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pubmed-article:1408142pubmed:abstractTextBreast cancer development is associated with several genetic abnormalities. Loss of heterozygosity in the short arm of chromosome 11 has been observed in 30% of tumors. We found homozygosity at five chromosome 11 polymorphic loci in genomic DNA of the MCF-7 breast carcinoma cell line, suggesting a possible loss of one chromosome 11. We have studied the transformed and tumorigenic phenotypes of MCF-7 cells following introduction of a normal human chromosome 11 via microcell fusion. MCF-7/H11 cell hybrids, containing chromosome 11, showed in vitro characteristics similar to the parental cell line. However, tumorigenicity in athymic mice was completely suppressed. Since tumor formation by MCF-7 cells is estrogen dependent, we have analysed the expression of the estrogen receptor and of the estrogen-activated gene pS2. No difference was detected between the parental MCF-7 cells and the derived chromosome 11 cell hybrids, indicating that the mechanism of MCF-7 tumor suppression by chromosome 11-associated functions does not directly involve the estrogen/estrogen receptor molecular pathway.lld:pubmed
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pubmed-article:1408142pubmed:articleTitleSuppression of tumorigenesis by the breast cancer cell line MCF-7 following transfer of a normal human chromosome 11.lld:pubmed
pubmed-article:1408142pubmed:affiliationInterdepartment Centre for Cancer Research, University of Ferrara, Italy.lld:pubmed
pubmed-article:1408142pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:1408142pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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