Riva, and Esther Oliva

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Published
2023
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4. PB2670: EQOL-MDS TRIAL: PATIENT-REPORTED OUTCOMES IN PATIENTS WITH LOWER RISK MYELODYSPLASTIC SYNDROMES WITH SEVERE THROMBOCYTOPENIA.

Author

Esther Oliva, Giuseppe Iannì, Marta Riva, Pasquale Niscola, Valeria Santini, Massimo Breccia, Valentina Gaidano, Antonella Poloni, Andrea Patriarca, Elena Crisà, Isabella Capodanno, Prassede Salutari, Gianluigi Reda, Grazia Sanpaolo, Dario Ferrero, Attilio Guarini, Giovanni Tripepi, Andrea Castelli, Bruno Fattizzo, Germana Beltrami, Monica Bocchia, Alfredo Molteni, Pierre Fenaux, Ulrich Germing, Alessandra Ricco, Giuseppe A. Palumbo, Stefana Impera, Nicola DI Renzo, Francesco Buccisano, Aspasia Stamatoullas, Anna Marina Liberati, Anna Candoni, Ilaria Maria Delfino, Patrizia Cufari, Lorenzo Rizzo, and Roberto Latagliata

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Published
2023
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5. Adult‐type granulosa cell tumor of the ovary: a FOXL2‐centric disease

Author

Jessica A Pilsworth, Dawn R Cochrane, Samantha J Neilson, Bahar H Moussavi, Daniel Lai, Aslı D Munzur, Janine Senz, Yi Kan Wang, Sina Zareian, Ali Bashashati, Adele Wong, Jacqueline Keul, Annette Staebler, Hannah S vanMeurs, Hugo M Horlings, Stefan Kommoss, Friedrich Kommoss, Esther Oliva, Anniina EM Färkkilä, Blake Gilks, and David G Huntsman

Subjects
adult‐type granulosa cell tumor of the ovary, FOXL2, TERT promoter, KMT2D, targeted sequencing, mutation profiling, Pathology, RB1-214
Abstract

Abstract Adult‐type granulosa cell tumors (aGCTs) account for 90% of malignant ovarian sex cord‐stromal tumors and 2–5% of all ovarian cancers. These tumors are usually diagnosed at an early stage and are treated with surgery. However, one‐third of patients relapse between 4 and 8 years after initial diagnosis, and there are currently no effective treatments other than surgery for these relapsed patients. As the majority of aGCTs (>95%) harbor a somatic mutation in FOXL2 (c.C402G; p.C134W), the aim of this study was to identify genetic mutations besides FOXL2 C402G in aGCTs that could explain the clinical diversity of this disease. Whole‐genome sequencing of 10 aGCTs and their matched normal blood was performed to identify somatic mutations. From this analysis, a custom amplicon‐based panel was designed to sequence 39 genes of interest in a validation cohort of 83 aGCTs collected internationally. KMT2D inactivating mutations were present in 10 of 93 aGCTs (10.8%), and the frequency of these mutations was similar between primary and recurrent aGCTs. Inactivating mutations, including a splice site mutation in candidate tumor suppressor WNK2 and nonsense mutations in PIK3R1 and NLRC5, were identified at a low frequency in our cohort. Missense mutations were identified in cell cycle‐related genes TP53, CDKN2D, and CDK1. From these data, we conclude that aGCTs are comparatively a homogeneous group of tumors that arise from a limited set of genetic events and are characterized by the FOXL2 C402G mutation. Secondary mutations occur in a subset of patients but do not explain the diverse clinical behavior of this disease. As the FOXL2 C402G mutation remains the main driver of this disease, progress in the development of therapeutics for aGCT would likely come from understanding the functional consequences of the FOXL2 C402G mutation.

Published
2021
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6. Identification of recurrent FHL2-GLI2 oncogenic fusion in sclerosing stromal tumors of the ovary

Author

Sarah H. Kim, Arnaud Da Cruz Paula, Thais Basili, Higinio Dopeso, Rui Bi, Fresia Pareja, Edaise M. da Silva, Rodrigo Gularte-Mérida, Zhen Sun, Sho Fujisawa, Caitlin G. Smith, Lorenzo Ferrando, Ana Paula Martins Sebastião, Yonina Bykov, Anqi Li, Catarina Silveira, Charles W. Ashley, Anthe Stylianou, Pier Selenica, Wesley R. Samore, Achim A. Jungbluth, Dmitriy Zamarin, Nadeem R. Abu-Rustum, Kristian Helin, Robert A. Soslow, Jorge S. Reis-Filho, Esther Oliva, and Britta Weigelt

Subjects
Science
Abstract

Little is known about the genetics of sclerosing stromal tumor of the ovary, a rare type of sex cord-stromal tumor. Here, the authors use sequencing strategies to show that in a cohort of 26 tumor samples 65% carry a FHL2-GLI2 fusion gene and demonstrate in vitro that the fusion gene has oncogenic properties.

