niacinamide has been researched along with dactolisib in 3 studies
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 3 (100.00) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Demartines, N; Dormond, O; Dormond-Meuwly, A; Dufour, M; Roulin, D; Waselle, L | 1 |
| de Gramont, A; Dos Santos, C; Faivre, S; Raymond, E; Riveiro, ME; Serova, M; Slimane, K; Tijeras-Raballand, A | 1 |
| Cho, E; Choi, KM; Chung, YH; Han, EH; Kang, M; Kim, B; Kim, E; Kim, JY; Shin, JH | 1 |
3 other study(ies) available for niacinamide and dactolisib
| Article | Year |
|---|---|
Targeting renal cell carcinoma with NVP-BEZ235, a dual PI3K/mTOR inhibitor, in combination with sorafenib.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Carcinoma, Renal Cell; Cell Line, Tumor; Female; Humans; Imidazoles; Kidney Neoplasms; Mice; Mice, Nude; Molecular Targeted Therapy; Niacinamide; Phenylurea Compounds; Phosphoinositide-3 Kinase Inhibitors; Protein Kinase Inhibitors; Pyridines; Quinolines; Sorafenib; TOR Serine-Threonine Kinases; Treatment Outcome; Xenograft Model Antitumor Assays | 2011 |
Benchmarking effects of mTOR, PI3K, and dual PI3K/mTOR inhibitors in hepatocellular and renal cell carcinoma models developing resistance to sunitinib and sorafenib.
Topics: Aminopyridines; Antineoplastic Agents; Bridged Bicyclo Compounds, Heterocyclic; Carcinoma, Hepatocellular; Carcinoma, Renal Cell; Cell Line, Tumor; Cell Proliferation; Dose-Response Relationship, Drug; Drug Resistance, Neoplasm; Everolimus; Humans; Imidazoles; Indoles; Kidney Neoplasms; Liver Neoplasms; Mechanistic Target of Rapamycin Complex 1; Morpholines; Multiprotein Complexes; Niacinamide; Phenylurea Compounds; Phosphoinositide-3 Kinase Inhibitors; Pyrimidines; Pyrroles; Quinolines; Signal Transduction; Sirolimus; Sorafenib; Sunitinib; TOR Serine-Threonine Kinases | 2013 |
Prolonged MEK inhibition leads to acquired resistance and increased invasiveness in KRAS mutant gastric cancer.
Topics: Cell Line, Tumor; Crizotinib; Drug Resistance, Neoplasm; Humans; Imidazoles; Mitogen-Activated Protein Kinase Kinases; Mutation; Neoplasm Invasiveness; Niacinamide; Phenotype; Phosphatidylinositol 3-Kinases; Phosphorylation; Phosphotyrosine; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Proto-Oncogene Proteins p21(ras); Quinolines; Stomach Neoplasms; TOR Serine-Threonine Kinases | 2018 |