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Growth interaction between different tumor populations in human endometrial adenocarcinoma growing in nude mice

Horvath, G; Fernö, Mårten LU ; Baldetorp, Bo LU and Johansson, Maria C LU (1993) In In Vivo 7(6A). p.511-517
Abstract
In these studies of tumor cell growth interaction we have used two tumors differing from each other in sensitivity to estradiol, transplanted to opposite sites of the same nude mice. In the first experiment we found that the growth of an estradiol-sensitive tumor may be delayed by the presence of an estradiol-resistant tumor in the same animal. Although the growth pattern was changed, proliferative activity, as reflected in the S-phase fraction measured by flow cytometry, and the steroid receptor concentrations were unchanged. Increase of circulating estradiol, however, protects the estradiol-sensitive population from this down-regulation of growth. Findings in a second experiment suggest that this growth delay is probably caused by... (More)
In these studies of tumor cell growth interaction we have used two tumors differing from each other in sensitivity to estradiol, transplanted to opposite sites of the same nude mice. In the first experiment we found that the growth of an estradiol-sensitive tumor may be delayed by the presence of an estradiol-resistant tumor in the same animal. Although the growth pattern was changed, proliferative activity, as reflected in the S-phase fraction measured by flow cytometry, and the steroid receptor concentrations were unchanged. Increase of circulating estradiol, however, protects the estradiol-sensitive population from this down-regulation of growth. Findings in a second experiment suggest that this growth delay is probably caused by changes such as decrease in labelling index, increase of non BrdU-incorporating cells in the S-phase, and cell loss in estradiol-sensitive tumors. We concluded that the estradiol-resistant tumor population may secrete some factor(s) acting as endocrine product(s) which may delay the growth of estradiol-sensitive cell populations when the tumors are grown in an estradiol-poor environment. If our model also represents interactions between tumor subpopulations within a single tumor, these findings may have implications for our understanding of the biology of tumor progression in some hormone-related human tumors. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
In Vivo
volume
7
issue
6A
pages
511 - 517
publisher
In vivo
external identifiers
  • pmid:8193269
  • scopus:0027137566
ISSN
0258-851X
language
English
LU publication?
yes
id
055d594f-48b6-4c7b-b396-80ece130c614 (old id 1107008)
date added to LUP
2008-07-30 09:19:36
date last changed
2017-07-30 04:33:02
@article{055d594f-48b6-4c7b-b396-80ece130c614,
  abstract     = {In these studies of tumor cell growth interaction we have used two tumors differing from each other in sensitivity to estradiol, transplanted to opposite sites of the same nude mice. In the first experiment we found that the growth of an estradiol-sensitive tumor may be delayed by the presence of an estradiol-resistant tumor in the same animal. Although the growth pattern was changed, proliferative activity, as reflected in the S-phase fraction measured by flow cytometry, and the steroid receptor concentrations were unchanged. Increase of circulating estradiol, however, protects the estradiol-sensitive population from this down-regulation of growth. Findings in a second experiment suggest that this growth delay is probably caused by changes such as decrease in labelling index, increase of non BrdU-incorporating cells in the S-phase, and cell loss in estradiol-sensitive tumors. We concluded that the estradiol-resistant tumor population may secrete some factor(s) acting as endocrine product(s) which may delay the growth of estradiol-sensitive cell populations when the tumors are grown in an estradiol-poor environment. If our model also represents interactions between tumor subpopulations within a single tumor, these findings may have implications for our understanding of the biology of tumor progression in some hormone-related human tumors.},
  author       = {Horvath, G and Fernö, Mårten and Baldetorp, Bo and Johansson, Maria C},
  issn         = {0258-851X},
  language     = {eng},
  number       = {6A},
  pages        = {511--517},
  publisher    = {In vivo},
  series       = {In Vivo},
  title        = {Growth interaction between different tumor populations in human endometrial adenocarcinoma growing in nude mice},
  volume       = {7},
  year         = {1993},
}