Cookie Settings

We use cookies to optimize our website. These include cookies that are necessary for the operation of the site, as well as those that are only used for anonymous statistic. You can decide for yourself which categories you want to allow. Further information can be found in our data privacy protection .

Essential

These cookies are necessary to run the core functionalities of this website and cannot be disabled.

Name Webedition CMS
Purpose This cookie is required by the CMS (Content Management System) Webedition for the system to function correctly. Typically, this cookie is deleted when the browser is closed.
Name econda
Purpose Session cookie emos_jcsid for the web analysis software econda. This runs in the “anonymized measurement” mode. There is no personal reference. As soon as the user leaves the site, tracking is ended and all data in the browser are automatically deleted.
Statistics

These cookies help us understand how visitors interact with our website by collecting and analyzing information anonymously. Depending on the tool, one or more cookies are set by the provider.

Name econda
Purpose Statistics
External media

Content from external video platforms is blocked by default. If cookies from external media are accepted, access to this content no longer requires manual consent.

Name Youtube
Purpose External media

Junior Research Group Soft-Tissue Sarcoma

Dr. Ana Banito

Endogenous tagging of the SS18-SSX fusion oncogene using CRISPR/Cas9-mediated homologous directed repair with Flag-HA epitopes in synovial sarcoma cells. The figure shows detection of SS18-SSX using anti-HA-tag immunofluorescence (red). This tool allowed to study genome-wide occupancy and protein-protein interactions of this oncogenic driver.
© dkfz.de

Sarcomas are an extremely heterogeneous group of mesenchymal tumors that arise in a multitude of tissues and cell types. Several genetic events have been identified in different sarcoma sub-types, but very few models were developed to study their role in tumorigenesis aiming at exploiting them as therapeutic vulnerabilities. As a result, the treatment of sarcoma has had extremely limited advancement in treatment options compared to other cancers. Thus, the generation of in vitro and in vivo models for sarcoma research is urgently needed, to provide insights into the pathobiology of these tumors and discover novel vulnerabilities in these often lethal but yet understudied diseases.

A common molecular mechanism
Many types of soft tissue sarcomas arising in children and young adults have a unifying underlying genetic mechanism, where chromosomal translocations generate fusion oncoproteins that serve as drivers of the disease. This genetic simplicity provides an exceptional opportunity to develop effective and specific therapies. My past research has applied cutting edge technology to define epigenetic vulnerabilities associated with the SS18-SSX gene fusion, the defining event in synovial sarcoma, and to study its oncogenic molecular mechanism. Our current goal is to combine a toolbox consisting of CRISPR/Cas9, RNAi technology and mouse modeling tools to systematically address key genetic and epigenetic mechanisms in the pathobiology of pediatric sarcomas. Our goal is to comprehensively study the impact of gene fusions and other genetic drivers in sarcomagenesis, uncover specific vulnerabilities they create, ultimately aiming at maximizing the potential for rapid clinical translation.

Contact

Dr. Ana Banito
Soft-Tissue Sarcoma (B380)
Deutsches Krebsforschungszentrum
Im Neuenheimer Feld 581
69120 Heidelberg
Tel: +49 6221 42-1581

Selected Publications

  • Banito A, Li X, Laporte A, Roe JS, Sanchez-Vega F, Huang CH, Dancsok A, Hatzi K, Chen CC, Tschaharganeh DF, Chandwani R, Tasdemir N, Ladanyi M, Jones KB, Capecchi MR, Vakoc CR, Torsten N, Lowe SW. The SS18-SSX oncoprotein hijacks KDM2B-PRC1.1 to drive synovial sarcoma. Cancer Cell. 2018 Mar 12;33(3):527-541.
  • Tasdemir N*, Banito A*, Roe JS*, Alonso-Curbelo D*, Camiolo M, Tschaharganeh DF, Huang CH, Aksoy O, Bolden JE, Chen C, Fennell M, Chicas A, Vakoc C, Lowe SW. Brd4 connects enhancer remodeling to senescence immune surveillance. Cancer Discov. (2016) June; 6(6): 612-29.
  • Acosta JC*, Banito A*, Wuestefeld T, Georgilis A, Janich P, Morton JP, Athineos D, Kang TW, Lasitschka F, Andrulis M, Pascual G, Morris KJ, Khan S, Jin H, Dharmalingam G, Snijders AP, Carroll T, Capper D, Pritchard C, Inman GJ, Longerich T, Sansom OJ, Benitah SA, Zender L, Gil J. A complex secretory program orchestrated by the inflammasome controls paracrine senescence. Nat Cell Biol. (2013) Aug;15(8):978-90.
  • Banito A, Rashid ST, Acosta JC, Li S, Pereira CF, Geti I, Pinho S, Silva JC, Azuara V, Walsh M, Vallier L, Gil J. Senescence impairs successful reprogramming to pluripotent stem cells. Genes Dev (2009) 23, 2134-2139.
to top
powered by webEdition CMS