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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Gastrointestinal stromal tumors in a mouse model by targeted mutation of the Kit receptor tyrosine kinase
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Gastrointestinal stromal tumors in a mouse model by targeted mutation of the Kit receptor tyrosine kinase

机译：Kit受体酪氨酸激酶的靶向突变在小鼠模型中的胃肠道间质瘤

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Oncogenic Kit mutations are found in somatic gastrointestinal (GI) stromal tumors (GISTs) and mastocytosis. A mouse model for the study of constitutive activation of Kit in oncogenesis has been produced by a knock-in strategy introducing a Kit exon 11-activating mutation into the mouse genome based on a mutation found in a case of human familial GIST syndrome. Heterozygous mutant Kit(V558Delta)/+ mice develop symptoms of disease and eventually die from pathology in the GI tract. Patchy hyperplasia of Kit-positive cells is evident within the myenteric plexus of the entire GI tract. Neoplastic lesions indistinguishable from human GISTs were observed in the cecum of the mutant mice with high penetrance. in addition, mast cell numbers in the dorsal skin were increased. Therefore Kit(V558Delta)/+ mice reproduce human familial GISTs, and they may be used as a model for the study of the role and mechanisms of Kit in neoplasia. Importantly, these results demonstrate that constitutive Kit signaling is critical and sufficient for induction of GIST and hyperplasia of interstitial cells of Cajal. [References: 48]
机译：在躯体胃肠道（GI）基质肿瘤（GIST）和肥大细胞增多症中发现了致癌试剂盒突变。通过在人类家族性GIST综合征病例中发现的突变，将Kit Kit外显子11激活突变引入小鼠基因组的敲入策略，已经产生了用于研究Kit在肿瘤发生中的组成性激活的小鼠模型。杂合突变体Kit（V558Delta）/ +小鼠出现疾病症状，最终死于胃肠道病理。 Kit阳性细胞的斑块状增生在整个胃肠道的肌间神经丛内很明显。在具有高渗透性的突变小鼠的盲肠中观察到与人GIST没有区别的肿瘤性病变。此外，背部皮肤的肥大细胞数量增加。因此，Kit（V558Delta）/ +小鼠可复制人类家族性GIST，可作为研究Kit在肿瘤形成中的作用和机制的模型。重要的是，这些结果表明，组成性Kit信号传导对于诱导GIST和Cajal间质细胞增生至关重要，并且足够。 [参考：48]

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