TRANSFORMING GROWTH FACTORS FROM HUMAN MAMMARY TISSUES

正在进行实验，以确定 α转化生长因子（AlphaTGF）在正常和恶性肿瘤中的作用 啮齿动物和人类乳腺上皮细胞。 初级 二甲基苯蒽（DMBA）和亚硝基甲基脲（NMU）大鼠 乳腺腺癌的生物学特性 与可移植的DMBA-1和NMU-Ⅱ相比， 癌 此外，在大肠杆菌中可以检测到一种特异的5.0kb mRNA种类， 原发性DMBA和NMU肿瘤在多聚A（+）RNA与 a人和小鼠AlphaTGF cDNA探针，但不在DMBA-I或NMU-II中 肿瘤的 卵巢切除术后， 在原发性DMBA肿瘤中，α TGF-β表达减少， AlphaTGF mRNA的表达。 小鼠乳腺上皮细胞， 用点突变的c-Ha-ras原癌基因转化的NMuMG/rasH细胞， 对EGF的生长促进作用产生抵抗力，因为这些细胞 合成AlphaTGF mRNA的能力增加。 人乳腺 癌细胞系也产生AlphaTGF并具有AlphaTGF mRNA。 在MCF-7细胞中，可以通过以下方式增强α TGF的产生水平： 雌激素 免疫反应性AlphaTGF和AlphaTGF mRNA水平升高 可在约50%的原发性人类乳腺癌中检测到。 α TGF β的存在与肿瘤细胞的增殖之间有很强的正相关性。 mRNA和功能性雌激素受体的存在，在一个子集，这些 肿瘤的

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.