Published
2020
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7. Allele Loss and Reduced Expression of CYCLOPS Genes is a Characteristic Feature of Chromophobe Renal Cell Carcinoma

Author

Riuko Ohashi, Peter Schraml, Aashil Batavia, Silvia Angori, Patrik Simmler, Niels Rupp, Yoichi Ajioka, Esther Oliva, and Holger Moch

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Copy-number alterations Yielding Cancer Liabilities Owing to Partial losS (CYCLOPS) genes have been recently identified as the most enriched class of copy-number associated gene dependencies in human cancer. These genes are cell essential and render tumor cells highly sensitive to the expression of the remaining copy. Chromophobe renal cell carcinoma (chRCC) is characterized by frequent chromosomal deletions, but the relevance of CYCLOPS genes in this tumor subtype is unclear. We found 39 (31%) of 124 recently published candidate CYCLOPS genes (B. Paolella et al., eLife 2017;6:e23268) located on 7 autosomes that are frequently lost in chRCC. GISTIC and RNA-seq data obtained from the TCGA-KICH database showed that 62% of these CYCLOPS genes had significantly lower expression levels in samples with deletion of the respective gene. As copy number (CN) loss of the CYCLOPS gene SF3B1 (Splicing factor 3B subunit 1) has been recently reported in 71% chRCC, we explored the relevance of SF3B1 CN alteration and SF3B1 expression in a set of chRCC and additional oncocytic renal neoplasms. The frequency of SF3B1 CN loss (65%) was similar to that obtained from the TCGA-KICH database and correlated significantly with both lower SF3B1 mRNA (P

Published
2019
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8. SARS-CoV-2 in Myelodysplastic Syndromes: A Snapshot From Early Italian Experience

Author

Sandra Mossuto, Enrico Attardi, Francesco Alesiani, Emanuele Angelucci, Enrico Balleari, Massimo Bernardi, Gianni Binotto, Costanza Bosi, Anna Calvisi, Isabella Capodanno, Antonella Carbone, Andrea Castelli, Marco Cerrano, Rosanna Ciancia, Daniela Cilloni, Marino Clavio, Cristina Clissa, Elena Crisà, Monica Crugnola, Matteo G. Della Porta, Nicola Di Renzo, Ambra Di Veroli, Roberto Fattizzo, Carmen Fava, Susanna Fenu, Ida L. Ferrara, Luana Fianchi, Carla Filì, Carlo Finelli, Valentina Giai, Francesco Frattini, Valentina Gaidano, Gianluca Guaragna, Svitlana Gumenyuk, Roberto Latagliata, Stefano Mancini, Emanuela Messa, Alfredo Molteni, Pellegrino Musto, Pasquale Niscola, Esther Oliva, Giuseppe A. Palumbo, Annamaria Pelizzari, Federica Pilo, Antonella Poloni, Marta Riva, Flavia Rivellini, Chiara Sarlo, Mariarita Sciumé, Roberto Secchi, Carmine Selleri, Agostino Tafuri, and Valeria Santini

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Published
2020
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9. Proceedings of Patient Reported Outcome Measure’s (PROMs) Conference Oxford 2017: Advances in Patient Reported Outcomes Research

