Growth factor receptors and the progression of breast cancer.
Interference with autocrine or paracrine loops offers a potential means of treatment of tumors which currently lack effective therapies. Hormonally responsive breast cancers generally respond to treatment with antiestrogens but a frequent occurrence is an outgrowth of populations of tumor cells that are no longer dependent on estrogen for growth. If the acquisition of the ability to constitutively express growth factors or growth factor receptors is associated with this form of tumor progression, identification of the growth factors and their receptors having the capability of reducing the dependence on estrogen for growth is an important first step in the design of strategies aimed at interfering with their function. Experimental systems employing transfection with eukaryotic expression vectors are described that are designed to test the hypothesis that overexpression of epidermal growth factor receptor or the related protein C-ERB-B2 may confer an increased growth rate under conditions of estrogen deprivation. The transfected cells are also being used to explore the molecular mechanisms underlying the regulation of epidermal growth factor receptor expression by estrogen.
Kern
F G
FG
Vincent T. Lombardi Cancer Research Center, Georgetown University Medical Center, Washington, DC 20007.
Cheville
A L
AL
Liu
Y L
YL
D000818:Animals; D001943:Breast Neoplasms / Q000235:genetics / Q000473:pathology / Q000648:ultrastructure*; D002285:Carcinoma, Intraductal, Noninfiltrating / Q000235:genetics / Q000473:pathology / Q000648:ultrastructure*; D002455:Cell Division / Q000502:physiology; D066246:ErbB Receptors / Q000235:genetics / Q000502:physiology*; D005260:Female; D015870:Gene Expression; D006133:Growth Substances / Q000502:physiology; D006801:Humans
D006133:Growth Substances; D066246:ErbB Receptors