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Erschienen in: Cancer and Metastasis Reviews 4/2010

01.12.2010 | NON-THEMATIC REVIEW

DNA methylation or histone modification status in metastasis and angiogenesis-related genes: a new hypothesis on usage of DNMT inhibitors and S-adenosylmethionine for genome stability

verfasst von: Mehmet Şahin, Emel Şahin, Saadet Gümüşlü, Abdullah Erdoğan, Meral Gültekin

Erschienen in: Cancer and Metastasis Reviews | Ausgabe 4/2010

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Abstract

Metastasis is a leading cause of mortality and morbidity in cancer. This process needs angiogenesis. The biology underlying cancer, metastasis, and angiogenesis has been investigated so as to determine the therapeutic targets. Invasive and metastatic cancer cells have undergone numerous genetic and epigenetic changes, manifested by cytoskeletal changes, loss of adhesion, and expression of proteolytic enzymes that degrade the basement membrane. Additionally, in endothelial cells, some epigenetic modifications occur during the formation of angiogenesis. Researchers have used some methylation inhibitors, histone deacetylase inhibitors, or methylating agents (such as S-adenosylmethionine, SAM) against cancer and angiogenesis. Although they are effective to beat these diseases, each one results in differentiation or changes in genome structure. We review epigenetically modified genes related with angiogenesis and metastasis in cancer and endothelial cells, and suggest a new proposal. This hypothesis has discussed the importance of the usage of DNA methylation inhibitors together with SAM to prevent tumor progression and genome instability or changes resulting in additional diseases.
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Metadaten
Titel
DNA methylation or histone modification status in metastasis and angiogenesis-related genes: a new hypothesis on usage of DNMT inhibitors and S-adenosylmethionine for genome stability
verfasst von
Mehmet Şahin
Emel Şahin
Saadet Gümüşlü
Abdullah Erdoğan
Meral Gültekin
Publikationsdatum
01.12.2010
Verlag
Springer US
Erschienen in
Cancer and Metastasis Reviews / Ausgabe 4/2010
Print ISSN: 0167-7659
Elektronische ISSN: 1573-7233
DOI
https://doi.org/10.1007/s10555-010-9253-0

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