Franco Noreli, Arnould Laurent, Mege Florence, Picard Samy-Felix, Arveux Patrick, Lizard-Nacol Sarab
Laboratory of Molecular Genetics, Centre Georges-François Leclerc, Dijon, France.
Arch Surg. 2003 Mar;138(3):291-5. doi: 10.1001/archsurg.138.3.291.
The cause of breast cancer is linked to many macroscopic events, including benign breast disease. In this study we asked whether molecular changes could discriminate fibroadenoma, which is one of the most common benign breast disease lesions associated or not with breast cancer.
Retrospective cohort study.
Anticancer medical center.
Archival tissues in 32 cases of fibroadenoma, diagnosed in the same breast as a breast carcinoma, are compared with a control group of 26 cases of fibroadenomas unaffected by breast cancer.
Histological features are characterized in all samples. The epithelial and stromal components are analyzed for a loss of heterozygosity and a microsatellite instability using a polymerase chain reaction-based method with 11 polymorphic microsatellite markers at 7 chromosomal regions frequently altered in breast cancer. The p53 gene mutations were also determined at exons 5 to 9.
The frequency of complex fibroadenomas was similar in both groups (P =.42). Only in the case group did we observe proliferative lesions confined in fibroadenomas, including atypical ductal hyperplasia (2 cases), lobular neoplasia (3 cases), or low-grade ductal carcinoma in situ (2 cases). There is no significant morphological difference between the 2 groups. Neither microsatellite alterations nor p53 gene mutations are present in the fibroadenoma components. Loss of heterozygosity is found only in the epithelial component of the 2 ductal carcinomas in situ confined in fibroadenomas.
Genetic alterations, which are most frequently involved in malignant breast carcinomas, are not present in fibroadenomas, regardless of their association with breast cancer or their histological complexity. These findings suggest that fibroadenomas are not associated with breast carcinogenesis.
乳腺癌的病因与许多宏观事件有关，包括乳腺良性疾病。在本研究中，我们探讨分子变化是否能够区分纤维腺瘤（这是最常见的与乳腺癌相关或不相关的乳腺良性疾病病变之一）。
回顾性队列研究。
抗癌医疗中心。
选取32例与乳腺癌在同一侧乳房诊断出的纤维腺瘤的存档组织，并与26例未受乳腺癌影响的纤维腺瘤对照组进行比较。
对所有样本的组织学特征进行表征。使用基于聚合酶链反应的方法，采用11个多态性微卫星标记，对7个在乳腺癌中经常发生改变的染色体区域进行分析，以检测上皮和间质成分的杂合性缺失和微卫星不稳定性。同时还测定了p53基因第5至9外显子的突变情况。
两组中复杂性纤维腺瘤的发生率相似（P = 0.42）。仅在病例组中，我们观察到局限于纤维腺瘤内的增殖性病变，包括非典型导管增生（2例）、小叶肿瘤（3例）或低级别导管原位癌（2例）。两组之间在形态学上无显著差异。纤维腺瘤成分中既未发现微卫星改变，也未发现p53基因突变。仅在局限于纤维腺瘤内的2例导管原位癌的上皮成分中发现了杂合性缺失。
无论纤维腺瘤与乳腺癌的关联情况或其组织学复杂性如何，纤维腺瘤中均不存在最常与恶性乳腺癌相关的基因改变。这些发现表明纤维腺瘤与乳腺癌发生无关。
