Growth interaction between different tumor populations in human endometrial adenocarcinoma growing in nude mice
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1107008
- author
- Horvath, G ; Fernö, Mårten LU ; Baldetorp, Bo LU and Johansson, Maria C LU
- organization
- publishing date
- 1993
- 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
- 2016-04-01 16:05:25
- date last changed
- 2021-01-03 07:18:51
@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}},
}