Author

Galina Velikova, Jose M. Valderas, Caroline Potter, Laurie Batchelder, Christine A’Court, Matthew Baker, Jennifer Bostock, Angela Coulter, Ray Fitzpatrick, Julien Forder, Diane Fox, Louise Geneen, Elizabeth Gibbons, Crispin Jenkinson, Karen Jones, Laura Kelly, Michele Peters, Brendan Mulhern, Alexander Labeit, Donna Rowen, Keith Meadows, Jackie Elliott, John Brazier, Emma Knowles, Anju Keetharuth, Janice Connell, Jill Carlton, Lizzie Taylor Buck, Thomas Ricketts, Michael Barkham, Pushpendra Goswami, Sam Salek, Tatyana Ionova, Esther Oliva, Adele K. Fielding, Marina Karakantza, Saad Al-Ismail, Graham P. Collins, Stewart McConnell, Catherine Langton, Daniel M. Jennings, Roger Else, Jonathan Kell, Helen Ward, Sophie Day, Elizabeth Lumley, Patrick Phillips, Rosie Duncan, Helen Buckley-Woods, Ahmed Aber, Gerogina Jones, Jonathan Michaels, Ian Porter, Jaheeda Gangannagaripalli, Antoinette Davey, Ignacio Ricci-Cabello, Kirstie Haywood, Stine Thestrup Hansen, Jose Valderas, Deb Roberts, Anil Gumber, Bélène Podmore, Andrew Hutchings, Jan van der Meulen, Ajay Aggarwal, Sujith Konan, Andrew Price, William Jackson, Nick Bottomley, Michael Philiips, Toby Knightley-Day, David Beard, Joanne Greenhalgh, Kate Gooding, Chema Valderas, Judy Wright, Sonia Dalkin, David Meads, Nick Black, Carol Fawkes, Robert Froud, Dawn Carnes, Jonathan Cook, Helen Dakin, James Smith, Sujin Kang, The ACHE Study Team, Catrin Griffiths, Ella Guest, Diana Harcourt, Mairead Murphy, Sandra Hollinghurst, Chris Salisbury, Anqi Gao, Agnieszka Lemanska, Tao Chen, David P. Dearnaley, Rajesh Jena, Matthew Sydes, Sara Faithfull, A. E. Ades, Daphne Kounali, Guobing Lu, Ines Rombach, Alastair Gray, Oliver Rivero-Arias, Patricia Holch, Marie Holmes, Zoe Rodgers, Sarah Dickinson, Beverly Clayton, Susan Davidson, Jacqui Routledge, Julia Glennon, Ann M. Henry, Kevin Franks, Roma Maguire, Lisa McCann, Teresa Young, Jo Armes, Jenny Harris, Christine Miaskowski, Grigorios Kotronoulas, Morven Miller, Emma Ream, Elizabeth Patiraki, Alexander Geiger, Geir V. Berg, Adrian Flowerday, Peter Donnan, Paul McCrone, Kathi Apostolidis, Patricia Fox, Eileen Furlong, Nora Kearney, Chris Gibbons, Felix Fischer, Joel Coste, Jose Valderas Martinez, Matthias Rose, Alain Leplege, Sarah Shingler, Natalie Aldhouse, Tamara Al-Zubeidi, Andrew Trigg, Helen Kitchen, Colin Green, Joanna Coast, Sarah Smith, Jolijn Hendriks, Koonal Shah, Juan-Manuel Ramos-Goni, Simone Kreimeier, Mike Herdman, Nancy Devlin, Aureliano Paolo Finch, John E. Brazier, Clara Mukuria, Bernarda Zamora, David Parkin, Yan Feng, Andrew Bateman, Thomas Patton, and Nils Gutacker

Subjects
Computer applications to medicine. Medical informatics, R858-859.7
Published
2017
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10. Single-cell sequencing of neonatal uterus reveals an Misr2+ endometrial progenitor indispensable for fertility

Author

Hatice Duygu Saatcioglu, Motohiro Kano, Heiko Horn, Lihua Zhang, Wesley Samore, Nicholas Nagykery, Marie-Charlotte Meinsohn, Minsuk Hyun, Rana Suliman, Joy Poulo, Jennifer Hsu, Caitlin Sacha, Dan Wang, Guangping Gao, Kasper Lage, Esther Oliva, Mary E Morris Sabatini, Patricia K Donahoe, and David Pépin

Subjects
uterus development, AMH, MIS, infertility, Mullerian duct, mesenchyme, Medicine, Science, Biology (General), QH301-705.5
Abstract

The Mullerian ducts are the anlagen of the female reproductive tract, which regress in the male fetus in response to MIS. This process is driven by subluminal mesenchymal cells expressing Misr2, which trigger the regression of the adjacent Mullerian ductal epithelium. In females, these Misr2+ cells are retained, yet their contribution to the development of the uterus remains unknown. Here, we report that subluminal Misr2+ cells persist postnatally in the uterus of rodents, but recede by week 37 of gestation in humans. Using single-cell RNA sequencing, we demonstrate that ectopic postnatal MIS administration inhibits these cells and prevents the formation of endometrial stroma in rodents, suggesting a progenitor function. Exposure to MIS during the first six days of life, by inhibiting specification of the stroma, dysregulates paracrine signals necessary for uterine development, eventually resulting in apoptosis of the Misr2+ cells, uterine hypoplasia, and complete infertility in the adult female.

Published
2019
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