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  • genes
  • The mechanism for inactivation of the KIP family cyclin-dependent kinase inhibitor (CDKI) genes, the p21 , p27 , and p57 genes, in gastric cancer cells was tested by treating the cells with either the DNA demethylation agent, 5-aza-2′-deoxycytidine or the histone deacetylase inhibitor, n -butyric acid or trichostatin A. RNA expression of the gene was determined by reverse transcription PCR. (aacrjournals.org)
  • melanoma
  • In contrast to BRAF V600E or NRAS G12D-expressing melanocytes, melanoma cells have an inherent resistance to suppression of AP-1 activity by BRAFV600E- or MEK-inhibitors. (harvard.edu)
  • selective
  • The development of a new generation of selective CDK 4/6 inhibitors, including palbociclib, abemaciclib and ribociclib has ability to target CDK 4/6 with fewer adverse effects and improved effectiveness, as they have a vital role in the G1 to S phase cell-cycle transition. (psmarketresearch.com)
  • tumor
  • Favorable results with palbociclib and its recent U.S. Food and Drug Administration approval demonstrate that CDK inhibitors with narrow selectivity profiles can have clinical utility for therapy based on individual tumor genetics. (aspetjournals.org)
  • rapamycin
  • In addition, the efficacy of flavopiridol against MCL cell lines was synergistically enhanced by co-treatment with agents that modulate the Akt pathway, including the PI3-K inhibitor LY294002, as well as rapamycin, an mTOR inhibitor. (aacrjournals.org)
  • chromosomal
  • The recent successes of CDK inhibitors in the clinic, combined with the potential for structure-based routes to the development of non-ATP-competitive CDK inhibitors, and evidence that CDK inhibitors may have use in suppressing chromosomal instability and in synthetic lethal drug combinations inspire optimism that CDK inhibitors will become important weapons in the fight against cancer. (aspetjournals.org)
  • targets
  • To identify downstream effectors of MAPK signaling that could be used as potential additional therapeutic targets for BRAFV600E inhibitors, we used hTERT/CDK4R24C/p53DD-immortalized primary human melanocytes genetically modified to ectopically express BRAF V600E or NRAS G12D and observed induction of the AP-1 transcription factor family member c-Jun. (harvard.edu)
  • known
  • This highly effective, functional approach allowed for rapid benchmarking against known CDK inhibitors with undesirable side effects, such as flavopiridol ( Fig. 1B ), and showed SCH 727965 to be a compound with a significantly superior therapeutic profile. (aacrjournals.org)