Preliminary Investigation of the Role of Cellular Immunity in Estrous Cycle Modulation of Post-Resection Breast Cancer Spread
Abstract
It is proposed to use this breast cancer of C(3)H mice to determine whether or not hormone dependent immunocyte suppression is, in part, responsible for the mammalian fertility cycle modulation of the capacity of the cancer to spread after attempted surgical cure. These studies will determine which female sex steroid hormone(s) control(s) post resection metastatic spread. They will determine whether estrogen and/or progesterone affect depth and duration of surgery-induced natural killer cell activity suppression, numbers of NK and/or helper T and/or suppressor T cells following tumor resection. They will determine whether deleting specific immune cell types by the in vivo administration of antibodies directed against these cell types (asialo GM(1)+CD(4)+, CD(8) abrogate the estrous cycle and sex hormone specific modulation of the post resection pattern of metastatic cancer spread. The results of the proposed studies, if negative, will exclude sex hormone modulation of cellular immune function as the most likely or important cause of the observed estrous cycle dependence of post surgical cancer spread. If these results demonstrate that NK and/or T helper and/or T suppressor cells are essential prerequisites of sex hormone modulation of post resection cancer spread, they will raise the hypothetical value of both neoadjuvant sex hormone and other specific cellular immune enhancement strategies prior to and/or immediately following primary breast cancer resection in order to potentially improve breast cancer cure frequency.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 1999
- Accession Number
- ADA388611
Entities
People
- William J. Hrushesky