TRANSFORMING GROWTH FACTORS FROM HUMAN MAMMARY TISSUES

正在进行实验，以确定细菌的分布和作用 α-转化生长因子在正常和恶性肿瘤中的表达 啮齿动物和人乳腺上皮细胞。主要 二甲基苯(α-)菲(DMBA)和亚硝基甲基脲(NMU)大鼠 从生物学角度看，乳腺癌的发病率要高出三到七倍。 比可移植的DMBA-I和NMU-II更具活性和免疫活性的α-TGFs 癌症。此外，还可以检测到特定的5.0kb的mrna物种。 Poly A(+)RNA与NMU杂交后的原发DMBA和NMU肿瘤 人和小鼠α-转化生长因子的cDNA探针，但不在DMBA-I或NMU-II中 肿瘤。卵巢摘除后，血浆中的 原发性DMBA肿瘤中的α-TGFs，在此之前 α-转化生长因子基因的表达。小鼠乳腺上皮细胞 用点突变的c-Ha-ras原癌基因转化NMuMG/Rash细胞， 对EGF的促生长作用产生抵抗力，因为这些细胞 合成α-转化生长因子基因的能力增强。人类乳房 癌细胞株也产生α-转化生长因子，并具有α-转化生长因子mRNA。 在MCF-7细胞中，α-转化生长因子的产生水平可以通过 雌激素。α-转化生长因子和α-转化生长因子基因表达水平升高 在大约50%的原发人类乳腺癌中可以检测到。 在阿尔法转化生长因子的存在之间存在强烈的正相关 MRNA和功能性雌激素受体在这些细胞中的存在 肿瘤。

Experiments are being conducted to determine the distribution and role of alpha transforming growth factors (AlphaTGFs) in normal and malignant rodent and human mammary epithelial cells. Primary dimethylbenz(Alpha)anthracene (DMBA) and nitrosomethylurea (NMU) rat mammary adenocarcinomas possess three to seven-fold more biologically active and immunoreactive AlphaTGFs than transplantable DMBA-I and NMU-II carcinomas. Moreover, a specific 5.0 kb mRNA species could be detected in the primary DMBA and NMU tumors following hybridization of poly A(+) RNA to a human and mouse AlphaTGF cDNA probes but not in the DMBA-I or NMU-II tumors. Ovariectomy produced a two to three-fold decrease in the level of AlphaTGFs in the primary DMBA tumors which was preceeded by a loss in the expression of AlphaTGF mRNA. Mouse mammary epithelial which have been transformed with a point-mutated c-Ha-ras proto-oncogene, NMuMG/rasH cells, become resistant to the growth promoting effects of EGF because these cells have an increased capacity to synthesize AlphaTGF mRNA. Human breast cancer cell lines are also producing AlphaTGF and possess AlphaTGF mRNA. In MCF-7 cells, the level of production of AlphaTGF can be enhanced by estrogens. Elevated levels of immunoreactive AlphaTGF and AlphaTGF mRNA can be detected in approximately 50% of primary human breast carcinomas. There is a strong positive correlation between the presence of AlphaTGF mRNA and the presence of functional estrogen receptors in a subset of these tumors.