nu7441  (Tocris)

Journal: Hematological Oncology

Article Title: Synthetic Lethal Combinations of DNA Repair Inhibitors and Genotoxic Agents to Target High‐Risk Diffuse Large B Cell Lymphoma

doi: 10.1002/hon.70131

Figure Lengend Snippet: Synthetic lethal combinations enhance apoptosis, induce cell cycle defect and activate DDR. (A, B) U2932 and DB cell lines were treated as indicated with IC20 of each drug (U2932 cell line: Cyclophosphamide 1 µM, PF477736 0.31, AZD‐6738 1.01 µM, Doxorubicin 30 nM, NU7441 3.1 µM; DB cell line: Cyclophosphamide: 0.8 μM, PF477736 0.39, AZD‐6738 3.13 µM, Doxorubicin 30 nM, NU7441 3.1 µM). Apoptosis was studied by AnnexinV‐PE staining and cell cycle was studied using BrdU incorporation and DAPI after 72H of treatment. Data are the mean ± SD of three independent experiments. Statistical significance was tested using t ‐test for pairs. * p < 0.05, ** p < 0.01, *** p < 0.001, NS: non‐significant.

Article Snippet: The compounds used in this study are PJ‐34 (PARP1/2 inhibitor; 3255 Tocris Bioscience), NU‐7441 (DNAPK inhibitor; S2638 Selleckchem), KU‐55933 (ATM inhibitor; S1092 Selleckchem), PF‐477736 (CHK1/2 inhibitor; S2904 Selleckchem), AZD‐6738 (ATR inhibitor; S7693 Selleckchem), MK‐8776 (CHK1 inhibitor; S2735 Selleckchem), AZD‐1775 (Wee1 inhibitor; S1525 Selleckchem), MP‐470 (Rad51 inhibitor; S1244 Selleckchem), Gemcitabine (nucleic acid synthesis inhibitor; S1714 Selleckchem), Doxorubicin and Etoposide (topoisomerase II inhibitors; D1515 Sigma Aldrich and S1225 Selleckchem, respectively), Mafosfamide (nitrogen mustard, active form of 4‐OH‐Cyclophosphamide; SC‐211761 Santa Cruz Biotechnology.

Techniques: Staining, BrdU Incorporation Assay

Journal: Hematological Oncology

Article Title: Synthetic Lethal Combinations of DNA Repair Inhibitors and Genotoxic Agents to Target High‐Risk Diffuse Large B Cell Lymphoma

doi: 10.1002/hon.70131

Figure Lengend Snippet: Synthetic lethal combinations enhance apoptosis, induce cell cycle defect and activate DDR. (A, B) U2932 and DB cell lines were treated as indicated with IC20 of each drug (U2932 cell line: Cyclophosphamide 1 µM, PF477736 0.31, AZD‐6738 1.01 µM, Doxorubicin 30 nM, NU7441 3.1 µM; DB cell line: Cyclophosphamide: 0.8 μM, PF477736 0.39, AZD‐6738 3.13 µM, Doxorubicin 30 nM, NU7441 3.1 µM). Apoptosis was studied by AnnexinV‐PE staining and cell cycle was studied using BrdU incorporation and DAPI after 72H of treatment. Data are the mean ± SD of three independent experiments. Statistical significance was tested using t ‐test for pairs. * p < 0.05, ** p < 0.01, *** p < 0.001, NS: non‐significant.

Article Snippet: The compounds used in this study are PJ‐34 (PARP1/2 inhibitor; 3255 Tocris Bioscience), NU‐7441 (DNAPK inhibitor; S2638 Selleckchem), KU‐55933 (ATM inhibitor; S1092 Selleckchem), PF‐477736 (CHK1/2 inhibitor; S2904 Selleckchem), AZD‐6738 (ATR inhibitor; S7693 Selleckchem), MK‐8776 (CHK1 inhibitor; S2735 Selleckchem), AZD‐1775 (Wee1 inhibitor; S1525 Selleckchem), MP‐470 (Rad51 inhibitor; S1244 Selleckchem), Gemcitabine (nucleic acid synthesis inhibitor; S1714 Selleckchem), Doxorubicin and Etoposide (topoisomerase II inhibitors; D1515 Sigma Aldrich and S1225 Selleckchem, respectively), Mafosfamide (nitrogen mustard, active form of 4‐OH‐Cyclophosphamide; SC‐211761 Santa Cruz Biotechnology.

Techniques: Staining, BrdU Incorporation Assay