Converting cancer therapies into cures: lessons from infectious diseases - Wikidata - wikimedia - TriplyDB

Converting cancer therapies into cures: lessons from infectious diseases

Converting cancer therapies into cures: lessons from infectious diseases

http://www.wikidata.org/entity/Q36301709

about

Autophagy and Apoptotic Crosstalk: Mechanism of Therapeutic Resistance in HER2-Positive Breast Cancer Co-Targeting of JNK and HUNK in Resistant HER2-Positive Breast Cancer Systems biology approaches for advancing the discovery of effective drug combinations Overcoming mutation-based resistance to antiandrogens with rational drug design Mapping the Pathways of Resistance to Targeted Therapies Systems biology of cancer: entropy, disorder, and selection-driven evolution to independence, invasion and "swarm intelligence"MicroRNA-147 induces a mesenchymal-to-epithelial transition (MET) and reverses EGFR inhibitor resistance Annotating STEAP1 regulation in prostate cancer with 89Zr immuno-PET Targeting substrate-site in Jak2 kinase prevents emergence of genetic resistance Lipid metabolism emerges as a promising target for malignant glioma therapy.Identifying kinase dependency in cancer cells by integrating high-throughput drug screening and kinase inhibition data Targeted therapy resistance mediated by dynamic regulation of extrachromosomal mutant EGFR DNA.Addiction to multiple oncogenes can be exploited to prevent the emergence of therapeutic resistance.Nonamplified FGFR1 is a growth driver in malignant pleural mesothelioma Glucocorticoid receptor confers resistance to antiandrogens by bypassing androgen receptor blockade.Selective anti-cancer agents as anti-aging drugs The role of epithelial plasticity in prostate cancer dissemination and treatment resistance Integrating phenotypic small-molecule profiling and human genetics: the next phase in drug discovery.Single-cell tracking reveals antibiotic-induced changes in mycobacterial energy metabolism.Systematic identification of signaling pathways with potential to confer anticancer drug resistance.RAS signaling promotes resistance to JAK inhibitors by suppressing BAD-mediated apoptosis.An Inducible TGF-β2-TGFβR Pathway Modulates the Sensitivity of HNSCC Cells to Tyrosine Kinase Inhibitors Targeting Dominant Receptor Tyrosine Kinases.Leveraging DNA damage response signaling to identify yeast genes controlling genome stability.Kinome RNAi Screens Reveal Synergistic Targeting of MTOR and FGFR1 Pathways for Treatment of Lung Cancer and HNSCC.Divergent Androgen Receptor and Beta-Catenin Signaling in Prostate Cancer Cells.Prediction of resistance development against drug combinations by collateral responses to component drugs.Compromising the 19S proteasome complex protects cells from reduced flux through the proteasome.Improving Cancer Treatment via Mathematical Modeling: Surmounting the Challenges Is Worth the Effort Skin-safe photothermal therapy enabled by responsive release of acid-activated membrane-disruptive polymer from polydopamine nanoparticle upon very low laser irradiation.Is the Improved Efficacy of Trastuzumab and Lapatinib Combination Worth the Added Toxicity? A Discussion of Current Evidence, Recommendations, and Ethical Issues Regarding Dual HER2-Targeted Therapy.Ovarian cancer treatment: The end of empiricism?Diverse drug-resistance mechanisms can emerge from drug-tolerant cancer persister cells.BRAF inhibitors in clinical oncology.A Perspective on Implementing a Quantitative Systems Pharmacology Platform for Drug Discovery and the Advancement of Personalized Medicine.Mapping the molecular determinants of BRAF oncogene dependence in human lung cancer.Molecular pathways: targeting resistance in the androgen receptor for therapeutic benefit Frequent amplification of receptor tyrosine kinase genes in welldifferentiated/ dedifferentiated liposarcoma.Drug synergy screen and network modeling in dedifferentiated liposarcoma identifies CDK4 and IGF1R as synergistic drug targets.Adaptation or selection--mechanisms of castration-resistant prostate cancer.That which does not kill me makes me stronger; combining ERK1/2 pathway inhibitors and BH3 mimetics to kill tumour cells and prevent acquired resistance.

