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Your search keyword '"Ventura Ferreira, Monica S."' showing total 15 results
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15 results on '"Ventura Ferreira, Monica S."'

2. Telomere shortening correlates with leukemic stem cell burden at diagnosis of chronic myeloid leukemia

Author

Bouillon, Anne-Sophie, Ventura Ferreira, Monica S., Awad, Shady Adnan, Richter, Johan, Hochhaus, Andreas, Kunzmann, Volker, Dengler, Jolanta, Janssen, Jeroen, Ossenkoppele, Gert, Westerweel, Peter E., te Boekhorst, Peter A.W., Mahon, Francois-Xavier, Hjorth-Hansen, Henrik, Isfort, Susanne, Fioretos, Thoas, Hummel, Sebastian, Schemionek, Mirle, Wilop, Stefan, Koschmieder, Steffen, Saußele, Susanne, Mustjoki, Satu, Beier, Fabian, and Brümmendorf, Tim H.

Published
2018
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3. Recurrent somatic mutations are rare in patients with cryptic dyskeratosis congenita

Author

Kirschner, Martin, Maurer, Angela, Wlodarski, Marcin W., Ventura Ferreira, Monica S., Bouillon, Anne-Sophie, Halfmeyer, Insa, Blau, Wolfgang, Kreuter, Michael, Rosewich, Martin, Corbacioglu, Selim, Beck, Joachim, Schwarz, Michaela, Bittenbring, Jörg, Radsak, Markus P., Wilk, Christian Matthias, Koschmieder, Steffen, Begemann, Matthias, Kurth, Ingo, Schemionek, Mirle, Brümmendorf, Tim H., and Beier, Fabian

Published
2018
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4. Telomere dynamics in patients with del (5q) MDS before and under treatment with lenalidomide

Author

Beier, Fabian, Masouleh, Behzad Kharabi, Buesche, Guntram, Ventura Ferreira, Monica S., Schneider, Rebekka K., Ziegler, Patrick, Wilop, Stefan, Vankann, Lucia, Gattermann, Norbert, Platzbecker, Uwe, Giagounidis, Aristoteles, Götze, Katharina S., Nolte, Florian, Hofmann, Wolf-Karsten, Haase, Detlef, Kreipe, Hans, Panse, Jens, Blasco, Maria A., Germing, Ulrich, and Brümmendorf, Tim H.

Published
2015
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9. Telomerase and pluripotency factors jointly regulate stemness in pancreatic cancer stem cells

Author

German Cancer Aid, German Research Foundation, The Hector Foundation, Ministerio de Economía y Competitividad (España), Asociación Española Contra el Cáncer, Ulm University, Walter, Karolin, Rodriguez-Aznar, Eva, Ventura Ferreira, Monica S., Frappart, Pierre-Olivier, Dittrich, Tabea, Tiwary, Kanishka, Meessen, Sabine, Lerma, L., Daiss, Nora, Schulte, Lucas-Alexander, Najafova, Zeynab, Arnold, Frank, Usachov, Valentyn, Azoitei, Ninel, Erkan, Mert M., Lechel, André, Brümmendorf, Tim H., Seufferlein, Thomas, Kleger, Alexander, Tabarés, E., German Cancer Aid, German Research Foundation, The Hector Foundation, Ministerio de Economía y Competitividad (España), Asociación Española Contra el Cáncer, Ulm University, Walter, Karolin, Rodriguez-Aznar, Eva, Ventura Ferreira, Monica S., Frappart, Pierre-Olivier, Dittrich, Tabea, Tiwary, Kanishka, Meessen, Sabine, Lerma, L., Daiss, Nora, Schulte, Lucas-Alexander, Najafova, Zeynab, Arnold, Frank, Usachov, Valentyn, Azoitei, Ninel, Erkan, Mert M., Lechel, André, Brümmendorf, Tim H., Seufferlein, Thomas, Kleger, Alexander, and Tabarés, E.

Abstract

To assess the role of telomerase activity and telomere length in pancreatic CSCs we used different CSC enrichment methods (CD133, ALDH, sphere formation) in primary patient-derived pancreatic cancer cells. We show that CSCs have higher telomerase activity and longer telomeres than bulk tumor cells. Inhibition of telomerase activity, using genetic knockdown or pharmacological inhibitor (BIBR1532), resulted in CSC marker depletion, abrogation of sphere formation in vitro and reduced tumorigenicity in vivo. Furthermore, we identify a positive feedback loop between stemness factors (NANOG, OCT3/4, SOX2, KLF4) and telomerase, which is essential for the self-renewal of CSCs. Disruption of the balance between telomerase activity and stemness factors eliminates CSCs via induction of DNA damage and apoptosis in primary patient-derived pancreatic cancer samples, opening future perspectives to avoid CSC-driven tumor relapse. In the present study, we demonstrate that telomerase regulation is critical for the “stemness” maintenance in pancreatic CSCs and examine the effects of telomerase inhibition as a potential treatment option of pancreatic cancer. This may significantly promote our understanding of PDAC tumor biology and may result in improved treatment for pancreatic cancer patients.

