乳腺导管原位癌与浸润性导管癌的细胞学分化:个人观点及文献综述

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摘要

虽然有些人认为有争议,但仅用细胞学来区分乳腺导管原位癌(DCIS)和浸润性导管癌(IDC)是可能的,但有一定的局限性。侵袭性是恶性细胞特异性生物学的结果,即侵袭性潜力,这与先前存在的DCIS不同,因此具有不同的形态。在侵袭过程中,恶性细胞经历多种形态变化,在奇妙的上皮-间质转化过程中失去上皮,获得间质特征,这解释了它们与环境共存的形态,包括细胞间连接的破坏、流动性的增加和原始上皮的释放。这种间充质样表型支持细胞的迁移和侵袭,即上皮-间充质转化保证了肿瘤的播散和转移。因此,侵袭性可以通过检测恶性细胞生物侵袭性增加的形态学迹象来细胞学上“测量”——通过其外观的变化(恶性鳞状细胞的细胞质伸长,即腺癌细胞质内腔,非典型核仁,粗团块染色质,eu-/副染色质),以及基质参数(细胞间基质的破坏,弹性蛋白片段,毛细血管内皮)表现为肿瘤特征,成纤维细胞增殖,弹性基质碎片,结缔组织和/或脂肪组织被成群或个别恶性细胞侵袭。对于侵袭也有非常可预测的管状恶性结构,内聚性降低的不规则成角簇,无良性裸核,多形态单个肿瘤细胞,肿瘤组肌上皮细胞较少,微钙化和泡沫巨噬细胞较少。相反的形态学结果提示DCIS。尽管细胞学上我们没有看到基底膜,也无法看到基底膜,但我们很有可能预测其侵袭——必须而且总是采用三重诊断方法,或对每个乳腺病变进行临床-放射-形态学关联,在有代表性的细胞样本中,并具备良好的病理组织学和细胞学知识
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Cytological Differentiation of Ductal Carcinoma in Situ and Invasive Ductal Carcinoma of the Breast: A Personal View and a Literature Review
Although some find it controversial, it is possible to differentiate breast ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC) using cytology only, with certain limitations. Invasiveness is the consequence of specific biological, i.e. aggressiveness potential of malignant cells, which is different with respect to the pre-existent DCIS, consequentially with different morphology. During the invasion, malignant cells go through multiple morphological changes, losing their epithelial and acquiring mesenchymal features in the fantastic process of epithelial-mesenchymal transition, which explains their morphology in cohabitation with the environment, includes the disruption of intercellular junctions, the increase of mobility and the release of the original epithelium. This mesenchymal-like phenotype supports the migration and invasion of cells, i.e. thus epithelial-mesenchymal transition ensures the tumor dissemination and metastasizing. Therefore, invasiveness can cytologically be “measured” by detecting morphological signs of increase of biological aggressiveness of malignant cells – through the change of their appearance (cytoplasm elongation in malignant squamous cells, i.e. in adenocarcinoma intracytoplasmic lumina, atypical nucleoli, coarsely clumped chromatin, eu-/parachromatin), but also with stromal parameters (disruption of the intercellular matrix, elastin fragments, capillaries endothelium) presented by tumour diathesis, fibroblast proliferation, fragments of elastoid stroma, invasion of connective and/or adipose tissue by groups and individual malignant cells. For the invasion are also very predictive tubular malignant structures, irregular angulated clusters of reduced cohesiveness, absence of benign naked nuclei, polymorph single tumour cells, less myoepithelial cells on tumour groups, fewer microcalcifications and foamy macrophages. Opposite morphological findings suggest DCIS. Even though cytologically we do not see and cannot see the basement membrane, highly likely we can predict the invasion – necessarily and always with the triple-diagnostic approach or clinical-radiological-morphological correlation to every breast lesion, in the representative well cellular sample and with good knowledge of patohistology and cytology
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