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4. Triple combination therapy comprising osimertinib, an AXL inhibitor, and an FGFR inhibitor improves the efficacy of EGFR-mutated non-small cell lung cancer

6. Adaptive resistance to lorlatinib via EGFR signaling in ALK-rearranged lung cancer

7. AXL signal mediates adaptive resistance to KRAS G12C inhibitors in KRAS G12C-mutant tumor cells

12. HER3 activation contributes toward the emergence of ALK inhibitor-tolerant cells in ALK-rearranged lung cancer with mesenchymal features

13. Initial AXL and MCL‐1 inhibition contributes to abolishing lazertinib tolerance in EGFR‐mutant lung cancer cells.

16. Chemoprevention with low-dose aspirin, mesalazine, or both in patients with familial adenomatous polyposis without previous colectomy (J-FAPP Study IV): a multicentre, double-blind, randomised, two-by-two factorial design trial

20. Supplementary Table2 from Effects of Combined Therapeutic Targeting of AXL and ATR on Pleural Mesothelioma Cells

22. Effects of Combined Therapeutic Targeting of AXL and ATR on Pleural Mesothelioma Cells

25. MO68-4 A chemoproteoinformatics approach demonstrates that aspirin increases sensitivity to MEK inhibition by directly binding to RPS5

27. Discovery of Selective Histone Deacetylase 1 and 2 Inhibitors: Screening of a Focused Library Constructed by Click Chemistry, Kinetic Binding Analysis, and Biological Evaluation

32. Cancer-Cell-Selective Targeting by Arylcyclopropylamine-Vorinostat Conjugates

36. Data from Efficacy of Low-Dose Aspirin in Colorectal Cancer Risk Prevention is Dependent on ADH1B and ALDH2 Genotype in Japanese Familial Adenomatous Polyposis Patients

37. Supplementary Data from Efficacy of Low-Dose Aspirin in Colorectal Cancer Risk Prevention is Dependent on ADH1B and ALDH2 Genotype in Japanese Familial Adenomatous Polyposis Patients

39. Supplementary Figure 4. from The Novel Histone Deacetylase Inhibitor, OBP-801, Induces Apoptosis in Rhabdoid Tumors by Releasing the Silencing of NOXA

40. Supplementary Figure 3. from The Novel Histone Deacetylase Inhibitor, OBP-801, Induces Apoptosis in Rhabdoid Tumors by Releasing the Silencing of NOXA

41. Supplementary Figure S4: The combination induces apoptosis in a TRAIL-independent manner in UM-UC-11 cells. from A Histone Deacetylase Inhibitor, OBP-801, and Celecoxib Synergistically Inhibit the Cell Growth with Apoptosis via a DR5-Dependent Pathway in Bladder Cancer Cells

42. Supplementary Figure S2: Expressions of DR5 mRNA and cell-surface DR5 are different between two bladder cancer cell lines. from A Histone Deacetylase Inhibitor, OBP-801, and Celecoxib Synergistically Inhibit the Cell Growth with Apoptosis via a DR5-Dependent Pathway in Bladder Cancer Cells

44. Supplementary Figure S1: Combined treatment with OBP-801 and celecoxib reduces FLIP and survivin expression at mRNA level. from A Histone Deacetylase Inhibitor, OBP-801, and Celecoxib Synergistically Inhibit the Cell Growth with Apoptosis via a DR5-Dependent Pathway in Bladder Cancer Cells

45. Supplementary Figure 1. from The Novel Histone Deacetylase Inhibitor, OBP-801, Induces Apoptosis in Rhabdoid Tumors by Releasing the Silencing of NOXA

46. Supplementary Figure 2. from The Novel Histone Deacetylase Inhibitor, OBP-801, Induces Apoptosis in Rhabdoid Tumors by Releasing the Silencing of NOXA

47. Suuplementary Figure S3: Combined treatment with OBP-801 and celecoxib induces binding of caspase-8 to DR5, and Bim expression in bladder cancer cells. from A Histone Deacetylase Inhibitor, OBP-801, and Celecoxib Synergistically Inhibit the Cell Growth with Apoptosis via a DR5-Dependent Pathway in Bladder Cancer Cells

49. Supplementary table from The Novel Histone Deacetylase Inhibitor, OBP-801, Induces Apoptosis in Rhabdoid Tumors by Releasing the Silencing of NOXA

50. Supplementary Data from Histone Deacetylase Inhibitors and 15-Deoxy-Δ12,14-Prostaglandin J2 Synergistically Induce Apoptosis

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