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Image Search Results
Journal: Cancer Informatics
Article Title: Pathway Interactions Based on Drug-Induced Datasets
doi: 10.1177/1176935119851518
Figure Lengend Snippet: Pairs of pathway interactions from 2 different drugs with the greatest DCSC score.
Article Snippet: 17-AAG_wort , 3/1 ,
Techniques: Infection
Journal: Cancer Informatics
Article Title: Pathway Interactions Based on Drug-Induced Datasets
doi: 10.1177/1176935119851518
Figure Lengend Snippet: Interactions of drugs, pathways, and diseases in our and previous studies. (A) Red arrows present the drug to cancer pathway via MTOR as in Chiu et al. (B) Blue arrows present sirolimus to pancreatic cancer pathways via MTOR and ERBB as in Hynes and MacDonald. (C) The ERBB signaling pathway is the primary choice for the breast cancer treatment. – (D) Description of our findings (black arrows) compared with previous studies.
Article Snippet: 17-AAG_wort , 3/1 ,
Techniques:
Journal: Oncotarget
Article Title: Evaluation of in vitro effects of various targeted drugs on plasma cells and putative neoplastic stem cells in patients with multiple myeloma
doi: 10.18632/oncotarget.11593
Figure Lengend Snippet: Effects of various targeted drugs on proliferation of myeloma cell lines
Article Snippet: A number of anti-neoplastic drugs were tested for their ability to inhibit growth of MM cells: the tyrosine kinase inhibitors (TKI) bosutinib, dasatinib, imatinib, sorafenib, sunitinib, and nilotinib, the ErbB-receptor inhibitors lapatinib, erlotinib, and gefitinib, the Aurora-kinase inhibitor VX-680, the
Techniques: Produced
Journal: Oncotarget
Article Title: Evaluation of in vitro effects of various targeted drugs on plasma cells and putative neoplastic stem cells in patients with multiple myeloma
doi: 10.18632/oncotarget.11593
Figure Lengend Snippet: Effects of the most effective targeted drugs on proliferation of primary neoplastic BM cells
Article Snippet: A number of anti-neoplastic drugs were tested for their ability to inhibit growth of MM cells: the tyrosine kinase inhibitors (TKI) bosutinib, dasatinib, imatinib, sorafenib, sunitinib, and nilotinib, the ErbB-receptor inhibitors lapatinib, erlotinib, and gefitinib, the Aurora-kinase inhibitor VX-680, the
Techniques: Produced
Journal: Oncotarget
Article Title: Evaluation of in vitro effects of various targeted drugs on plasma cells and putative neoplastic stem cells in patients with multiple myeloma
doi: 10.18632/oncotarget.11593
Figure Lengend Snippet: Effects of various targeted drugs on survival (apoptosis) of myeloma cell lines
Article Snippet: A number of anti-neoplastic drugs were tested for their ability to inhibit growth of MM cells: the tyrosine kinase inhibitors (TKI) bosutinib, dasatinib, imatinib, sorafenib, sunitinib, and nilotinib, the ErbB-receptor inhibitors lapatinib, erlotinib, and gefitinib, the Aurora-kinase inhibitor VX-680, the
Techniques: Produced
Journal: Oncotarget
Article Title: Evaluation of in vitro effects of various targeted drugs on plasma cells and putative neoplastic stem cells in patients with multiple myeloma
doi: 10.18632/oncotarget.11593
Figure Lengend Snippet: MM cell lines (MM.1S, NCI-H929, OPM-2, RPMI-8226, U-266) were incubated in control medium (Co) or in various concentrations of 17AAG, BI2536, or BEZ235 (0.001-1 μM) at 37°C for 48 hours. Then, the percentage of apoptotic cells was determined by AnnexinV/PI staining and flow cytometry. Results show the percentage of AnnexinV/PI+ cells and represent the mean±S.D. from 3 independent experiments. Asterisk (*): p<0.05.
Article Snippet: A number of anti-neoplastic drugs were tested for their ability to inhibit growth of MM cells: the tyrosine kinase inhibitors (TKI) bosutinib, dasatinib, imatinib, sorafenib, sunitinib, and nilotinib, the ErbB-receptor inhibitors lapatinib, erlotinib, and gefitinib, the Aurora-kinase inhibitor VX-680, the
Techniques: Incubation, Control, Staining, Flow Cytometry
Journal: Oncotarget
Article Title: Evaluation of in vitro effects of various targeted drugs on plasma cells and putative neoplastic stem cells in patients with multiple myeloma
doi: 10.18632/oncotarget.11593
Figure Lengend Snippet: Primary BM cells derived from 6 patients with MM were incubated in control medium (Co) or in medium containing 17AAG, BI2536, or BEZ235 (each 1 μM) at 37°C for 48 hours. Thereafter, cells were stained with antibodies against AnnexinV A. or active caspase-3 B. by multicolor flow cytometry as described in the text. The following subsets of cells were examined: CD138 + MM cells (black bars), CD138 − /CD27 + /CD20 + putative MMSC (grey bars), CD34 + /CD38 − hematopoietic stem cells (open bars), and CD34 + /CD38 + cells (hatched bars). Results are expressed as percent AnnexinV+ cells (A) or percent active caspase-3+ cells (B) and represent the mean±S.D. from 6 independent experiments. Asterisk (*): p<0.05.
