Genotype-selective combination therapies for melanoma identified by high-throughput drug screening. - Wikidata - wikimedia - TriplyDB

Genotype-selective combination therapies for melanoma identified by high-throughput drug screening.

Genotype-selective combination therapies for melanoma identified by high-throughput drug screening.

http://www.wikidata.org/entity/Q39226193

about

Targeting melanoma by small molecules: challenges ahead Pathways and therapeutic targets in melanoma Quantitative phenotypic and pathway profiling guides rational drug combination strategies Landscape of Targeted Anti-Cancer Drug Synergies in Melanoma Identifies a Novel BRAF-VEGFR/PDGFR Combination Treatment Systems Analysis of Adaptive Responses to MAP Kinase Pathway Blockade in BRAF Mutant Melanoma.Distinctive Behaviors of Druggable Proteins in Cellular Networks Combinatorial drug screening and molecular profiling reveal diverse mechanisms of intrinsic and adaptive resistance to BRAF inhibition in V600E BRAF mutant melanomas.p70S6 kinase is a critical node that integrates HER-family and PI3 kinase signaling networks.Enhancing reproducibility in cancer drug screening: how do we move forward?Combinatorial drug screening identifies compensatory pathway interactions and adaptive resistance mechanisms Synergistic apoptosis in head and neck squamous cell carcinoma cells by co-inhibition of insulin-like growth factor-1 receptor signaling and compensatory signaling pathways.Synthetic lethality: emerging targets and opportunities in melanoma.A comprehensive review of the preclinical efficacy profile of the ErbB family blocker afatinib in cancer.Significance of glioma-associated oncogene homolog 1 (GLI1) expression in claudin-low breast cancer and crosstalk with the nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) pathway.The broad-spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF-mutant melanoma cells in combination with other signaling pathway inhibitors.BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume.Combining genomic and network characteristics for extended capability in predicting synergistic drugs for cancer.A FAK scaffold inhibitor disrupts FAK and VEGFR-3 signaling and blocks melanoma growth by targeting both tumor and endothelial cells A Computational Approach for Identifying Synergistic Drug Combinations.Prediction of multidimensional drug dose responses based on measurements of drug pairs.Activities of multiple cancer-related pathways are associated with BRAF mutation and predict the resistance to BRAF/MEK inhibitors in melanoma cells.Clarifying intact 3D tissues on a microfluidic chip for high-throughput structural analysis.Towards combinatorial targeted therapy in melanoma: from pre-clinical evidence to clinical application (review).Biological networks and drug discovery--where do we stand?BRAFV600E cooperates with PI3K signaling, independent of AKT, to regulate melanoma cell proliferation.Integrative network and transcriptomics-based approach predicts genotype- specific drug combinations for melanoma.Advances in computational approaches in identifying synergistic drug combinations.Combinatorial Screening of Pancreatic Adenocarcinoma Reveals Sensitivity to Drug Combinations Including Bromodomain Inhibitor Plus Neddylation Inhibitor.Nanoparticle-Based Celecoxib and Plumbagin for the Synergistic Treatment of Melanoma.Systematic Drug Screening Identifies Tractable Targeted Combination Therapies in Triple-Negative Breast Cancer.Combine and conquer: challenges for targeted therapy combinations in early phase trials.The impact of melanoma genetics on treatment response and resistance in clinical and experimental studies.Regulation of viability, differentiation and death of human melanoma cells carrying neural stem cell biomarkers: a possibility for neural trans-differentiation.High-Throughput RNAi Screening Identifies a Role for the Osteopontin Pathway in Proliferation and Migration of Human Aortic Smooth Muscle Cells.Cooperative induction of apoptosis in NRAS mutant melanoma by inhibition of MEK and ROCK.Expression and activity of EGFR in human cutaneous melanoma cell lines and influence of vemurafenib on the EGFR pathway.Combined treatment with low concentrations of decitabine and SAHA causes cell death in leukemic cell lines but not in normal peripheral blood lymphocytes Predicting synergistic effects between compounds through their structural similarity and effects on transcriptomes.Combenefit: an interactive platform for the analysis and visualization of drug combinations.Targeting Notch enhances the efficacy of ERK inhibitors in BRAF-V600E melanoma.

