Cetta F, Chiappetta G, Melillo R M, Petracci M, Montalto G, Santoro M, Fusco A
Istituto di Clinica Chirurgica, Università di Siena, Nuovo Policlinico, Italy.
J Clin Endocrinol Metab. 1998 Mar;83(3):1003-6. doi: 10.1210/jcem.83.3.4614.
Familial adenomatous polyposis (FAP) is caused by germ-line mutations of the apc gene, and it is associated with an increased risk of developing papillary thyroid carcinomas. We have previously reported that a significant fraction of sporadic human papillary thyroid carcinomas is characterized by gene rearrangements affecting the ret protooncogene. These rearrangements generate chimeric transforming oncogenes designated ret/ptc. By a combined immunohistochemical and RT-PCR approach, we analyzed, for ret/ptc oncogene activation, papillary thyroid carcinomas occurred in two FAP kindreds, both showing typical apc gene mutations. Kindred 1 had seven members affected by FAP, and among these, three patients showed papillary thyroid carcinomas. Kindred 2 had two patients, mother and daughter, affected by colonic polyposis; the 20-yr-old daughter showed also a papillary carcinoma. Here we report that ret/ptc1 oncogene was activated in two of the three papillary carcinomas of FAP kindred 1 and in the papillary carcinoma of FAP kindred 2. These findings document that loss of function of apc coexists with gain of function of ret in some papillary thyroid carcinomas, suggesting that ret/ptc1 oncogene activation could be a progression step in the development of FAP-associated thyroid tumors.
家族性腺瘤性息肉病(FAP)由apc基因的种系突变引起,且与甲状腺乳头状癌的发病风险增加相关。我们之前报道过,相当一部分散发性人类甲状腺乳头状癌的特征是影响ret原癌基因的基因重排。这些重排产生了名为ret/ptc的嵌合转化癌基因。通过免疫组织化学和逆转录聚合酶链反应相结合的方法,我们分析了两个FAP家系中发生的甲状腺乳头状癌ret/ptc癌基因的激活情况,这两个家系均显示出典型的apc基因突变。家系1有7名成员受FAP影响,其中3例患者患有甲状腺乳头状癌。家系2有两名患者,母亲和女儿,患有结肠息肉病;20岁的女儿也患有乳头状癌。在此我们报道,ret/ptc1癌基因在FAP家系1的3例乳头状癌中的2例以及FAP家系2的乳头状癌中被激活。这些发现证明,在一些甲状腺乳头状癌中,apc功能丧失与ret功能获得并存,提示ret/ptc1癌基因激活可能是FAP相关甲状腺肿瘤发生发展过程中的一个进展步骤。