Bondy M L, Lustbader E D, Buffler P A, Schull W J, Hardy R J, Strong L C
Division of Pediatrics, University of Texas M.D. Anderson Cancer Center, Houston.
Genet Epidemiol. 1991;8(4):253-67. doi: 10.1002/gepi.1370080406.
The study goal was to determine the genetic (heritable) contribution to childhood brain tumors (CBT) which cause nearly one quarter of all childhood cancer deaths. Their etiology remains unknown, but previous studies have suggested a proportion of CBT may be heritable. In this study we collected family histories of 243 confirmed CBT patients referred to The University of Texas M. D. Anderson Cancer Center between the years 1944 and 1983, diagnosed before age 15, and residents of the United States or Canada. Family histories were obtained for all the probands' first degree relatives (parents, siblings, and offspring) and extended to include selected second degree relatives (aunts, uncles, grandparents) using sequential sampling. To determine if these CBT families exhibited excess cancer, we compared their cancer experience to age-, race-, sex-, and calendar-year specific rates from the Connecticut Tumor Registry. No cancer excess was observed among 1,099 first and second degree relatives [39 cancers observed (O) and 44 expected (E) for a standardized incidence ratio (SIR) of 0.88]. For colon cancer, although small numbers, five cases were observed among the probands' first degree relatives with 1.6 expected, for a significant SIR of 3.10. Segregation analysis demonstrated that chance alone could not account for the observed cancer distribution with a multifactorial model providing the best overall explanation of the data. Overall, heredity played a role in the etiology of CBT in 4% of the study families: four (1.7%) due to known hereditary syndromes (nevoid basal cell carcinoma syndrome and von Recklinghausens neurofibromatosis--NF-1), four (1.7%) with multifactorial inheritance, and two additional families with cancers aggregating similar to the clinical criteria described for the Li-Fraumeni cancer family syndrome.
该研究的目标是确定导致近四分之一儿童癌症死亡的儿童脑肿瘤(CBT)的遗传(可遗传)因素。其病因尚不清楚,但先前的研究表明,一部分CBT可能具有遗传性。在本研究中,我们收集了1944年至1983年间转诊至德克萨斯大学MD安德森癌症中心的243例确诊CBT患者的家族史,这些患者在15岁之前被诊断,并且是美国或加拿大居民。通过序贯抽样获取了所有先证者的一级亲属(父母、兄弟姐妹和子女)的家族史,并扩展到包括选定的二级亲属(姑姑、叔叔、祖父母)。为了确定这些CBT家族是否存在癌症高发情况,我们将他们的癌症发病情况与康涅狄格肿瘤登记处按年龄、种族、性别和日历年划分的特定发病率进行了比较。在1099名一级和二级亲属中未观察到癌症高发情况[观察到39例癌症(O),预期44例(E),标准化发病比(SIR)为0.88]。对于结肠癌,虽然病例数较少,但在先证者的一级亲属中观察到5例,预期为1.6例,显著的SIR为3.10。分离分析表明,仅靠偶然性无法解释观察到的癌症分布情况,多因素模型对数据提供了最佳的总体解释。总体而言,在4%的研究家族中,遗传因素在CBT的病因中起了作用:4个家族(1.7%)是由于已知的遗传综合征(痣样基底细胞癌综合征和冯雷克林霍增氏神经纤维瘤病 - NF - 1),4个家族(1.7%)具有多因素遗传,另外还有两个家族的癌症聚集情况类似于李 - 弗劳梅尼癌症家族综合征所描述的临床标准。