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MCF7/164R-4 Cell Line

Invented by Dr Anne Lykkesfeldt from Danish Cancer Society
Invented at Danish Cancer Society

Info

Catalogue Number 152101
Antigen/Gene or Protein Targets Oestrogen receptor
Parental Line MCF7 S0.5
Host Human
Tissue Breast
Disease Keywords Breast cancer, fulvestrant resistant
Model Tumour line
Relevance The MCF7/164R-4 Cell line is a breast cancer cell line resistant to fulvestrant. Treatment with the steroidal antiestrogen fulvestrant has proven effective upon progression on tamoxifen therapy and is now approved for second-line treatment after tamoxifen or aromatase inhibitors. As for tamoxifen treatment of advanced breast cancer, resistance will inevitably occur also for fulvestrant. Clarification of the molecular changes associated with the resistant growth is needed to find targeted treatments to resistant tumour cells and treatments that can inhibit or delay the emergence of resistance.
Production Details The MCF7/164R-4 cell line has been established from a clone of MCF7/S0.5 cells surviving long term growth with the pure steroidal antiestrogen ICI 164,384 in 100 nM concentration. The MCF7/164R-4 cells are also resistant to the pure steroidal antiestrogen fulvestrant (ICI 182,780) and can be maintained continuously in growth medium with 100 nM fulvestrant.
Research Area Cancer, Drug Discovery & Development
Recommended Growing Conditions Phenol red free DMEM/F12 (1:1) supplemented with 1% FCS, Glutamax 2.5 mM and 6 ng/ml insulin. Supplemented with 100nM fulvestrant to maintain resistance.
Notes Upon withdrawal of fulvestrant, the cells express ER alpha, although at a reduced level compared to the parental MCF7/S0.5 cell line. The MCF7/164R-4 cells do not express progesterone receptor. The MCF7/164R-4 cells express increased level of EGFR, phosphorylated EGFR and phosphorylated ErbB3 and reduced level of ErbB4 compared to the parental MCF7/S0.5 cells.

Passage 403 (AL3810, AL3811)
Cellosaurus ID CVCL_1D49

References

There are 8 reference entries for this reagent.

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References: 8 entries

Thrane et al. 2015. Oncogene. 34(32):4199-210. PMID: 25362855.

A kinase inhibitor screen identifies Mcl-1 and Aurora kinase A as novel treatment targets in antiestrogen-resistant breast cancer cells.

Europe PMC ID: 25362855

Sonne-Hansen et al. 2010. Breast Cancer Res Treat. 121(3):601-13. PMID: 19697122.

Breast cancer cells can switch between estrogen receptor alpha and ErbB signaling and combined treatment against both signaling pathways postpones development of resistance.

Europe PMC ID: 19697122

Frogne et al. 2009. Breast Cancer Res Treat. 114(2):263-75. PMID: 18409071.

Activation of ErbB3, EGFR and Erk is essential for growth of human breast cancer cell lines with acquired resistance to fulvestrant.

Europe PMC ID: 18409071

Lykkesfeldt et al. 1995. Int J Cancer. 61(4):529-34. PMID: 7759159.

Human breast cancer cell lines resistant to pure anti-estrogens are sensitive to tamoxifen treatment.

Europe PMC ID: 7759159


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References: 8 entries

Thrane et al. 2015. Oncogene. 34(32):4199-210. PMID: 25362855.

A kinase inhibitor screen identifies Mcl-1 and Aurora kinase A as novel treatment targets in antiestrogen-resistant breast cancer cells.

Sonne-Hansen et al. 2010. Breast Cancer Res Treat. 121(3):601-13. PMID: 19697122.

Breast cancer cells can switch between estrogen receptor alpha and ErbB signaling and combined treatment against both signaling pathways postpones development of resistance.

Frogne et al. 2009. Breast Cancer Res Treat. 114(2):263-75. PMID: 18409071.

Activation of ErbB3, EGFR and Erk is essential for growth of human breast cancer cell lines with acquired resistance to fulvestrant.

Lykkesfeldt et al. 1995. Int J Cancer. 61(4):529-34. PMID: 7759159.

Human breast cancer cell lines resistant to pure anti-estrogens are sensitive to tamoxifen treatment.


Add a reference