P2860

Q26753162-EF615977-E3A4-4299-90C9-3F541FF50ABF Q27314840-2ED3D29D-2E5E-4269-BFD1-EC495DA237C7 Q27702922-CD729B8D-82E2-4B3B-94F9-03AC33C04E4A Q28044590-7FA9A0CB-1C9C-4924-966F-AB6367526875 Q28088791-E35B1407-3F69-43D1-B5CA-A000CD3A4F2F Q28391909-746A998A-190A-471F-8378-F42CEC056595 Q28538690-5BCC3A28-E8CE-44D4-80A9-292CACB27CAE Q30643770-A0B7C20F-4C34-4EE2-898B-8FA98F572057 Q30666276-17F531DF-039B-4D56-A7DD-645E7081847C Q30684049-E79A7B4C-D30A-439E-B512-A209E178364B Q30982375-B67E5556-1A07-46CE-BAF7-5AAF0F74DF2F Q33725972-16B04088-51DA-4EBD-AF81-08F58FF1BDB1 Q34060618-ACE55FC7-64C3-4F4C-8AE4-3CEC94869F62 Q34364821-C5912264-EDBC-4D44-99C3-7CE03E51FBA4 Q34390313-71E9354C-3781-488B-BD5E-B1C4ED90716D Q34392470-37616CE8-FF9C-449B-B0D7-C0EF20559DEA Q34505037-B3546B64-24FB-45B1-839A-E783308FE089 Q34797680-2EFEAAEA-1F4A-4816-BCB0-40B85E940B53 Q35115383-26CAB187-E462-4C84-8190-F86C71AFB62A Q35159023-92E24B03-264A-4404-9DE6-D0C9779BB9BB Q35159034-D5A01C1C-CBFD-4210-90E7-BA3DB89FA7FC Q35577672-C3D1E7D9-0B19-45E6-A41C-62A1EE1A9C8E Q35590051-F75DA694-C25E-4437-AA77-1F6A0E3FD195 Q35770299-A0153B88-BB95-4852-86A7-776C25B2FF4D Q35823999-80B414C7-1B3C-496B-A862-4526F8D3B28F Q35854877-FB74B7E3-B5DE-4F06-8B51-F54FFDDED43F Q36002378-B66A7EC6-242F-44C4-B9D7-ED1EC9A33FF1 Q36364933-5DAA82DC-05DD-44F8-803B-BD4AE49BB330 Q36366662-050BBEF8-0DC4-4669-80F6-E9BE2B3C1F01 Q36440625-3408877C-B1F1-4818-BDC9-A2D887E47233 Q36554444-10D1DF5F-7625-4821-A994-E729F5A5B1A7 Q36605057-9AEC6099-CCF4-419A-94EC-BFCA815AD5A4 Q36747050-8AA987D5-FC8E-4741-B551-90A6B5D0935B Q37029832-E69A281E-9DDF-4725-A3C1-DE3FB55D5B63 Q37599935-D4A71EF8-74D8-44A7-BE42-2B7A4E8C0E0E Q37620953-7E643352-303A-4F71-BCA1-4D7BCAC7FCCA Q37706527-799B92E4-E529-43CC-B473-67CDC5D80010 Q37723910-A8DC452A-ABAD-4EF5-BFE7-A7868F818720 Q38068116-E46A2F33-82EB-41CC-82EF-88BEBE08D29E Q38104439-72D117F9-96F5-4940-B323-BF9F1252475B