Article Snippet: A number of anti-neoplastic drugs were tested for their ability to inhibit growth of MM cells: the tyrosine kinase inhibitors (TKI) bosutinib, dasatinib, imatinib, sorafenib, sunitinib, and nilotinib, the ErbB-receptor inhibitors lapatinib, erlotinib, and gefitinib, the Aurora-kinase inhibitor VX-680, the
Techniques: Derivative Assay, Incubation, Control, Staining, Flow Cytometry
Journal: Oncotarget
Article Title: Evaluation of in vitro effects of various targeted drugs on plasma cells and putative neoplastic stem cells in patients with multiple myeloma
doi: 10.18632/oncotarget.11593
Figure Lengend Snippet: MM.1S cells (upper left panel), NCI-H929 cells (upper right panel), OPM-2 cells (middle left panel), RPMI-8226 cells (middle right panel) and U-266 cells (lower panel) were incubated in control medium (Co) or various concentrations of 17AAG, BI2536, or BEZ235 (0.001-1 μM each) at 37°C for 48 hours. Then, cell cycle distribution was analyzed by flow cytometry as described in the text. Asterisk (*): p<0.05.
Article Snippet: A number of anti-neoplastic drugs were tested for their ability to inhibit growth of MM cells: the tyrosine kinase inhibitors (TKI) bosutinib, dasatinib, imatinib, sorafenib, sunitinib, and nilotinib, the ErbB-receptor inhibitors lapatinib, erlotinib, and gefitinib, the Aurora-kinase inhibitor VX-680, the
Techniques: Incubation, Control, Flow Cytometry
Journal: Oncotarget
Article Title: Evaluation of in vitro effects of various targeted drugs on plasma cells and putative neoplastic stem cells in patients with multiple myeloma
doi: 10.18632/oncotarget.11593
Figure Lengend Snippet: MM.1S cells A. , OPM-2 cells B. , and RPMI-8226 cells C. were incubated in control medium (Co), in medium containing individual drugs alone, or in medium containing drug combinations (at fixed ratio) at 37°C for 48 hours. Then, uptake of 3 H-thymidine was measured. MM.1S cells (A) were incubated in various concentrations of BI2536 ( ○ - ○ ), BEZ235 ( ◇ - ◇ ), or combinations of both drugs ( ◾ - ◾ ). OPM-2 cells (B) were incubated with various concentrations of BI2536 ( ○ - ○ ) or obatoclax ( ◇ - ◇ ) or combinations of both drugs ( ○ - ○ ). RPMI-8226 cells (C) were incubated with various concentrations of 17AAG ( ○ - ○ ) or BEZ235 ( ◇ - ◇ ) or combinations of both drugs ( ○ - ○ ). Results show the percentage of 3 H-thymidine uptake compared to medium control and represent the mean±S.D. of one typical experiment.
Article Snippet: A number of anti-neoplastic drugs were tested for their ability to inhibit growth of MM cells: the tyrosine kinase inhibitors (TKI) bosutinib, dasatinib, imatinib, sorafenib, sunitinib, and nilotinib, the ErbB-receptor inhibitors lapatinib, erlotinib, and gefitinib, the Aurora-kinase inhibitor VX-680, the
Techniques: Incubation, Control
Journal: Oncotarget
Article Title: Evaluation of in vitro effects of various targeted drugs on plasma cells and putative neoplastic stem cells in patients with multiple myeloma
doi: 10.18632/oncotarget.11593
Figure Lengend Snippet: Effects of various drug combinations on proliferation of myeloma cell lines
Article Snippet: A number of anti-neoplastic drugs were tested for their ability to inhibit growth of MM cells: the tyrosine kinase inhibitors (TKI) bosutinib, dasatinib, imatinib, sorafenib, sunitinib, and nilotinib, the ErbB-receptor inhibitors lapatinib, erlotinib, and gefitinib, the Aurora-kinase inhibitor VX-680, the
Techniques: Produced