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人类乳腺癌的生长调节是通过调控生长因子的分泌来实现的。

Growth regulation of human breast carcinoma occurs through regulated growth factor secretion.

作者信息

Lippman M E, Dickson R B, Gelmann E P, Rosen N, Knabbe C, Bates S, Bronzert D, Huff K, Kasid A

机构信息

Medical Breast Cancer Section, National Cancer Institute, Bethesda, Maryland 20892.

出版信息

J Cell Biochem. 1987 Sep;35(1):1-16. doi: 10.1002/jcb.240350102.

DOI:10.1002/jcb.240350102
PMID:3312244
Abstract

We describe studies on human breast cancer in which it is shown that specific growth factors (IGF-I, TGF alpha, PDGF) are secreted by human breast cancer cells and likely to be involved in tumor growth and progression. These activities are regulated by estradiol in hormone-dependent breast cancer and secreted constitutively by hormone-independent cells. These growth factor activities can induce the growth of hormone-dependent cells in vivo in athymic nude mice. Hormone-dependent breast cancer cells also secrete TGF beta, a growth-inhibitory substance, when treated with antiestrogens. TGF beta functions as a negative autocrine growth regulator and is responsible for some of the growth-inhibitory effects of antiestrogens.

摘要

我们描述了对人类乳腺癌的研究,研究表明特定生长因子(胰岛素样生长因子-I、转化生长因子α、血小板衍生生长因子)由人类乳腺癌细胞分泌,且可能参与肿瘤生长和进展。在激素依赖性乳腺癌中,这些活性受雌二醇调节,而在激素非依赖性细胞中则持续分泌。这些生长因子活性可在无胸腺裸鼠体内诱导激素依赖性细胞生长。当用抗雌激素处理时,激素依赖性乳腺癌细胞也会分泌一种生长抑制物质——转化生长因子β。转化生长因子β作为一种负性自分泌生长调节因子,介导了抗雌激素的一些生长抑制作用。

相似文献

1
Growth regulation of human breast carcinoma occurs through regulated growth factor secretion.人类乳腺癌的生长调节是通过调控生长因子的分泌来实现的。
J Cell Biochem. 1987 Sep;35(1):1-16. doi: 10.1002/jcb.240350102.
2
Effect of estrogens and antiestrogens on growth of human breast cancer cells in athymic nude mice.雌激素和抗雌激素对无胸腺裸鼠体内人乳腺癌细胞生长的影响。
Cancer Res. 1985 Feb;45(2):584-90.
3
Growth regulatory peptide production by human breast carcinoma cells.人乳腺癌细胞产生的生长调节肽
J Steroid Biochem. 1988;30(1-6):53-61. doi: 10.1016/0022-4731(88)90076-3.
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Evidence for a novel pituitary factor that potentiates the mitogenic effect of estrogen in human breast cancer cells.一种新型垂体因子增强雌激素对人乳腺癌细胞促有丝分裂作用的证据。
Cancer Res. 1985 Jul;45(7):3083-9.
5
Transforming growth factor beta 1 can induce estrogen-independent tumorigenicity of human breast cancer cells in athymic mice.转化生长因子β1可诱导人乳腺癌细胞在无胸腺小鼠体内产生雌激素非依赖性致瘤性。
Cell Growth Differ. 1993 Mar;4(3):193-201.
6
Required presence of both estrogen and pituitary factors for the growth of human breast cancer cells in athymic nude mice.在无胸腺裸鼠中,人乳腺癌细胞生长需要雌激素和垂体因子同时存在。
Cancer Res. 1981 Feb;41(2):546-51.
7
Enhanced invasion and tumor growth of fibroblast growth factor 8b-overexpressing MCF-7 human breast cancer cells.成纤维细胞生长因子8b过表达的MCF-7人乳腺癌细胞侵袭性增强及肿瘤生长加快。
Cancer Res. 2001 May 15;61(10):4229-37.
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Estrogens regulate production of specific growth factors in hormone-dependent human breast cancer.
J Lab Clin Med. 1987 Mar;109(3):230-5.
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Alterations in transforming growth factor-alpha and -beta production and cell responsiveness during the progression of MCF-7 human breast cancer cells to estrogen-autonomous growth.在MCF-7人乳腺癌细胞向雌激素自主生长进展过程中转化生长因子-α和-β产生及细胞反应性的改变。
Cancer Res. 1994 Nov 15;54(22):5867-74.
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Human breast carcinoma desmoplasia is PDGF initiated.人类乳腺癌的促纤维增生是由血小板衍生生长因子引发的。
Oncogene. 2000 Sep 7;19(38):4337-45. doi: 10.1038/sj.onc.1203785.

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Tumour necrosis factor-alpha and transforming growth factor-beta are significantly associated with better prognosis in non-small cell lung carcinoma: putative relation with BCL-2-mediated neovascularization.肿瘤坏死因子-α和转化生长因子-β与非小细胞肺癌的较好预后显著相关:与BCL-2介导的新生血管形成的假定关系。
Br J Cancer. 2000 Aug;83(4):480-6. doi: 10.1054/bjoc.2000.1345.
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Human breast cancer cell lines as models of growth regulation and disease progression.作为生长调控和疾病进展模型的人乳腺癌细胞系
J Mammary Gland Biol Neoplasia. 1996 Jan;1(1):111-21. doi: 10.1007/BF02096306.
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IGF-II mRNA and protein are expressed in the stroma of invasive breast cancers: an in situ hybridization and immunohistochemistry study.
Breast Cancer Res Treat. 1996;41(1):43-50. doi: 10.1007/BF01807035.
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Changes in expression of transforming growth factor beta mRNA isoforms in patients undergoing tamoxifen therapy.
Br J Cancer. 1996 Aug;74(3):474-8. doi: 10.1038/bjc.1996.385.
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