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|Antigen/Gene or Protein Targets||Breast cancer anti-estrogen resistance genes|
|Disease Keywords||Mammary ductal carcinoma, estrogen independent|
Breast cancer is widely and effectively treated with endocrine treatment. However, in advanced disease cases the tumours will eventually progress into an estrogen-independent and therapy-resistant phenotype. Retroviral insertion mutagenesis was used to generate this cell line in order to elucidate the molecular mechanisms underlaying endocrine therapy failure. Using this method the main genes conferring estrogen independence in human breast cancer cells where identified. Genes located in the immediate proximity of the retroviral integration site were characterised. Out of 15 candidate breast cancer antigen resistance (BCAR) genes, seven (AKT1, AKT2, BCAR1, BCAR3, EGFR2, GRB7 and TRERF1/BCAR2) were shown to directly underline estrogen independence.
This cell line is part of a panel of 71 cell lines (Cat No 154549-154619) plus the parental (Cat No 154547).
These cell lines are a powerful tool for studying the molecular and cellular mechanisms of breast tumour progression, therapy resistance and to test the effectiveness of novel drugs to combat different modes of anti-estrogen insensitivity.
|Production Details||ZR-75-1 cells were infected with amphotropic, defective murine retrovirus and plated in medium containing 1uM of 4-hydroxy-tamoxifen. Within 5 weeks after the start of selection proliferating colonies were individually picked and expanded to stable cell lines|
|Research Area||Cancer, Drug Discovery & Development|
|Recommended Growing Conditions||RPMI 1640 medium supplemented with 10% heat-inactivated bovine calf serum (RBCS)|
|Notes||Cell line with unique integration events in the following genes, of which one is the most likely cause for estrogen independence: KPNA3 and AP2S1|
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