Intracystic papillary carcinomas of the breast: A reevaluation using a panel of myoepithelial cell markers

Intracystic papillary carcinomas of the breast: A reevaluation using a panel of myoepithelial cell markers
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DOI:
10.1097/00000478-200608000-00011
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发表时间:
2006-08-01
影响因子:
5.6
通讯作者:
Schnitt, Stuart J.
Schnitt, Stuart J.
中科院分区:
医学1区
文献类型:
--
作者:
Collins, Laura C.;Carlo, Victor P.;Schnitt, Stuart J.

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乳腺囊内乳头状癌(IPC)传统上被认为是导管原位癌(DCIS)的变种。然而,目前还不清楚是否所有的组织学分类为IPC的病变都是真正的原位癌,或者一些这样的病变可能是浸润性乳头状癌的局限性或包裹性结节。鉴于癌细胞巢周围肌上皮细胞(MEC)层的显示是在有问题的病例中区分原位乳腺癌和浸润性乳腺癌的有用手段,评估构成这些病变的结节外围是否有MEC层可能有助于解决这一问题。我们对22例IPC和15例良性导管内乳头状瘤结节周边MEC的存在和分布进行了研究。免疫组织化学染色检测了5种识别MEC成分的高敏感性标记物:平滑肌肌球蛋白重链、钙蛋白、p63、CD10和细胞角蛋白5/6。22例IPC结节周围均无MEC,5种标记物均为阴性。相反,在与IPC结节相邻的传统DCI的病灶周围检测到MEC层。此外,所有良性导管内乳头状瘤,包括那些大小与IPC相当的肿瘤,几乎在病变的整个周边显示一层MEC,所有5种MEC标志物都有。总之,在组织学上归类为IPC的22个病变中,我们都没有在结节周围检测到MEC层。一种可能的解释是,这些病变是原位病变,其中界定MEC层的这些抗原的表达明显减弱或改变,可能是由于这些病变在囊性扩张的导管内扩张生长所致的压缩。另一种可能是,至少一些使用常规组织学标准被归类为IPC的病变实际上代表了浸润性乳头状癌的局限性包膜结节。无论这些病变是原位癌还是浸润性癌,现有的结果数据表明,仅通过适当的局部治疗,它们似乎具有良好的预后。因此,我们认为,最谨慎的做法是继续对这些病变的患者进行目前的管理(即类似于DCIS患者),并避免将此类病变归类为浸润性乳头状癌。鉴于我们的观察,我们倾向于术语“包裹性乳头状癌”而不是“囊内型乳头状癌”,因为乳头状癌的局限性结节被纤维包膜包围,其内无法辨认出MEC的外周层。
Intracystic papillary carcinomas (IPC) of the breast have traditionally been considered to be variants of ductal carcinoma in situ (DCIS). However, it is not clear if all lesions categorized histologically as IPC are truly in situ carcinomas, or if some such lesions might represent circumscribed or encapsulated nodules of invasive papillary carcinoma. Given that the demonstration of a myoepithelial cell (MEC) layer around nests of carcinoma cells is a useful means to distinguish in situ from invasive carcinomas of the breast in problematic cases, assessment of the presence or absence of a MEC layer at the periphery of the nodules that comprise these lesions could help resolve this issue. We studied the presence and distribution of MEC at the periphery of the nodules of 22 IPC and, for comparison, 15 benign intraductal papillomas using immunostaining for 5 highly sensitive markers that recognize various MEC components: smooth muscle myosin heavy chain, calponin, p63, CD10, and cytokeratin 5/6. All 22 lesions categorized as IPC showed complete absence of MEC at the periphery of the nodules with all 5 markers. In contrast, a MEC layer was detected around foci of conventional DCIS present adjacent to the nodules of IPC. Furthermore, all benign intraductal papillomas, including those of sizes comparable to those of IPC, showed a MEC layer around virtually the entire periphery of the lesion with all 5 MEC markers. In conclusion we could not detect a MEC layer at the periphery of the nodules of any of 22 lesions categorized histologically as IPC. One possible explanation for this observation is that these are ill situ lesions in which the delimiting MEC layer has become markedly attenuated or altered with regard to expression of these antigens, perhaps due to their compression by the expansile growth of these lesions within a cystically dilated duct. Alternatively, it may be that at least some lesions that have been categorized as IPC using conventional histologic criteria actually represent circumscribed, encapsulated nodules of invasive papillary carcinoma. Regardless of whether these lesions are in situ or invasive carcinomas, available outcome data indicate that they seem to have an excellent prognosis with adequate local therapy alone. Therefore, we believe it is most prudent to continue to manage patients with these lesions as they are currently managed (ie., similar to patients with DCIS) and to avoid categorization of such lesions as frankly invasive papillary carcinomas. Given our observations, we favor the term "encapsulated papillary carcinoma" over "intracystic papillary carcinoma" for circumscribed nodules of papillary carcinoma surrounded by a fibrous capsule in which a peripheral layer of MEC is not identifiable.