MCF-7
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 due to metastatic breast cancer.[5] Her cells were the source of much of current knowledge about breast cancer.[2][6] 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.[7] MCF-7 has potential for new drug development, including anti-cancer drug testing, anti-estrogen drug resistance and antiplatelet drug development.[8]
Characteristics of MCF-7 cells
[edit]MCF-7 cells have the following characteristics:[2][6][7][9][10][11]
- Primary tumor (invasive breast ductal carcinoma)
- Originate from pleural effusion
- Estrogen receptors present[12]
- Proliferative response to estrogens
- Presence of progesterone receptors
- Contains 17β-estradiol-binding protein[8]
- 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[13]
- 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.[14]
PIK3CA helical mutations were identified in MCF-7,[15] but with low AKT activation.[16]
References
[edit]- ^ Lee, Adrian V.; et al. (1 July 2015). "MCF-7 Cells—Changing the Course of Breast Cancer Research and Care for 45 Years". Journal of the National Cancer Institute. 107 (7): djv073. doi:10.1093/jnci/djv073. PMID 25828948.
- ^ a b c Soule, HD; Vazquez J; Long A; Albert S; Brennan M. (1973). "A human cell line from a pleural effusion derived from a breast carcinoma". Journal of the National Cancer Institute. 51 (5): 1409–1416. doi:10.1093/jnci/51.5.1409. PMID 4357757.
- ^ http://www.cancer.gov "NCI Cancer Bulletin for April 29, 2008 - National Cancer Institute". Archived from the original on 2010-05-27. Retrieved 2010-04-28. Retrieved on 2010-04-28
- ^ Glodek, Cass, Ph.D., "A History of the Michigan Cancer Foundation, the Beginnings & Growth of Detroit's Anticancer Movement," 1990, page 68, Michigan Cancer Foundation, Detroit.
- ^ Lee, A. V.; Oesterreich, S.; Davidson, N. E. (2015-03-31). "MCF-7 Cells--Changing the Course of Breast Cancer Research and Care for 45 Years". JNCI Journal of the National Cancer Institute. 107 (7): djv073. doi:10.1093/jnci/djv073. ISSN 0027-8874.
- ^ a b Levenson, AS; Jordan VC. (1997). "MCF-7: the first hormone-responsive breast cancer cell line". Cancer Research. 57 (15): 3071–3078. PMID 9242427.
- ^ a b Lacroix, M; Leclercq G. (2004). "Relevance of breast cancer cell lines as models for breast tumours: an update". Breast Research and Treatment. 83 (3): 249–289. doi:10.1023/B:BREA.0000014042.54925.cc. PMID 14758095. S2CID 207628369.
- ^ a b Comşa, Şerban; Cîmpean, Anca Maria; Raica, Marius (2015-06-01). "The Story of MCF-7 Breast Cancer Cell Line: 40 years of Experience in Research". Anticancer Research. 35 (6): 3147–3154. ISSN 0250-7005.
- ^ Ross, DT; Perou CM. (2001). "A comparison of gene expression signatures from breast tumors and breast tissue derived cell lines". Disease Markers. 17 (2): 99–109. doi:10.1155/2001/850531. PMC 3850857. PMID 11673656.
- ^ Charafe-Jauffret, E; Ginestier C; Monville F; Finetti P; Adelaide J; Cervera N; Fekairi S; Xerri L; Jacquemier J; Birnbaum D; Bertucci F. (2006). "Gene expression profiling of breast cell lines identifies potential new basal markers". Oncogene. 25 (15): 2273–2284. doi:10.1038/sj.onc.1209254. PMID 16288205.
- ^ Lacroix, M; Toillon RA; Leclercq G. (2006). "p53 and breast cancer, an update". Endocrine-Related Cancer. 13 (2). Bioscientifica: 293–325. doi:10.1677/erc.1.01172. PMID 16728565.
- ^ Fanelli, Alex (2016). "MCF-7 Cells: human breast adenocarcinoma cell line". Retrieved 3 December 2017.
- ^ Sflomos, George; Dormoy, Valerian; Metsalu, Tauno; Jeitziner, Rachel; Battista, Laura; Scabia, Valentina; Raffoul, Wassim; Delaloye, Jean-Francois; Treboux, Assya (2016). "A Preclinical Model for ERα-Positive Breast Cancer Points to the Epithelial Microenvironment as Determinant of Luminal Phenotype and Hormone Response". Cancer Cell. 29 (3): 407–422. doi:10.1016/j.ccell.2016.02.002. PMID 26947176.
- ^ Mansara, Prakash P.; Deshpande, Rashmi A.; Vaidya, Milind M.; Kaul-Ghanekar, Ruchika (1 September 2015). "Differential Ratios of Omega Fatty Acids (AA/EPA+DHA) Modulate Growth, Lipid Peroxidation and Expression of Tumor Regulatory MARBPs in Breast Cancer Cell Lines MCF7 and MDA-MB-231". PLOS ONE. 10 (9): e0136542. Bibcode:2015PLoSO..1036542M. doi:10.1371/journal.pone.0136542. ISSN 1932-6203. PMC 4556657. PMID 26325577.
- ^ Cosmic. "COSMIC: Sample overview for 1289391". cancer.sanger.ac.uk. Retrieved 2017-05-10.
- ^ Vasudevan, Krishna M.; Barbie, David A.; Davies, Michael A.; Rabinovsky, Rosalia; McNear, Chontelle J.; Kim, Jessica J.; Hennessy, Bryan T.; Tseng, Hsiuyi; Pochanard, Panisa (2009-07-07). "AKT-independent signaling downstream of oncogenic PIK3CA mutations in human cancer". Cancer Cell. 16 (1): 21–32. doi:10.1016/j.ccr.2009.04.012. ISSN 1878-3686. PMC 2752826. PMID 19573809.
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