Ertorer M Eda, Tuncer Feyza N, Ciftci Sema, Tanrikulu Seher, Selcukbiricik Ozlem Soyluk, Topaloğlu Ömercan, Evran Mehtap, Kadioglu Pinar, Aydin Sevcan, Can Bulent, Sehit Canan, Pekkolay Zafer, Oruk Guzide Gonca, Cetinarslan Berrin, Yarman Sema
Division of Endocrinology and Metabolism, Baskent University Faculty of Medicine, Adana, Turkey.
Department of Translational Medicine, Institute of Health Sciences, Cukurova University, Adana, Turkey.
Sci Rep. 2025 Jul 7;15(1):24279. doi: 10.1038/s41598-025-08610-1.
Genetic causes of familial isolated pituitary adenomas (FIPAs) remain mostly elusive. A cohort of 20 FIPA cases from 12 different geographical regions of Türkiye was included to characterize clinical and genetic features. Whole exome sequencing (WES) was performed on genomic DNA of index cases, followed by confirmation through Sanger sequencing utilizing indexes and their relatives to interpret disease associated variants. Index cases among homogeneous (n = 10) and heterogeneous (n = 10) FIPA groups (45% female /55% male), age at diagnosis was 36.3 ± 11.98 years, median follow-up was 103 months. GH-secreting adenomas dominated homogeneous group (60% vs. 30% of heterogeneous group). Two predefined AIP variants [p.(Arg304Ter) and p.(Arg81Ter)] and a novel AIP variant at splice acceptor site [(c.646-1G > C)] were detected in three families (15%). Syndromic heterozygous novel NF1 [p.(Thr1295Ala)], TSC1 [p.(Arg517Gln)], SDHB [p.(Glu176Gly)] and CDH23 [p.(Ala765Val)] variants were detected in four FIPA families, along with novel candidate genes in the remaining patients of the cohort. Among all detected variants, three [p.(Arg81Ter) and (c.646-1G > C) in AIP, and p.(Glu216GlysfsTer61) in TINF2] were classified as pathogenic according to ACMG. AIP mutation frequency was 15% in our cohort. A novel AIP variant, and novel variations in syndromic genes were identified, along with the introduction of candidate genes. WES method is a crucial approach to identify new rare genetic variants in familial settings, and it will pave the way for future studies on targeted therapies.
家族性孤立性垂体腺瘤(FIPA)的遗传病因大多仍不清楚。本研究纳入了来自土耳其12个不同地理区域的20例FIPA病例,以表征其临床和遗传特征。对先证者的基因组DNA进行全外显子组测序(WES),随后通过桑格测序利用先证者及其亲属来确认,以解释与疾病相关的变异。在同质性(n = 10)和异质性(n = 10)FIPA组中的先证者(45%为女性/55%为男性),诊断时年龄为36.3±11.98岁,中位随访时间为103个月。生长激素分泌型腺瘤在同质性组中占主导(60%,而异质性组为30%)。在三个家族(15%)中检测到两个预定义的AIP变异[p.(Arg304Ter)和p.(Arg81Ter)]以及一个位于剪接受体位点的新型AIP变异[(c.646-1G>C)]。在四个FIPA家族中检测到综合征性杂合新型NF1[p.(Thr1295Ala)]、TSC1[p.(Arg517Gln)]、SDHB[p.(Glu176Gly)]和CDH23[p.(Ala765Val)]变异,以及该队列其余患者中的新型候选基因。在所有检测到的变异中,根据美国医学遗传学与基因组学学会(ACMG)的标准,三个变异[AIP中的p.(Arg81Ter)和(c.646-1G>C),以及TINF2中的p.(Glu216GlysfsTer61)]被分类为致病性变异。在我们的队列中,AIP突变频率为15%。鉴定出一个新型AIP变异以及综合征性基因中的新型变异,同时引入了候选基因。WES方法是在家族性背景中鉴定新的罕见遗传变异的关键方法,它将为未来的靶向治疗研究铺平道路。