Almeida Madson Q, Kaupert Laura C, Brito Luciana P, Lerario Antonio M, Mariani Beatriz M P, Ribeiro Marta, Monte Osmar, Denes Francisco T, Mendonca Berenice B, Bachega Tânia A S S
Divisão de Endocrinologia e Metabologia, Laboratório de Hormônios e Genética Molecular/LIM42, Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, Av, Dr, Enéas de Carvalho Aguiar, 155, 2 andar, Bloco 6, São Paulo, SP 05403-900, Brasil.
BMC Endocr Disord. 2014 May 12;14:42. doi: 10.1186/1472-6823-14-42.
Although chronic adrenocorticotropic hormone (ACTH) and androgen hyperstimulation are assumed to be involved in the pathogenesis of adrenal myelolipomas associated with poor-compliance patients with congenital adrenal hyperplasia (CAH), the expression of their receptors has not yet been demonstrated in these tumors so far.
We analyzed Melanocortin 2 receptor (MC2R), Androgen Receptor (AR), Leptin (LEP), and Steroidogenic factor 1 (SF1) expression using real-time qRT-PCR in two giant bilateral adrenal myelolipomas from two untreated simple virilizing CAH cases and in two sporadic adrenal myelolipomas. In addition, the X-chromosome inactivation pattern and CAG repeat numbers in AR exon 1 gene were evaluated in the 4 cases.
The MC2R gene was overexpressed in myelolipomas from 3 out of 4 patients. AR overexpression was detected in 2 tumors: a giant bilateral myelolipoma in a CAH patient and a sporadic case. Simultaneous overexpression of AR and MC2R genes was found in two of the cases. Interestingly, the bilateral giant myelolipoma associated with CAH that had high androgen and ACTH levels but lacked MC2R and AR overexpression presented a significantly shorter AR allele compared with other tumors. In addition, X-chromosome inactivation pattern analysis showed a polyclonal origin in all tumors, suggesting a stimulatory effect as the trigger for tumor development.
These findings are the first evidence for MC2R or AR overexpression in giant bilateral myelolipomas from poor-compliance CAH patients.
尽管慢性促肾上腺皮质激素(ACTH)和雄激素过度刺激被认为与先天性肾上腺皮质增生症(CAH)依从性差的患者所患肾上腺髓质脂肪瘤的发病机制有关,但迄今为止,这些肿瘤中尚未证实其受体的表达情况。
我们使用实时定量逆转录聚合酶链反应(qRT-PCR)分析了来自2例未经治疗的单纯男性化型CAH患者的2个巨大双侧肾上腺髓质脂肪瘤以及2个散发性肾上腺髓质脂肪瘤中黑素皮质素2受体(MC2R)、雄激素受体(AR)、瘦素(LEP)和类固醇生成因子1(SF1)的表达。此外,还评估了这4例患者中AR外显子1基因的X染色体失活模式和CAG重复数。
4例患者中有3例的髓质脂肪瘤中MC2R基因过度表达。在2个肿瘤中检测到AR过度表达:1例CAH患者的巨大双侧髓质脂肪瘤和1例散发性病例。其中2例同时出现AR和MC2R基因的过度表达。有趣的是,与CAH相关的双侧巨大髓质脂肪瘤,其雄激素和ACTH水平较高,但缺乏MC2R和AR过度表达,与其他肿瘤相比,其AR等位基因明显较短。此外,X染色体失活模式分析显示所有肿瘤均起源于多克隆,提示存在刺激作用作为肿瘤发生的触发因素。
这些发现首次证明了MC2R或AR在依从性差的CAH患者的巨大双侧髓质脂肪瘤中过度表达。