Abstract |
Existing data identify EWS-FLI1 as indispensable for sustained Ewing's sarcoma growth and as the ideal therapeutic target in this disease. The siRNA may hold great promises as a fusion gene specific agent. RNAi mediated suppression of EWS-FLI1 is likely to result in an altered tumor cell phenotype including changes in chemosensitivity, and a restored differentiation potential. Thus, RNAi may serve as an adjuvant to chemotherapy. As a therapeutic means however, RNAi is hampered by limitations in the delivery of the agent and emergence of resistant clones. In vitro suppression of EWS-FLI1 expression will allow to define the phenotypic characteristics of dormant tumor cells that may give rise to late relapses, enabling improved diagnosis and treatment even of minimal residual disease.
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Authors | Heinrich Kovar, Josef Ban, Sarka Pospisilova |
Journal | Seminars in cancer biology
(Semin Cancer Biol)
Vol. 13
Issue 4
Pg. 275-81
(Aug 2003)
ISSN: 1044-579X [Print] England |
PMID | 14563122
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- EWS-FLI fusion protein
- Oncogene Proteins, Fusion
- Proto-Oncogene Protein c-fli-1
- RNA-Binding Protein EWS
- Transcription Factors
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Topics |
- Animals
- Genetic Therapy
(methods)
- Humans
- Models, Biological
- Oncogene Proteins, Fusion
(genetics)
- Proto-Oncogene Protein c-fli-1
- RNA Interference
- RNA-Binding Protein EWS
- Sarcoma, Ewing
(genetics, therapy)
- Transcription Factors
(genetics)
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