Sensitivity of the hormone dependent MXT-mouse mammary carcinoma to estradiol during tumoral growth. An autoradiographic study

Kiss, Róbert; Paridaens, Robert; Leclercq, G; Danguy, André

doi:10.1016/0277-5379(86)90373-1

Cited by 10 publications

(6 citation statements)

References 12 publications

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“…MXT carcinoma maintains a constant sensitivity to a physiological dose of estrogen during the first 6-7 weeks of its growth after transplantation in intact mice [29]. However, the tumor consists of dependent and independent cancer cell populations and its phenotype can be changed during serial transplantation, under continuous hormonal stimulation, or after estrogen depletion [29,30]. The hormone sensitive variant is a well differentiated, steroid hormone receptor-positive adenocarcinoma, the growth of which is significantly slowed down by ovariectomy, whereas estrogen independent tumors are poorly differentiated or anaptastic and their growth is not influenced by castration [31].…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Growth inhibition of estrogen independent MXT mouse mammary carcinomas in mice treated with an agonist or antagonist of LH-RH, an analog of somatostatin, or a combination

Szepesházi

Milovanović

Lapis

et al. 1992

Breast Cancer Res Tr

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Female BDF1 mice inoculated with MXT (3.2) estrogen independent mouse mammary carcinoma were treated for three weeks with microcapsules of the luteinizing hormone-releasing hormone (LH-RH) agonist [D-Trp6]LH-RH, the antagonist SB-75, the somatostatin analog RC-160, or combinations. The lack of estrogen dependence of the tumor was proved by bilateral surgical ovariectomy, which had no effect. In two experiments, treatment with 25 micrograms/day doses of each analog alone resulted in a significant inhibition of tumor growth as shown by a 40-53% inhibition of tumor volumes, 38-43% decrease in tumor weights, and histological signs of tumor regression. However, the combination of SB-75 or [D-Trp6]LH-RH with somatostatin analog RC-160 caused greater reduction of tumor volume (68 and 61%) or tumor weights (59 and 56%), than single analogs, and histologically the occurrence of apoptosis and decrease in AgNOR numbers was more pronounced in the groups receiving combination therapy. Specific binding sites for [D-Trp6]LH-RH, EGF, and IGF-I were demonstrated in the tumor membranes. The binding capacity of LH-RH receptors was decreased by treatment with the analogs, the greatest down-regulation being caused by combination therapy. A significant decrease in EGF binding capacity was observed after treatment with the LH-RH analogs, alone or especially in combination with somatostatin analog RC-160. The combination of these analogs also caused a reduction in IGF-I receptors. The finding that LH-RH agonists and antagonists and somatostatin analogs inhibit the growth of estrogen independent mammary tumors, and that combinations are more effective than single analogs, might be of practical importance in human breast cancer therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Growth inhibition of estrogen independent MXT mouse mammary carcinomas in mice treated with an agonist or antagonist of LH-RH, an analog of somatostatin, or a combination

Szepesházi

Milovanović

Lapis

et al. 1992

Breast Cancer Res Tr

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“…Among these models, the MXT mouse neoplasm is subcutaneously transplantable and was initially devel oped by Watson et al [3]. It has been shown to contain subpopulations of neoplastic cells which react dif ferently to the same hormonal stimulus [4], MXT cell proliferation is significantly modulated by estradiol (E2) [5][6][7], progesterone (Pg) [8. 9).…”

Section: Introductionmentioning

confidence: 99%

Influence of Fetal Calf Serum in Combination with Pharmacological Doses of Progesterone or Estradiol on Proliferation and Cell Cycle Kinetics of Cultured Mammary Cancer Cells

Kiss

Launoit²,

Danguy³

et al. 1989

Oncology

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We describe an original method to monitor clonal cell density (hyperplasia) and the cell cycle kinetics of neoplastic cells simultaneously. We thus characterize the in vitro influence of two different types of fetal calf serum (FCS), defined as FCS-S and FCS-I, on the progesterone- or estradiol-induced effect on proliferation and cell cycle kinetic parameters of the MXT mouse and MCF-7 human mammary cancer cell lines. The two sera were treated with dextran-coated charcoal. The FCS-S serum showed a stimulatory influence on MXT and MCF-7 growth, whereas FCS-I was devoid of any clear-cut influence. The cells were cultured on glass coverslips, placed in Petri dishes containing either a control or a hormone-added medium, fixed for histology and submitted to the Feulgen reaction, which allows selective and quantitative (stoichiometric) staining of DN A. Proliferation and cell cycle kinetics were analyzed on the same sample of cells by means of the SAMBA 200 cell image processor. Our results show that steroid-mediated effects were dramatically modulated according to the type of serum used. Furthermore, they also show that pharmacological doses of progesterone or estradiol decrease MXT cell growth by at least two different mechanisms: the first is related to cell cycle kinetics, i.e. an inhibition of the cells into the S phase, while the second remains unknown but seems to be cell cycle independent. High dose estradiol, but not progesterone, induced the same inhibitory influence on the MCF-7 cells.

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“…12,24.36 and 48 h after the administration of the hormone or growth factor. This experimen tal schedule was chosen on the basis o f previous ones validated with respect to the MXT mouse mammary carcinoma [20][21][22][23].…”

Section: Experimental Schedule For the Characterization O F The Influmentioning

confidence: 99%

“…basic fibroblast growth factor (bFGF) and bombesin ( B). These two sets of experiments were carried out according to experimental schedules previously validated with respect to the MXT mouse mammary adenocarcinoma [20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Characterization of the Hormone-Sensitivity of Three Human Non-Small-Cell Lung Cancers Grafted onto Nude Mice

et al. 1993

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The in vivo hormone sensitivity of three human NSCLCs grafted onto female nude mice (labelled KLX7, KLX9 and KLX14) was characterized on a dynamic level, i.e. on the level of both the macroscopic growth and the proliferative fraction (PF = percentage of cells in the S + G2 + M Fractions). Two sets of experiments were performed. The first set showed the influence on the macroscopic growth of the NSCLC xenograft of castration performed either before or after tumor grafting. The second set showed the influence of a pulse of 6 different hormones or growth factors on the PF index magnitude recorded 36 h after their administration to the xenograft-bearing mice. These 6 hormones or growth factors were EGF, estradiol-17-beta (E2). gastrin (G), platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF) and bombesin (B). The results show that the KLX7 model grew definitely faster on the nude mice than the other two models. Ovariectomy before or after tumor grafting did not significantly modify the growth pattern of the KLX7 model, while castration before tumor grafting significantly increased the macroscopic growth of both the KLX9 and the KLX14 tumors. In contrast, E2, bFGF, G and B significantly increased the proliferative activity of the KLX7 model 36 h after their administration to the tumor-bearing mice while remaining without any apparent statistically significant effects in both the KLX9 and the KLX14 models.

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Sensitivity of the hormone dependent MXT-mouse mammary carcinoma to estradiol during tumoral growth. An autoradiographic study

Cited by 10 publications

References 12 publications

Growth inhibition of estrogen independent MXT mouse mammary carcinomas in mice treated with an agonist or antagonist of LH-RH, an analog of somatostatin, or a combination

Growth inhibition of estrogen independent MXT mouse mammary carcinomas in mice treated with an agonist or antagonist of LH-RH, an analog of somatostatin, or a combination

Influence of Fetal Calf Serum in Combination with Pharmacological Doses of Progesterone or Estradiol on Proliferation and Cell Cycle Kinetics of Cultured Mammary Cancer Cells

Characterization of the Hormone-Sensitivity of Three Human Non-Small-Cell Lung Cancers Grafted onto Nude Mice

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