P2860

Q26824642-251EFBF2-2599-4AF9-96EB-48A7D81F71E0 Q26865736-F6C4E002-75A4-4603-A170-4B7C7CF14051 Q27021150-45764183-F203-4D43-A885-2C858F544E6A Q27313653-02CC08DC-D47B-409C-BD49-1C890A0AB677 Q28548486-831DBC59-90B5-438B-9887-DCB3008A24DA Q28551715-22AAA873-9EEF-4623-8C5B-A6B52208789E Q30277902-9ABA69B7-427F-484F-9E5D-2DF63AA1274C Q30371561-E26D4D61-6363-423B-AA76-E067789F6C23 Q30405622-E7B1C6B1-B051-458C-81C0-6DAA769AA26D Q30418057-36223F37-B374-4856-9555-984A3EFCC394 Q30458494-9AAB0453-14D0-4500-9F68-691BB40918D0 Q33578398-976A8AD3-D42D-4B74-BA52-7F3F7C9E5DB9 Q33605906-0B9249A8-D198-4C00-9CFB-769B35795492 Q35000293-222BE98A-6C40-4EA1-BF2E-C55B89473A27 Q35597799-0BEF6251-8F36-4345-9F46-C0A498725926 Q35836409-7A45DF95-7704-48D3-BC88-26234EC9DAE9 Q36139333-7E28694B-D64B-4592-ACC4-627947BD6BEC Q36188833-4116F740-04D2-4969-83E8-402743EDB7F3 Q36248734-DAA30A1E-CCA9-4F7D-B114-B7F7CD8A41A6 Q37264069-49F90E8D-C2AF-49B9-902D-6B5F11EA26ED Q37529969-FBD3C9B6-1B5B-4BF9-9A19-96809927D2EB Q37549815-DB098355-981F-46EA-B51C-9F408FC3B6A8 Q38219616-284A17DC-3FDC-4F54-A59C-4A1EB287FAB8 Q38243624-9AE734AA-4CBC-4219-8F26-9A08F4BB474A Q38520679-CA52E5F3-A995-44CC-AE3F-1B0CC6EB64DC Q38621140-A1C0454D-0E75-4E27-A4D0-D0CB5179C7CD Q38687343-C8856330-EB1B-4F90-AE72-F286BCC7178B Q38712272-4CB9C487-3231-4B21-B2CC-E95658E1740F Q38724921-3F8E8A53-A50F-474E-9B4D-911FF295F59B Q38729732-38F907D1-4C05-4045-8833-553B3293352C Q38734451-E0D538BE-047E-44BD-B96B-6B67918DE2A2 Q38756275-426B0F26-0798-466E-9F4E-5AC14FBAD7CD Q38877894-3156820D-F77F-483B-B309-28B18EC83459 Q38878829-7B2C26DC-1D9F-4F51-ACE6-D0AACA6AE055 Q38904777-F6CBFCA2-8892-48C3-A407-7E063F42C627 Q38995370-051ED454-D5A1-43C3-8FE9-FADD7E319FB4 Q39100888-FD328F86-E1B4-40BA-B59F-E0C5F6A99860 Q39474699-FEE6D23B-8950-4110-9F43-447A3BCCA593 Q39788218-D715701E-C827-4B29-9BB3-FE64F05E7CEA Q42317543-1A71581A-BB1F-4724-8B1B-26F8BD357C09

P2860

Genotype-selective combination therapies for melanoma identified by high-throughput drug screening.

http://www.wikidata.org/entity/Q39226193

description

2012 nî lūn-bûn

@nan

2012年の論文

@ja

2012年論文

@yue

2012年論文

@zh-hant

2012年論文

@zh-hk

2012年論文

@zh-mo

2012年論文

@zh-tw

2012年论文

@wuu

2012年论文

@zh

2012年论文

@zh-cn

name

Genotype-selective combination ...... igh-throughput drug screening.

@en

Genotype-selective combination ...... igh-throughput drug screening.

@nl

type

label

Genotype-selective combination ...... igh-throughput drug screening.

@en

Genotype-selective combination ...... igh-throughput drug screening.

@nl

prefLabel

Genotype-selective combination ...... igh-throughput drug screening.

@en

Genotype-selective combination ...... igh-throughput drug screening.

