MCF-7 is a breast cancer cell line isolated in 1970 from a 69-year-old White woman.^[1] MCF-7 is the acronym of Michigan Cancer Foundation-7, referring to the institute in Detroit where the cell line was established in 1973 by Herbert Soule and co-workers.^[2] The Michigan Cancer Foundation is now known as the Barbara Ann Karmanos Cancer Institute.^[3]

Prior to MCF-7, it was not possible for cancer researchers to obtain a mammary cell line that was capable of living longer than a few months.^[4]

The patient, Frances Mallon died in 1970. Her cells were the source of much of current knowledge about breast cancer.^[2][5] At the time of sampling, she was a nun in the convent of Immaculate Heart of Mary in Monroe, Michigan under the name of Sister Catherine Frances.

MCF-7 and two other breast cancer cell lines, named T-47D and MDA-MB-231, account for more than two-thirds of all abstracts reporting studies on mentioned breast cancer cell lines, as concluded from a Medline-based survey.^[6]

MCF-7 cells have the following characteristics:^{[2][5][6][7][8][9]}

• Primary tumor (invasive breast ductal carcinoma)
• Originate from pleural effusion
• Estrogen receptors present^[10]
• Proliferative response to estrogens
• Presence of progesterone receptors
• Cannot have ERBB2 gene amplification (with Her2/neu protein overexpression)
• Tumorigenic in mice but only with estrogen supplementation if engrafted into the subcutaneous fat or mammary fat pad
• Tumorigenic in mice without estrogen supplementation if engrafted intraductally^[11]
• Luminal epithelial phenotype

This cell line retained several characteristics of differentiated mammary epithelium, including the ability to process estradiol via cytoplasmic estrogen receptors and the capability of forming domes.^{[citation needed]}

Tumor necrosis factor alpha (TNF alpha) inhibits the growth of MCF-7 breast cancer cells. Treatment with anti-estrogens can modulate the secretion of insulin-like growth factor binding proteins. Omega-3 and 6 fatty acids such as EPA, DHA and AA has been reported to inhibit MCF-7 cell line growth and proliferation.^[12]

PIK3CA helical mutations were identified in MCF-7,^[13] but with low AKT activation.^[14]