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| Status |
Public on Feb 19, 2018 |
| Title |
PHLDA1 mediates drug resistance in receptor tyrosine kinase driven cancer |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by array
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| Summary |
Mutations or amplifications of receptor tyrosine kinases (RTKs) are common in many cancers. Given the emergence of small molecule inhibitors specific to RTKs, these signalling cascades are attractive therapeutic targets. However, compensatory and adaptation mechanisms limit the clinical utility of compounds that target nodes in RTK networks.
Here we show that PHLDA1 down-regulation is critical to acquisition and maintenance of drug resistance in RTK-driven cancer.
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| Overall design |
Total RNA obtained from cell lines resistant to small molecule FGFR inhibitors AZD4547 or PD173074 were profiled together with RNA from the parental cell line (MFE-296).
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| Contributor(s) |
Fearon AE, Grose RP |
| Citation(s) |
29490281 |
| |
| Submission date |
May 05, 2016 |
| Last update date |
Aug 13, 2018 |
| Contact name |
Jun Wang |
| E-mail(s) |
j.a.wang@qmul.ac.uk
|
| Organization name |
Barts Cancer Institute, Queen Mary, London
|
| Street address |
Charterhouse Square
|
| City |
London |
| ZIP/Postal code |
EC1M 6BQ |
| Country |
United Kingdom |
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| Platforms (1) |
| GPL10558 |
Illumina HumanHT-12 V4.0 expression beadchip |
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| Samples (12)
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| Relations |
| BioProject |
PRJNA320773 |
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