| Autor: |
Drusbosky, Leylah M., Vidva, Robinson, Gera, Saji, Das, Arko, Tiwari, Krishna K, Joseph, Vishwas, Mohapatra, Subrat, Lunkad, Neelesh, Abbasi, Taher, Vali, Shireen, Tognon, Cristina E., Kurtz, Stephen E, Tyner, Jeffrey W., Druker, Brian J., Cogle, Christopher R. |
| Zdroj: |
Blood; December 2017, Vol. 130 Issue: 1, Number 1 Supplement 1 p3907-3907, 1p |
| Abstrakt: |
Background: Isocitrate dehydrogenase (IDH) is an essential enzyme in the TCA cycle. Recurrent mutations in IDH1or IDH2are prevalent in several cancers, including glioma and acute myeloid leukemia (AML). IDHmutations reduce cellular levels of α-ketoglutarate (α-KG), resulting in accumulation of 2-hydroxyglutarate (2-HG), an α-KG antagonist. This leads to the inhibition of both α-KG-dependent histone lysine demethylases and the TET family of DNA hydroxylases. Even though current IDH inhibitors have high specificity towards the IDH1and IDH2mutant forms, the overall clinical response rate to these drugs remains ~19%, suggesting the presence of IDH mutations alone does not reflect positive clinical outcome. However, defining biomarkers and developing methods to predict response to IDH inhibitors will expedite the drug development process and provide patient selection criteria for future clinical trials. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
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