Nabarra Bernadette, Pontoux Christiane, Godard Cecile, Osborne-Pellegrin Mary, Ezine Sophie
U 591 INSERM, Centre Hospitalier Universitaire-NECKER, Paris, France.
Int J Exp Pathol. 2005 Dec;86(6):397-413. doi: 10.1111/j.0959-9673.2005.00451.x.
Using several techniques, we have assessed morphological characteristics of a malignant thymic tumour in SV12 transgenic (Tg) mice expressing SV40 T and t antigens under control of an L-PK promoter. We describe the development of a carcinoma originating from thymic hyperplasia and followed by the formation of a benign tumour composed chiefly of medullary epithelial cells expressing the transgene and of lymphocytes, a pathology very rarely reported in mice. Our study of the SV12 Tg mice represents the first description of a model of a pure malignant thymic tumour associated with extensive angiogenesis maintained in numerous descendants. The formation of a large tumoral neovascular network, observed here, has never been described in human and/or experimental thymic tumours. Tumoral transformation and angiogenesis are demonstrated by immunolabelling with antibodies against various cytokeratins (CKs) of different molecular weights, vascular endothelial cell markers and VEGF/receptor-2 (Flk-1) present on the neovascular endothelial cells. Different points raised by the originality of this model are discussed. These include the medullary nature of the cells expressing the SV40 transgene and their relationship with the tumoral development. The subset of different molecular weight CK components and their modifications are also considered, as well as the presence of type IV epithelial cells, progenitors of medullary epithelial cells. Finally, the cell signals involved in angiogenesis and the possible action of an angiogenic factor, probably secreted by the tumoral cells themselves, are discussed.
我们运用多种技术,评估了在L-PK启动子控制下表达SV40大T抗原和小t抗原的SV12转基因(Tg)小鼠中恶性胸腺肿瘤的形态学特征。我们描述了一种起源于胸腺增生的癌的发展过程,随后形成了一个主要由表达转基因的髓质上皮细胞和淋巴细胞组成的良性肿瘤,这种病理情况在小鼠中很少报道。我们对SV12 Tg小鼠的研究首次描述了一种与广泛血管生成相关的纯恶性胸腺肿瘤模型,该模型在众多后代中得以维持。此处观察到的大量肿瘤性新血管网络的形成,在人类和/或实验性胸腺肿瘤中从未有过描述。通过用针对不同分子量的各种细胞角蛋白(CKs)、血管内皮细胞标志物以及新血管内皮细胞上存在的VEGF/受体-2(Flk-1)的抗体进行免疫标记,证实了肿瘤转化和血管生成。讨论了该模型的独特性所引发的不同问题。这些问题包括表达SV40转基因的细胞的髓质性质及其与肿瘤发展的关系。还考虑了不同分子量CK成分的子集及其修饰,以及IV型上皮细胞(髓质上皮细胞的祖细胞)的存在。最后,讨论了参与血管生成的细胞信号以及可能由肿瘤细胞自身分泌的血管生成因子的作用。