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Status |
Public on Jan 19, 2012 |
Title |
Co-targeting of the PI3K pathway improves the response of BRCA1 deficient breast cancer cells to PARP1 inhibition |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by array
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Summary |
Although pre-clinical and clinical studies on PARP1 inhibitors, alone and in combination with DNA-damaging agents, show promising results, further ways to improve and broaden the scope of application of this therapeutic approach are warranted. To this end, we have investigated the possibility of improving the response of BRCA1 mutant breast cancer cells to PARP1 inhibition by co-targeting the PI3K pathway. The human breast cancer cell line MDA-MB-436, which lacks the expression of both BRCA1 and PTEN, was treated with the PARP1 inhibitor AG014699 as a single agent or in combination with the PI3K inhibitor LY294002 for 7 days.
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Overall design |
The human breast cancer cell line MDA-MB-436 was treated with the PARP1 inhibitor AG014699 as a single agent or in combination with the PI3K inhibitor LY294002 for 7 days. All treatments were performed in triplicates. Total RNA was extracted hybridized onto the Illumina HumanHT-12 v4.0 microarray platform.
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Contributor(s) |
Kimbung S, Biskup E, Johansson I, Aaltonen K, Ottosson-Wadlund A, Gruvberger-Saal S, Cunliffe H, Fadeel B, Loman N, Berglund P, Hedenfalk I |
Citation(s) |
22266096 |
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Submission date |
Jan 03, 2012 |
Last update date |
Aug 13, 2018 |
Contact name |
Ida Johansson |
E-mail(s) |
[email protected]
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Organization name |
Lund University
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Department |
Oncology
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Street address |
Department of Oncology Clinical Sciences Lund University BMC C13
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City |
Lund |
ZIP/Postal code |
SE-22184 |
Country |
Sweden |
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Platforms (1) |
GPL10558 |
Illumina HumanHT-12 V4.0 expression beadchip |
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Samples (15)
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Relations |
BioProject |
PRJNA150257 |