Accession Number : ADA336805
Title : Vasopressin and Breast Cancer
Descriptive Note : Final rept 1 Sep 94-31 Aug 97
Corporate Author : DARTMOUTH COLL HANOVER NH
Personal Author(s) : Fay, Michael J.
PDF Url : ADA336805
Report Date : AUG 1997
Pagination or Media Count : 25
Abstract : Previously we demonstrated expression of vasopressin and oxytocin gene-related products in breast cancer, but not benign fibrocystic breast disease, using the technique of immunohistochemistry. In vitro and in vivo studies suggest that both of these hormones have growth regulatory effects on breast cancer cells. Therefore, these hormones may represent autocrine/paracrine and/or endocrine factors for breast cancer. However, the receptors through which these hormones act and the effector mechanisms involved with cancer cell growth are not known. Using RT-PCR we demonstrated the expression of mRNA for the 4 known vasopressin receptors, including the novel VACM receptor, and the oxytocin receptor. During this last year we cloned VACM from cancer cells (NCI-H146 and MCF7), using the technique of 5' and 3'-RACE. The isolated clones contains an open reading frame of 2,343 nucleotides and encode a protein of 781 amino acids. Obtaining the cDNA for VACM will aid in determining the role of this receptor in breast cancer pathophysiology. In addition we have demonstrated vasopressin-induced calcium mobilization in breast cancer cells, and preliminary results indicate vasopressin-induced activation of MAPK. The studies suggest that vasopressin may stimulate cancer cell growth through VACM, V1a, or V1b vasopressin receptors by activating the MAP kinase cascade.
Descriptors : *PITUITARY HORMONES, *BREAST CANCER, PROTEINS, ISOLATION, DEOXYRIBONUCLEIC ACIDS, IN VITRO ANALYSIS, GENES, CLONES, IN VIVO ANALYSIS, PATHOPHYSIOLOGY, CELLS(BIOLOGY), RIBONUCLEIC ACIDS, ANTIGENS, MAMMARY GLANDS, GROWTH(PHYSIOLOGY), IMMUNOCHEMISTRY, HISTOCHEMISTRY.
Subject Categories : Biochemistry
Genetic Engineering and Molecular Biology
Anatomy and Physiology
Medicine and Medical Research
Distribution Statement : APPROVED FOR PUBLIC RELEASE