Transgenic Oncogenesis and Genomics Section, Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Building 37, Room 4054, Bethesda, MD 20892, USA.
Transgenic Res. 2011 Apr;20(2):247-59. doi: 10.1007/s11248-010-9406-5. Epub 2010 Jun 12.
The C3(1) component of the rat prostate steroid binding protein has been used to target expression of the SV40 T/t-antigen to the mammary epithelium of mice resulting in pre-neoplastic lesions that progress to invasive and metastatic cancer with molecular features of human basal-type breast cancer. However, there are major differences in the histologic architecture of the stromal and epithelial elements between the mouse and human mammary glands. The rat mammary gland is more enriched with epithelial and stromal components than the mouse and more closely resembles the cellular composition of the human gland. Additionally, existing rat models of mammary cancer are typically estrogen receptor positive and hormone responsive, unlike most genetically engineered mouse mammary cancer models. In an attempt to develop a mammary cancer model that might more closely resemble the pathology of human breast cancer, we generated a novel C3(1)/SV40 T/t-antigen transgenic rat model that developed progressive mammary lesions leading to highly invasive adenocarcinomas. However, aggressive tumor development prevented the establishment of transgenic lines. Characterization of the tumors revealed that they were primarily estrogen receptor and progesterone receptor negative, and either her2/neu positive or negative, resembling human triple-negative or Her2 positive breast cancer. Tumors expressed the basal marker K14, as well as the luminal marker K18, and were negative for smooth muscle actin. The triple negative phenotype has not been previously reported in a rat mammary cancer model. Further development of a C3(1)SV40 T/t-antigen based model could establish valuable transgenic rat lines that develop basal-type mammary tumors.
大鼠前列腺类固醇结合蛋白的 C3(1) 成分已被用于将 SV40 T/t-抗原的表达靶向到小鼠的乳腺上皮细胞,导致出现具有人类基底型乳腺癌分子特征的前肿瘤病变,进而进展为侵袭性和转移性癌症。然而,小鼠和人乳腺的基质和上皮成分的组织学结构存在很大差异。大鼠乳腺比小鼠更富含上皮和基质成分,并且更接近人类腺体的细胞组成。此外,现有的大鼠乳腺癌模型通常是雌激素受体阳性和激素反应性的,这与大多数基因工程小鼠乳腺癌模型不同。为了开发一种更类似于人类乳腺癌病理学的乳腺癌模型,我们生成了一种新型的 C3(1)/SV40 T/t-抗原转基因大鼠模型,该模型发展出进行性乳腺病变,导致高度侵袭性的腺癌。然而,侵袭性肿瘤的发展阻止了转基因系的建立。肿瘤的特征表明它们主要是雌激素受体和孕激素受体阴性,并且要么是 her2/neu 阳性,要么是阴性,类似于人类三阴性或 Her2 阳性乳腺癌。肿瘤表达基底标志物 K14,以及腔标志物 K18,并且平滑肌肌动蛋白呈阴性。三重阴性表型以前尚未在大鼠乳腺癌模型中报道过。进一步开发基于 C3(1)SV40 T/t-抗原的模型可以建立具有发展基底型乳腺肿瘤的有价值的转基因大鼠系。