P2860

Converting cancer therapies into cures: lessons from infectious diseases

http://www.wikidata.org/entity/Q36301709

description

2012 nî lūn-bûn

@nan

2012年の論文

@ja

2012年学术文章

@wuu

2012年学术文章

@zh-cn

2012年学术文章

@zh-hans

2012年学术文章

@zh-my

2012年学术文章

@zh-sg

2012年學術文章

@yue

2012年學術文章

@zh

2012年學術文章

@zh-hant

name

Converting cancer therapies into cures: lessons from infectious diseases

@ast

Converting cancer therapies into cures: lessons from infectious diseases

@en

type

label

Converting cancer therapies into cures: lessons from infectious diseases

@ast

Converting cancer therapies into cures: lessons from infectious diseases

@en

prefLabel

Converting cancer therapies into cures: lessons from infectious diseases

@ast

Converting cancer therapies into cures: lessons from infectious diseases

@en

P1433

Q36301709-9E20D8AB-8D5A-4689-A096-D5A9144A3D91

P1476

Q36301709-9A314436-6FFF-4CE7-98C2-0DA4E7A2D569

P2093

Q36301709-21914E85-91E5-4BAC-959B-CB00435265D0

Q36301709-B800CEBC-7DE7-496F-B749-6076E0265026

P2860

Q36301709-0421D7C8-8872-4C75-96F4-81FCDA81272A

Q36301709-0D32E268-630D-4540-A88D-2AF362E22C55

Q36301709-11798689-F2B2-433A-B509-328A697A6992

Q36301709-18168FFA-E9D2-4F94-ABEA-A6830F797674

Q36301709-1C30659C-AE6A-4C6F-BAC9-A3BE09D286F2

Q36301709-1DA3E2B3-33E3-4BD8-AEAD-6BE118DF3B4E

Q36301709-1DDF4B09-0FB5-4560-810B-AC2115B7EB22

Q36301709-29753AC8-AEB7-46BA-9F69-697784D5F696

Q36301709-2E3ACEAC-E248-4FD5-ADBA-1558A1F9F43C

Q36301709-2EA6FD82-EA7D-472E-9E8B-0C56EDA67B6D

P304

Q36301709-81FEF7A8-A6AF-41D7-B96B-DF8BF169514F

P31

Q36301709-25E60DA5-B292-4520-893E-C3533B0B50FA

P356

Q36301709-84338293-E254-4D9A-9931-C108EEFAD958

P407

Q36301709-F6C0264C-1FC3-4C29-91E0-0A48BBDC8BB8

P433

Q36301709-E3F3C68B-8C9C-43C1-8EEB-E5F44D715F80

P478

Q36301709-072931E3-E178-4234-8E15-68166BA73AEC

P577

Q36301709-2C983A08-3AA2-48E8-94DA-CE2B118C67CC

P5875

Q36301709-CF4E0D27-BCDB-42ED-9224-88AB60A23CDE

P698

Q36301709-76469F5F-FD2A-47C6-B89E-616985C002FA

P932

Q36301709-8356FB2A-21BC-4184-A3FB-FE7D672DAC42

P356

J.CELL.2012.02.015

P1433

P1476

Converting cancer therapies into cures: lessons from infectious diseases

@en

P2093

Charles L Sawyers

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

Michael S Glickman

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

P2860

Antitumour activity of MDV3100 in castration-resistant prostate cancer: a phase 1-2 study

Development of a second-generation antiandrogen for treatment of advanced prostate cancer

HIV-1 integrase inhibitor resistance and its clinical implications

MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib

STREPTOMYCIN treatment of pulmonary tuberculosis

hipA, a newly recognized gene of Escherichia coli K-12 that affects frequency of persistence after inhibition of murein synthesis

Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain

Structural mechanism for rifampicin inhibition of bacterial rna polymerase

A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.

MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

P304

1089-1098

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

P31

scholarly article

P356

10.1016/J.CELL.2012.02.015

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

P407

P433

6

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

P478

148

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

P577

2012-03-01T00:00:00Z

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

P5875

221712655

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

P698

22424221

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

P932

3465702

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