16 K Prolactin as an Angiogenic Inhibitor in Breast Cancer
Abstract
Tumors must induce the formation of new blood vessels in order to grow and metastasize. Active angiogenesis results from a dissipation in the balance between angiogenic and angiostatic factors produced by the tumor. In breast cancer, a high density of blood vessels is inversely correlated with patient survival. Suppressing tumor growth by targeting its vasculature thus offers a promising therapeutic strategy. Prolactin (PRL) is a 23 kDa pituitary hormone that has mitogenic, morphogenic, and lactogenic actions on the breast. The role of 23K PRL in breast cancer is controversial, but its N-terminal 16K fragment suppresses proliferation of endothelial cells from several species, inhibits capillary formation in chick embryos, and antagonizes the actions of angiogenic factors. However, the ability of 16K PRL to inhibit tumors in vivo has not been tested. The purpose of this thesis work was to test the following hypotheses: 1)16K PRL suppresses angiogenesis and tumor growth in vivo and 2) locally-produced 23K PRL promotes breast cancer growth. If our hypotheses are correct, treating breast tumors with 16K PRL should inhibit tumor vascularization and subsequent growth. In contrast, 23K PRL should increase breast cancer cell proliferation and tumor growth.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2002
- Accession Number
- ADA407632
Entities
People
- Karen Liby
- Nira Ben-jonsthan
Organizations
- University of Cincinnati