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首页> 外文期刊>Cell and Tissue Research >Pheochromocytoma and paraganglioma: genotype versus anatomic location as determinants of tumor phenotype
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Pheochromocytoma and paraganglioma: genotype versus anatomic location as determinants of tumor phenotype

机译：Pheochromytoma和Paraganglioma：基因型与解剖位置为肿瘤表型的决定因素

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To date, germline or somatic genetic events can be detected for at least 60% of paragangliomas. Strong genotype–phenotype associations have been recognized and become increasingly refined. Characteristics closely linked with genotype include syndromic presentation, age of onset, risk of metastatic disease and predominant anatomic site. In contrast, profiles of catecholamine secretion appear to be largely determined by anatomic location or cell type of origin. This review summarizes current knowledge of genotype–phenotype correlations for paragangliomas in different locations and scrutinizes previous publications on the respective tissues of origin to find potential explanations for site-related differences. We hypothesize that differential sensitivities of distinct chromaffin cell populations to hypoxia are major determinants of these differences, with increased sensitivity to hypoxia likely exacerbating vulnerability to mutation-derived disruption of hypoxic signaling pathways. Potential involvement of endothelin-1, tumor necrosis factor type 1 receptor-associated protein and the hypoxia-inducible miR-210 in the development of abdomino-thoracic or head and neck paragangliomas are discussed. Recognition of factors that predispose to chromosomal losses, or amplify sub-threshold molecular alterations towards tumorigenic events in different (chromaffin) cell types, may facilitate the leap from developing targeted therapies towards establishment of tumor preventative measures.
机译：迄今为止，可以检测到至少60％的Paragangliomas检测种系或体细胞遗传事件。已经认识到强基因型 - 表型关联并越来越成熟。与基因型密切相关的特征包括综合征介绍，发病年龄，转移性疾病风险和主要的解剖部位。相反，儿茶酚胺分泌的谱似乎通过解剖学位置或细胞类型来大大确定。本综述总结了当前关于不同地点的基因型 - 表型相关性的基因型表型相关性，并在原产地组织上审查先前的出版物，以找到与现场相关差异的潜在解释。我们假设不同的斑粘蛋白细胞群与缺氧的差异敏感性是这些差异的主要决定因素，其对缺氧的敏感性增加了对缺氧信号传导途径的突变衍生的破坏的缺氧可能加剧脆弱性。讨论了内皮素-1，肿瘤坏死因子类型1受体相关蛋白和缺氧诱导的miR-210的潜在参与在腹部 - 胸部或头部和颈部癌症癌症术中的缺氧诱导的miR-210。识别致力于染色体损失的因素，或扩增诸如不同（磷素）细胞类型的致瘤事件的亚阈值分子改变，可以促进朝向建立肿瘤预防措施的靶向疗法的飞跃。

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