von Salomé Jenny, Boonstra Philip S, Karimi Masoud, Silander Gustav, Stenmark-Askmalm Marie, Gebre-Medhin Samuel, Aravidis Christos, Nilbert Mef, Lindblom Annika, Lagerstedt-Robinson Kristina
Department of Molecular Medicine and Surgery, Karolinska Institutet, and Department of Clinical Genetics, Karolinska University Hospital, Solna, Stockholm, Sweden.
Department of Biostatistics, University of Michigan, Ann Arbor, Michigan, United States of America.
PLoS Genet. 2017 Oct 31;13(10):e1007012. doi: 10.1371/journal.pgen.1007012. eCollection 2017 Oct.
Among hereditary colorectal cancer predisposing syndromes, Lynch syndrome (LS) caused by mutations in DNA mismatch repair genes MLH1, MSH2, MSH6 or PMS2 is the most common. Patients with LS have an increased risk of early onset colon and endometrial cancer, but also other tumors that generally have an earlier onset compared to the general population. However, age at first primary cancer varies within families and genetic anticipation, i.e. decreasing age at onset in successive generations, has been suggested in LS. Anticipation is a well-known phenomenon in e.g neurodegenerative diseases and several reports have studied anticipation in heritable cancer. The purpose of this study is to determine whether anticipation can be shown in a nationwide cohort of Swedish LS families referred to the regional departments of clinical genetics in Lund, Stockholm, Linköping, Uppsala and Umeå between the years 1990-2013. We analyzed a homogenous group of mutation carriers, utilizing information from both affected and non-affected family members. In total, 239 families with a mismatch repair gene mutation (96 MLH1 families, 90 MSH2 families including one family with an EPCAM-MSH2 deletion, 39 MSH6 families, 12 PMS2 families, and 2 MLH1+PMS2 families) comprising 1028 at-risk carriers were identified among the Swedish LS families, of which 1003 mutation carriers had available follow-up information and could be included in the study. Using a normal random effects model (NREM) we estimate a 2.1 year decrease in age of diagnosis per generation. An alternative analysis using a mixed-effects Cox proportional hazards model (COX-R) estimates a hazard ratio of exp(0.171), or about 1.19, for age of diagnosis between consecutive generations. LS-associated gene-specific anticipation effects are evident for MSH2 (2.6 years/generation for NREM and hazard ratio of 1.33 for COX-R) and PMS2 (7.3 years/generation and hazard ratio of 1.86). The estimated anticipation effects for MLH1 and MSH6 are smaller.
在遗传性结直肠癌易感综合征中,由DNA错配修复基因MLH1、MSH2、MSH6或PMS2突变引起的林奇综合征(LS)最为常见。LS患者患早发性结肠癌和子宫内膜癌的风险增加,同时也有患其他肿瘤的风险,这些肿瘤的发病通常比普通人群更早。然而,家族中首例原发性癌症的发病年龄各不相同,并且在LS中已有人提出遗传早现现象,即连续几代人的发病年龄逐渐降低。早现是神经退行性疾病等领域中一种众所周知的现象,已有多篇报道研究了遗传性癌症中的早现现象。本研究的目的是确定在1990年至2013年间转诊至隆德、斯德哥尔摩、林雪平、乌普萨拉和于默奥等地临床遗传学区域部门的瑞典LS家族全国队列中是否能显示出早现现象。我们分析了一组同质的突变携带者,利用了受影响和未受影响家庭成员的信息。在瑞典LS家族中,共识别出239个有错配修复基因突变的家族(96个MLH1家族、90个MSH2家族,其中包括1个EPCAM-MSH2缺失的家族、39个MSH6家族、12个PMS2家族以及2个MLH1+PMS2家族),包括1028名有风险的携带者,其中1003名突变携带者有可用的随访信息并可纳入研究。使用正态随机效应模型(NREM),我们估计每代诊断年龄降低2.1岁。使用混合效应Cox比例风险模型(COX-R)进行的另一项分析估计,连续几代人诊断年龄的风险比为exp(0.171),约为1.19。MSH2(NREM为2.6岁/代,COX-R的风险比为1.33)和PMS2(7.3岁/代,风险比为1.86)的LS相关基因特异性早现效应明显。MLH1和MSH6的估计早现效应较小。