Publication Date:
1985-05-10
Description:
The natural history of estrogen-responsive breast cancers often involves a phenotypic change to an estrogen-unresponsive, more aggressive tumor. The human breast cancer cell line, MCF-7, which requires estradiol for tumor formation in vivo and shows growth stimulation in response to estradiol in vitro, is a model for hormone-responsive tumors. The v-rasH onc gene was transfected into MCF-7 cells. The cloned MCF-7ras transfectants, which expressed the v-rasH messenger RNA and v-rasH p21 protein (21,000 daltons), were characterized. In contrast to the parental cell line, MCF-7ras cells no longer responded to exogenous estrogen in culture and their growth was minimally inhibited by exogenous antiestrogens. When tested in the nude mouse, the MCF-7ras cells were fully tumorigenic in the absence of estrogen supplementation. Thus, cells acquiring an activated onc gene can bypass the hormonal regulatory signals that trigger the neoplastic growth of a human breast cancer cell line.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasid, A -- Lippman, M E -- Papageorge, A G -- Lowy, D R -- Gelmann, E P -- New York, N.Y. -- Science. 1985 May 10;228(4700):725-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4039465" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Breast Neoplasms/chemically induced/*genetics
;
Cell Line
;
Cell Transformation, Neoplastic/*chemically induced
;
DNA, Neoplasm/genetics
;
Estrogens/*pharmacology
;
Female
;
Humans
;
Mice
;
Mice, Nude
;
Neoplasms, Experimental/chemically induced/genetics
;
*Oncogenes
;
Pyrrolidines/pharmacology
;
Repetitive Sequences, Nucleic Acid
;
Thiophenes/pharmacology
;
*Transfection
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
Permalink
