Abstract |
Epigenetic alterations are strongly associated with cancer development and drug resistance. The use of the DNA methylation inhibitor decitabine (Dacogen®) has been approved in the treatment of hematological malignancies, and its clinical effects on solid tumors have gained attention. Here, we present a review of the molecular regulation mechanisms, clinical experiences and biological evaluation for novel decitabine-based therapies in solid tumors. We also discuss the following questions: What is the best administration schedule of decitabine in solid tumors? Is there tumor type specificity for decitabine-based epigenetic therapy? What are the biological function and mechanism of decitabine in suppressing tumor development? Is there a correlation between DNA demethylation and clinical response? Importantly, low-dose decitabine and combined therapy show significant improvement in solid tumor treatment. However, the correlation studies are preliminary, and key biomarkers for prognosis need further investigation.
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Authors | Jing Nie, Lin Liu, Xiang Li, Weidong Han |
Journal | Cancer letters
(Cancer Lett)
Vol. 354
Issue 1
Pg. 12-20
(Nov 01 2014)
ISSN: 1872-7980 [Electronic] Ireland |
PMID | 25130173
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Copyright | Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. |
Chemical References |
- Antimetabolites, Antineoplastic
- Biomarkers, Tumor
- Decitabine
- Azacitidine
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Topics |
- Antimetabolites, Antineoplastic
(administration & dosage, chemistry)
- Azacitidine
(administration & dosage, analogs & derivatives, chemistry)
- Biomarkers, Tumor
- Clinical Trials as Topic
- DNA Methylation
(drug effects)
- Decitabine
- Epigenesis, Genetic
- Humans
- Neoplasms
(drug therapy, genetics)
- Prognosis
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