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Metabolic re-programming of pancreatic cancer mediated by CDK4/6 inhibition elicits unique vulnerabilities
Due to loss of p16ink4a in pancreatic ductal adenocarcinoma (PDA), pharmacological suppression of CDK4/6 could represent a potent target for treatment. In PDA models CDK4/6 inhibition had variable effect on cell cycle, but yielded accumulation of ATP and mitochondria. Pharmacological CDK4/6 inhibito...
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| Vydáno v: | Cell Rep |
|---|---|
| Hlavní autoři: | , , , , |
| Médium: | Artigo |
| Jazyk: | Inglês |
| Vydáno: |
2016
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| Témata: | |
| On-line přístup: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4757440/ https://ncbi.nlm.nih.gov/pubmed/26804906 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.celrep.2015.12.094 |
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