Dual EGFR and BRAF blockade overcomes resistance to vemurafenib in BRAF mutated thyroid carcinoma cells
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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1475-2867
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
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online resource.
- Bibliographic citation
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Dual EGFR and BRAF blockade overcomes resistance to vemurafenib in BRAF mutated thyroid carcinoma cells ; volume:17 ; number:1 ; day:4 ; month:10 ; year:2017 ; pages:1-9 ; date:12.2017
Cancer cell international ; 17, Heft 1 (4.10.2017), 1-9, 12.2017
- Keyword
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Krebs
Onkologie
- Creator
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Notarangelo, Tiziana
- Contributor
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Sisinni, Lorenza
Condelli, Valentina
Landriscina, Matteo
SpringerLink (Online service)
- DOI
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10.1186/s12935-017-0457-z
- URN
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urn:nbn:de:1111-20171129295
- Rights
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Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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15.08.2025, 7:37 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Notarangelo, Tiziana
- Sisinni, Lorenza
- Condelli, Valentina
- Landriscina, Matteo
- SpringerLink (Online service)
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Dual targeting of MAPK and PI3K pathways unlocks redifferentiation of Braf-mutated thyroid cancer organoids
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TERT expression is susceptible to BRAF and ETS-factor inhibition in BRAF V600E /TERT promoter double-mutated glioma
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Targeted therapy with vemurafenib in BRAF(V600E)-mutated anaplastic thyroid cancer
Differential responsiveness to BRAF inhibitors of melanoma cell lines BRAF V600E-mutated
Response to BRAF/MEK Inhibition in A598_T599insV BRAF Mutated Melanoma
BRAF inhibitors in BRAF V600E-mutated ameloblastoma: systematic review of rare cases in the literature
The BRAF-inhibitor PLX4720 inhibits CXCL8 secretion in BRAFV600E mutated and normal thyroid cells: a further anti-cancer effect of BRAF-inhibitors
Metastatic BRAF V600E-Mutated Thyroid Carcinoma: Molecular/Genetic Profiling Brings a New Therapeutic Option
Targeting NG2 relieves the resistance of BRAF-mutant thyroid cancer cells to BRAF inhibitors
Dual targeting of MAPK and PI3K pathways unlocks redifferentiation of Braf-mutated thyroid cancer organoids
Targeting CDK 2 overcomes melanoma resistance against BRAF and Hsp90 inhibitors
RNF43 mutations predict response to anti-BRAF/EGFR combinatory therapies in BRAF V600E metastatic colorectal cancer