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Contributor Information

  • Name Anne Lykkesfeldt
  • Institute Danish Cancer Society

Tool Details

  • Tool name: T47D/S5 Cell Line
  • Tool type: Cell Lines
  • Tool sub-type: Continuous
  • Parental cell line: T47D
  • Organism: Human
  • Tissue: Breast
  • Cancer type: Breast cancer
  • Disease: Cancer
  • Model: Tumour line
  • Application: T47DS5 cells express ER alpha and progesterone receptor.
  • Description: The T47D/S5 Cell line is the control for the fulvestrant resistant T47D/182R-1 and T47D/182R-2 cell lines. Antiestrogen resistance is a major problem in breast cancer treatment. Therefore, the search for new therapeutic targets and biomarkers for antiestrogen resistance is crucial. T47DS5 cells express ER alpha and progesterone receptor. Passage 155 (AL3043, AL3044)
  • Research area: Cancer; Drug development
  • Production details: T47D/S5 cells grows continuously in presence of 5% fetal calf serum.
  • Cellosaurus ID: CVCL_1D46

  • For Research Use Only

Target Details

  • Target: Oestrogen receptor

Application Details

  • Application: T47DS5 cells express ER alpha and progesterone receptor.


  • Format: Frozen
  • Passage number: Passage 155 (AL3043, AL3044)
  • Growth medium: Phenol red free RPMI 1640 + 5% FCS + glutamax + 8?„?žg Insulin/ml
  • Shipping conditions: Dry ice



  •   Larsen et al. 2015. PLoS One. 10(2):e0118346. PMID: 25706943.
  •   Larsen et al. 2015. BMC Cancer. 15:239. PMID: 25885472.
  •   Aurora kinase B is important for antiestrogen resistant cell growth and a potential biomarker for tamoxifen resistant breast cancer.
  •   SRC drives growth of antiestrogen resistant breast cancer cell lines and is a marker for reduced benefit of tamoxifen treatment.
  •   Thrane et al. 2014. Oncogene. :. PMID: 25362855.
  •   A kinase inhibitor screen identifies Mcl-1 and Aurora kinase A as novel treatment targets in antiestrogen-resistant breast cancer cells.
  •   Kirkegaard et al. 2014. Cancer Lett. 344(1):90-100. PMID: 24513268.
  •   T47D breast cancer cells switch from ER/HER to HER/c-Src signaling upon acquiring resistance to the antiestrogen fulvestrant.