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首页> 外文期刊>Endocrine-related cancer >RET-mediated modulation of tumor microenvironment and immune response in multiple endocrine neoplasia type 2 (MEN2)
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RET-mediated modulation of tumor microenvironment and immune response in multiple endocrine neoplasia type 2 (MEN2)

机译：RET介导的多发性内分泌肿瘤2型（MEN2）的肿瘤微环境和免疫反应的调节。

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Medullary thyroid carcinomas (MTC) arise from thyroid parafollicular, calcitonin-producing C-cells and can occur either as sporadic or as hereditary diseases in the context of familial syndromes, including multiple endocrine neoplasia 2A (MEN2A), multiple endocrine neoplasia 2B (MEN2B) and familial MTC (FMTC). In a large fraction of sporadic cases, and virtually in all inherited cases of MTC, activating point mutations of the RET proto-oncogene are found. RET encodes for a receptor tyrosine kinase protein endowed with transforming potential on thyroid parafollicular cells. As in other cancer types, microenvironmental factors play a critical role in MTC. Tumor-associated extracellular matrix, stromal cells and immune cells interact and influence the behavior of cancer cells both in a tumor-promoting and in a tumor-suppressing manner. Several studies have shown that, besides the neoplastic transformation of thyroid C-cells, a profound modification of tumor microenvironment has been associated to the RET FMTC/MEN2-associated oncoproteins. They influence the surrounding stroma, activating cancer-associated fibroblasts (CAFs), promoting cancer-associated inflammation and suppressing anti-cancer immune response. These mechanisms might be exploited to develop innovative anti-cancer therapies and novel prognostic tools in the context of familial, RET-associated MTC.
机译：甲状腺髓样癌（MTC）源自甲状腺滤泡旁产生降钙素的C细胞，在家族性综合征的情况下可能以散发性疾病或遗传性疾病的形式出现，包括多发性内分泌肿瘤2A（MEN2A），多发性内分泌肿瘤2B（MEN2B）和家族MTC（FMTC）。在大部分零星的案例中，以及实际上在所有继承的MTC案例中，都发现了RET原癌基因的激活点突变。 RET编码受体酪氨酸激酶蛋白，该蛋白在甲状腺滤泡旁细胞上具有转化潜能。与其他癌症类型一样，微环境因素在MTC中起关键作用。肿瘤相关的细胞外基质，基质细胞和免疫细胞以促进肿瘤和抑制肿瘤的方式相互作用并影响癌细胞的行为。多项研究表明，除了甲状腺C细胞的肿瘤性转化外，与RET FMTC / MEN2相关的癌蛋白还涉及肿瘤微环境的深刻改变。它们影响周围的基质，激活与癌症相关的成纤维细胞（CAF），促进与癌症相关的炎症，并抑制抗癌免疫反应。在家族性，与RET相关的MTC的背景下，可以利用这些机制来开发创新的抗癌疗法和新颖的预后工具。

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