肾上腺皮质激素的分子遗传学。

IF 2.4 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Patricia Vaduva, Jerome Bertherat
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引用次数: 0

摘要

肾上腺库欣占内源性皮质功能亢进病例的 20%。单侧皮质醇分泌腺瘤(一种良性肿瘤)和肾上腺皮质癌(一种恶性肿瘤)的发病率高于双侧肾上腺结节性疾病(原发性双侧大结节性肾上腺增生症(PBMAH)和原发性色素性结节性肾上腺疾病(PPNAD))。在产生皮质醇的肾上腺肿瘤中,主要改变的信号通路是蛋白激酶 A 和 Wnt/β-catenin 通路。研究这些通路的组成成分以及探索这些肿瘤的综合征和家族病例,历来都能确定许多易感基因。最近,基因组测序发现了散发性肿瘤中的基因改变。在 ACC 中,主要是由于 TP53 基因改变导致了 Li-Fraumeni 综合征,种系易感性在儿童中很常见,而在成人中却很罕见。DNA 错配修复基因 MLH1、MSH2、MSH6 和 PMS2 的致病变体可导致林奇综合征,IGF2 和 CDKN1C(11p15 位点)的改变可导致贝克维-维德曼综合征,这些变体也可导致 ACC。在其他遗传性肿瘤综合征中,由于 MEN1 或 APC 的种系致病变异,以及在极少数情况下由于 NF1、SDH、PRKAR1A 或 BRCA2 的种系致病变异而导致 ACC 的病例也非常罕见。关于 ACC 的体细胞变异,TP53 和 11p15 基因座的遗传或表观遗传变异以及 CTNNB1 和 ZNRF3 致病变异也经常被描述。CPAs 主要携带 PRKACA 和 CTNNB1 的体细胞致病变异,PRKAR1A、PRKACB 或 GNAS1 致病变异则较少见。在 20% 至 25% 的病例中,孤立性 PBMAH 是由 ARMC5 失活致病变体引起的,而在食物依赖性库欣病例中,则是由 KDM1A 致病变体引起的。综合征型 PBMAH 可能是由 MEN1、APC 或 FH 的种系致病变体引起的,这些变体分别导致 1 型多发性内分泌瘤病、家族性腺瘤性息肉病或遗传性白肌瘤病-肾癌综合征。PRKAR1A种系致病变异是导致PPNAD(孤立的或卡尼复合体的一部分)的主要改变。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The molecular genetics of adrenal cushing.

Adrenal Cushing represents 20% of cases of endogenous hypercorticism. Unilateral cortisol-producing adenoma (CPA), a benign tumor, and adrenocortical carcinoma (ACC), a malignant tumor, are more frequent than bilateral adrenal nodular diseases (primary bilateral macronodular adrenal hyperplasia (PBMAH) and primary pigmented nodular adrenal disease (PPNAD)).In cortisol-producing adrenal tumors, the signaling pathways mainly altered are the protein kinase A and Wnt/β-catenin pathways. Studying components of these pathways and exploring syndromic and familial cases of these tumors has historically enabled identification of many of the predisposing genes. More recently, pangenomic sequencing revealed alterations in sporadic tumors.In ACC, mainly due to TP53 alterations causing Li-Fraumeni syndrome, germline predisposition is frequent in children, while it is rare in adults. Pathogenic variants in the DNA mismatch repair genes MLH1, MSH2, MSH6, and PMS2, which cause Lynch syndrome or alterations of IGF2 and CDKN1C (11p15 locus) in Beckwith-Wiedemann syndrome, can also cause ACC. Rarely, ACC is described in other hereditary tumor syndromes due to germline pathogenic variants in MEN1 or APC and, in very rare cases, NF1, SDH, PRKAR1A, or BRCA2. Concerning ACC somatic alterations, TP53 and genetic or epigenetic alterations at the 11p15 locus are also frequently described, as well as CTNNB1 and ZNRF3 pathogenic variants.CPAs mainly harbor somatic pathogenic variants in PRKACA and CTNNB1 and, less frequently, PRKAR1A, PRKACB, or GNAS1 pathogenic variants. Isolated PBMAH is due to ARMC5 inactivating pathogenic variants in 20 to 25% of cases and to KDM1A pathogenic variants in food-dependent Cushing. Syndromic PBMAH may be due to germline pathogenic variants in MEN1, APC, or FH, causing type 1 multiple endocrine neoplasia, familial adenomatous polyposis, or hereditary leiomyomatosis-kidney cancer syndrome, respectively. PRKAR1A germline pathogenic variants are the main alteration causing PPNAD (isolated or part of Carney complex).

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来源期刊
CiteScore
5.90
自引率
0.00%
发文量
76
审稿时长
6-12 weeks
期刊介绍: Hormones-International Journal of Endocrinology and Metabolism is an international journal published quarterly with an international editorial board aiming at providing a forum covering all fields of endocrinology and metabolic disorders such as disruption of glucose homeostasis (diabetes mellitus), impaired homeostasis of plasma lipids (dyslipidemia), the disorder of bone metabolism (osteoporosis), disturbances of endocrine function and reproductive capacity of women and men. Hormones-International Journal of Endocrinology and Metabolism particularly encourages clinical, translational and basic science submissions in the areas of endocrine cancers, nutrition, obesity and metabolic disorders, quality of life of endocrine diseases, epidemiology of endocrine and metabolic disorders.
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