Department of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo 160‑8582, Japan.
Center for Medical Genetics, Keio University School of Medicine, Tokyo 160‑8582, Japan.
Oncol Rep. 2019 Dec;42(6):2303-2308. doi: 10.3892/or.2019.7353. Epub 2019 Oct 4.
Endometrial polyps are common, yet the molecular mechanisms underlying their formation and progression remain unclear. We examined gene mutations possibly related to the pathogenesis of endometrial polyps, as well as to their clinical features. Four premenopausal patients with endometrial polyps, who were not under drug treatment, were recruited. Whole exomes of endometrial polyps and peripheral blood lymphocytes were analyzed by next‑generation sequencing, and somatic mutations were derived by subtraction. Then, 35 samples of endometrial polyps and 12 samples of atypical polypoid adenomyoma were newly recruited to validate the identified mutations by polymerase chain reaction‑reverse sequence specific oligonucleotide method. The mutations were also analyzed in separate stromal and glandular components of the polyps after laser‑capture microdissection. Whole exome sequencing revealed that KRAS mutations were the only type of mutation detectable in multiple cases (2/4). Targeted mutation analysis revealed that 16 of 35 samples (45.7%) of endometrial polyps harbored RAS mutations. Mutation‑positive cases exhibited a significantly higher number of endometrial polyps (3.25±2.70 vs. 1.74±0.87, P=0.045). Laser‑capture microdissection in NRAS‑mutated endometrial polyps revealed that both stromal and glandular components harbored RAS mutations. There was no RAS mutation in 12 samples of atypical polypoid adenomyoma. This is the first report demonstrating that pathogenic RAS mutations are frequent in non‑treated endometrial polyps. RAS mutations may have an important role in tumorigenesis and in the formation of multiple endometrial polyps.
子宫内膜息肉很常见,但其形成和进展的分子机制仍不清楚。我们研究了可能与子宫内膜息肉发病机制以及其临床特征相关的基因突变。招募了 4 名未经药物治疗的绝经前子宫内膜息肉患者。通过下一代测序分析子宫内膜息肉和外周血淋巴细胞的全外显子组,并通过减法获得体细胞突变。然后,新招募了 35 例子宫内膜息肉和 12 例非典型息肉样腺肌瘤样本,通过聚合酶链反应-反向序列特异性寡核苷酸方法验证鉴定的突变。还通过激光捕获微切割分析息肉的分离基质和腺体成分中的突变。全外显子组测序显示,KRAS 突变是多种情况下可检测到的唯一突变类型(2/4)。靶向突变分析显示,35 例子宫内膜息肉样本中有 16 例(45.7%)存在 RAS 突变。突变阳性病例的子宫内膜息肉数量明显更多(3.25±2.70 比 1.74±0.87,P=0.045)。在 NRAS 突变的子宫内膜息肉中进行激光捕获微切割显示,基质和腺体成分均存在 RAS 突变。12 例非典型息肉样腺肌瘤中没有 RAS 突变。这是首次报道表明治疗前的子宫内膜息肉中存在致病性 RAS 突变。RAS 突变可能在肿瘤发生和多发性子宫内膜息肉形成中具有重要作用。