@nl

P1433

Q39226193-E135F138-8270-4F94-BEAB-7C2B3C882C91

P1476

Q39226193-2F94E170-0343-47F7-A16B-44A89ED0B6AD

P2093

Q39226193-0942E703-8A4A-4F9D-AA60-0355D33A7212

Q39226193-630F8A4F-2CC9-4BAE-8570-356E619A2239

Q39226193-6444CCB2-2B4C-49A2-8ADE-75F4EDD29D75

Q39226193-6F92359E-AD31-412E-A2E1-4A49F2E83E9D

Q39226193-7B1777B4-9CEA-4286-B496-2233AC95E8E2

Q39226193-AC7FF737-BA60-49B9-AF29-D9366AB939D5

Q39226193-B0CA39FE-B7BE-4265-B691-1A9039005107

Q39226193-CB53E83C-0C06-452D-9D94-E1E41EC964EB

Q39226193-D97DFC1D-F799-402F-8847-224940FD7FE4

Q39226193-D9A0B618-A944-425E-97F4-65F17D9ECFAA

P2860

Q39226193-04F90919-FAB6-43D1-9663-82439141FE2A

Q39226193-055633EA-0875-41CC-981E-A2BAA0BEA931

Q39226193-062B5F13-4175-49A7-9182-C6EE79E0F8BD

Q39226193-16F6E87B-7436-4452-A396-3E6BE2F28567

Q39226193-17572AD6-3322-4E9A-806C-7CA3B6B81390

Q39226193-1C85D935-2162-4364-A4B5-76AA8319A827

Q39226193-20AB88D2-37A6-439E-9CE9-291AA8A0AAEB

Q39226193-25A8E0E4-EB6D-4C0B-8667-49173B3B7917

Q39226193-31BC4D55-3358-4AFF-9FB0-B4C8FB94A6A6

Q39226193-32E91EF4-51FA-4266-BD32-1F28498CAA76

P304

Q39226193-B0DC619F-04D7-409C-80AE-577010C5E7AE

P31

Q39226193-22894C2F-1208-4CC1-8664-CD24EFCA5797

P356

Q39226193-2325926B-25F0-43FC-B14D-4B8BAAB4A151

P433

Q39226193-E2ABAAC2-E69B-495D-8BAF-90E3ED6C890A

P478

Q39226193-E691F7E9-CFCD-450B-B61F-F7DFD59830D3

P50

Q39226193-578CA5DF-7AE0-4512-878B-F8DD7CE91921

P577

Q39226193-D40BCC6D-3804-433E-8E7E-DC7EB641AB66

P5875

Q39226193-A2C1C143-C3DC-42B3-A701-7D12958B4E6E

P698

Q39226193-72BD4C56-1928-4600-A3FF-3F160AA029A7

P921

Q39226193-3462F302-02C1-415D-9C23-E785211853A5

P932

Q39226193-C3AE1A2D-6ADB-42B6-B5CA-E68CA010AB87

P356

2159-8290.CD-12-0408

P1433

Cancer Discovery

P1476

Genotype-selective combination ...... igh-throughput drug screening.

@en

P2093

Andrew Koo

http://www.w3.org/2001/XMLSchema#string

Ashok Chakraborty

http://www.w3.org/2001/XMLSchema#string

Casey G Langdon

http://www.w3.org/2001/XMLSchema#string

David F Stern

http://www.w3.org/2001/XMLSchema#string

James T Platt

http://www.w3.org/2001/XMLSchema#string

Jonathan W Haskins

http://www.w3.org/2001/XMLSchema#string

Marcus W Bosenberg

http://www.w3.org/2001/XMLSchema#string

Matthew A Held

http://www.w3.org/2001/XMLSchema#string

Tisheeka Graham-Steed

http://www.w3.org/2001/XMLSchema#string

Zongzhi Liu

http://www.w3.org/2001/XMLSchema#string

P2860

Kinase-dead BRAF and oncogenic RAS cooperate to drive tumor progression through CRAF

Survival in BRAF V600-mutant advanced melanoma treated with vemurafenib

PLX4032, a selective BRAF(V600E) kinase inhibitor, activates the ERK pathway and enhances cell migration and proliferation of BRAF melanoma cells

Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation

Improved survival with vemurafenib in melanoma with BRAF V600E mutation

Combined targeting of BRAF and CRAF or BRAF and PI3K effector pathways is required for efficacy in NRAS mutant tumors

A synthetic lethal interaction between K-Ras oncogenes and Cdk4 unveils a therapeutic strategy for non-small cell lung carcinoma.

Reversing melanoma cross-resistance to BRAF and MEK inhibitors by co-targeting the AKT/mTOR pathway.

Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR.

Inhibition of Mutated, Activated BRAF in Metastatic Melanoma

P304

52-67

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1158/2159-8290.CD-12-0408

http://www.w3.org/2001/XMLSchema#string

P433

1

http://www.w3.org/2001/XMLSchema#string

P478

3

http://www.w3.org/2001/XMLSchema#string

P50

Antonella Bacchiocchi

P577

2012-12-13T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P5875

233915357

http://www.w3.org/2001/XMLSchema#string

P698

23239741

http://www.w3.org/2001/XMLSchema#string

P921

P932

3546137

http://www.w3.org/2001/XMLSchema#string