Published
2021

10. A feedback-loop between telomerase activity and stemness factors regulates PDAC stem cells

Author

Walter, Karolin, primary, Rodriguez-Aznar, Eva, additional, Ventura Ferreira, Monica S., additional, Frappart, Pierre-Olivier, additional, Dittrich, Tabea, additional, Tiwary, Kanishka, additional, Meessen, Sabine, additional, Lerma, Laura, additional, Daiss, Nora, additional, Schulte, Lucas-Alexander, additional, Arnold, Frank, additional, Usachov, Valentyn, additional, Azoitei, Ninel, additional, Erkan, Mert, additional, Lechel, Andre, additional, Brümmendorf, Tim H., additional, Seufferlein, Thomas, additional, Kleger, Alexander, additional, Tabarés, Enrique, additional, Günes, Cagatay, additional, Beier, Fabian, additional, Sainz, Bruno, additional, and Hermann, Patrick C., additional

Published
2020
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12. Presence of TERT Promoter Mutations is a Secondary Event and Associates with Elongated Telomere Length in Myxoid Liposarcomas.

Author

Ventura Ferreira, Monica S., Crysandt, Martina, Braunschweig, Till, Jost, Edgar, Voss, Barbara, Bouillon, Anne-Sophie, Knuechel, Ruth, Brümmendorf, Tim H., and Beier, Fabian

Subjects
*SOFT tissue tumors, *CHONDROSARCOMA, *TELOMERES, *SARCOMA, *GENETICS, *PREVENTION, *PHYSIOLOGY
Abstract

The occurrence of TERT promoter mutations has been well described in soft tissue sarcomas (STS). However, the biological role of these mutations as well as their impact on telomere length in STS is still unclear. We analyzed 116 patient samples diagnosed with 22 distinct histological subtypes of bone and STS for the occurrence of TERT promoter mutations by Sanger sequencing. We observed TERT promoter mutations at an overall frequency of 9.5% distributed over 7 different sarcoma subtypes. Except for one chondrosarcoma case harboring a C250T mutation, all other mutations were detected at location C228T. By far the far highest frequency of TERT promoter mutations was found in myxoid liposarcoma (MLS) (4 out of 9 cases studied, i.e., 44%). Assessment of telomere length from tumor biopsies revealed that TERT promoter-mutated MLSs had significantly fewer shortened telomeres in comparison to TERT wildtype MLSs. Based on the frequency of TERT promoter mutations and the elongated telomere length in mutated compared to wildtype MLS, we hypothesize that occurrence of TERT promoter mutations has a pivotal role in the disease progression as a secondary genetic event at a time when tumor cells face the need for telomere elongation to allow further proliferation. [ABSTRACT FROM AUTHOR]

Published
2018
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13. Enterocytes Of Patients With Uncontrolled Acute Graft Versus Host Disease Of The Gut Undergo Massive Telomere Shortening Compared To Unaffected Controls

Author

Hummel, Sebastian, primary, Heudobler, Daniel, additional, Huber, Elisabeth, additional, Ventura Ferreira, Monica S, additional, Fahrenkamp, Dirk, additional, Schmid, Karin, additional, Gremse, Felix, additional, Müller-Newen, Gerhard, additional, Ziegler, Patrick, additional, Jost, Edgar, additional, Brümmendorf, Tim H., additional, Holler, Ernst, additional, and Beier, Fabian, additional

Published
2013
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14. An engineered multicomponent bone marrow niche for the recapitulation of hematopoiesis at ectopic transplantation sites

Author

Ventura Ferreira, Mónica S., Bergmann, Christian, Bodensiek, Isabelle, Peukert, Kristina, Abert, Jessica, Kramann, Rafael, Kachel, Paul, Rath, Björn, Rütten, Stephan, Knuchel, Ruth, Ebert, Benjamin L., Fischer, Horst, Brümmendorf, Tim H., and Schneider, Rebekka K.

Abstract

Background: Bone marrow (BM) niches are often inaccessible for controlled experimentation due to their difficult accessibility, biological complexity, and three-dimensional (3D) geometry. Methods: Here, we report the development and characterization of a BM model comprising of cellular and structural components with increased potential for hematopoietic recapitulation at ectopic transplantation sites. Cellular components included mesenchymal stromal cells (MSCs) and hematopoietic stem and progenitor cells (HSPCs). Structural components included 3D β-tricalcium phosphate (β-TCP) scaffolds complemented with Matrigel or collagen I/III gels for the recreation of the osteogenic/extracellular character of native BM. Results: In vitro, β-TCP/Matrigel combinations robustly maintained proliferation, osteogenic differentiation, and matrix remodeling capacities of MSCs and maintenance of HSPCs function over time. In vivo, scaffolds promoted strong and robust recruitment of hematopoietic cells to sites of ectopic transplantation, vascularization, and soft tissue formation. Conclusions: Our tissue-engineered BM system is a powerful tool to explore the regulatory mechanisms of hematopoietic stem and progenitor cells for a better understanding of hematopoiesis in health and disease. Electronic supplementary material The online version of this article (doi:10.1186/s13045-016-0234-9) contains supplementary material, which is available to authorized users.

Published
2016
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