#152101

MCF7/164R-4 Cell Line

Cat. #152101

MCF7/164R-4 Cell Line

Cat. #: 152101

Sub-type: Continuous

Unit size: 1x10^6 cells / vial

Availability: 10-12 weeks

Organism: Human

Tissue: Breast

Disease: Cancer

Model: Tumour line

£800.00

This fee is applicable only for non-profit organisations. If you are a for-profit organisation or a researcher working on commercially-sponsored academic research, you will need to contact our licensing team for a commercial use license.

Contributor

Inventor: Anne Lykkesfeldt

Institute: Danish Cancer Society, Denmark

Primary Citation: Lykkesfeldt et al. 1995. Int J Cancer. 61(4):529-534. PMID: 7759159.

Tool Details
Target Details
Applications
Handling
References

Tool Details

*FOR RESEARCH USE ONLY (for other uses, please contact the licensing team)

  • Name: MCF7/164R-4 Cell Line
  • Alternate name: MCF-7/164R-4; 164R-4
  • Cancer: Breast cancer
  • Cancers detailed: Breast cancer;Fulvestrant resistant
  • Research fields: Cancer;Drug development
  • Tool sub type: Continuous
  • Parental cell: MCF7 S0.5
  • Organism: Human
  • Gender: Female
  • Tissue: Breast
  • Disease: Cancer
  • Model: Tumour line
  • Description: The MCF7/164R-4 cell line is a breast cancer cell line resistant to fulvestrant (Faslodex). The MCF7/164R-4 cell line is a human breast cancer cell line established from MCF7. The cellular classification is epithelial, and their shape is polygonal. The passage number of this cell line is 403 (AL3810, AL3811). 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.
  • Application: Investigation of signalling pathways involved in fulvestrant 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.
  • Additional 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.
  • Cellosaurus id: CVCL_1D49

Target Details

  • Target: Oestrogen receptor

Applications

  • Application: Investigation of signalling pathways involved in fulvestrant resistance
  • Application 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)

Handling

  • Format: Frozen
  • Passage number: Passage 403 (AL3810, AL3811)
  • Growth medium: 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.
  • Temperature: 37° C
  • Atmosphere: 5% CO2
  • Unit size: 1x10^6 cells / vial
  • Shipping conditions: Dry ice

References

  • Thrane et al. 2014. Oncogene. 34(32):4199-4210. PMID: 25362855.
  • Sonne-Hansen et al. 2010. Breast Cancer Res Treat. 121(3):601-613. PMID: 19697122.
  • Frogne et al. 2008. Breast Cancer Res Treat. 114(2):263-275. PMID: 18409071.
  • Lykkesfeldt et al. 1995. Int J Cancer. 61(4):529-534. PMID: 7759159.