The separation of benign and malignant mesothelial proliferations.

The separation of benign and malignant mesothelial proliferations.
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良性和恶性间皮增殖的分离。

DOI:
10.1097/00000478-200009000-00001
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发表时间:
2000
期刊:
The American journal of surgical pathology
影响因子:
--
通讯作者:
William D. Travis
William D. Travis
中科院分区:
--
文献类型:
--
作者:
A. Churg;Thomas V. Colby;P. Cagle;Joseph M. Corson;Allen R. Gibbs;Blake Gilks;Margaret M. Grimes;Samuel P. Hammar;V. Roggli;William D. Travis

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良性与恶性间皮增生的分离已成为浆膜病理学中的一个主要问题。对于上皮和梭形细胞间皮过程,真正的间质浸润是恶性肿瘤最准确的指标,但间质浸润往往很难评估,特别是在小活检。在胸膜腔内,增厚和纤维化胸膜的深度穿透或间皮细胞穿透胸壁脂肪是恶性肿瘤的良好指标;然而,组织性积液对间皮细胞和腺体的浅表包埋在良性反应中很常见,需要与浸润相区分。在腹膜腔,脂肪或器官壁的侵犯仍然是恶性肿瘤最可靠的指标,但良性细胞在肉芽组织或脂肪小叶之间的截留是常见的和易混淆的。局限于胸膜或腹膜腔的恶性肿瘤,特别是游离表面的非典型间皮细胞的线性排列,在没有明确浸润的情况下不应被称为恶性肿瘤。细胞学检查通常无助于区分良性和恶性反应,因为良性过程通常是不典型的,间皮瘤往往是欺骗性的单调。胸膜腔内密集的间皮细胞在良性反应中常见,但间质内密集的间皮细胞有利于恶性肿瘤的诊断。机化性渗出液(纤维性胸膜炎)通常表现为向胸膜腔的高细胞性和细胞学分层,向胸壁的纤维化增加,细胞性减少,细胞学分层较少,而肉瘤性(包括促结缔组织增生性)间皮瘤不表现出这种类型的分层。在机化渗出液中可见垂直于胸膜表面的细长毛细血管,但不是肉瘤性间皮瘤的特征。诊断促纤维增生性间皮瘤需要结合少细胞的故事状结构,以及间质(包括脂肪和邻近组织)的侵犯,或温和的坏死,明显的肉瘤灶,或远处转移。坏死通常是恶性肿瘤的征象,但偶尔见于良性间皮瘤反应。角蛋白染色可用于指示间皮细胞的分布,特别是显示间皮细胞渗透到间质或邻近结构中,但对区分良性和恶性增生没有帮助,因为两者都是角蛋白阳性的。虽然p53和EMA染色都被认为是间皮恶性肿瘤的标志物,但在我们的经验中,它们对个体病例没有帮助。
The separation of benign from malignant mesothelial proliferations has emerged as a major problem in the pathology of the serosal membranes. For both epithelial and spindle cell mesothelial processes, true stromal invasion is the most accurate indicator of malignancy, but stromal invasion is often difficult to assess, especially in small biopsies. In the pleural cavity, deep penetration of a thickened and fibrotic pleura or penetration of mesothelial cells into the fat of the chest wall are good indicators of malignancy; however, superficial entrapment of mesothelial cells and glands by organizing effusions is common in benign reactions and needs to be distinguished from invasion. In the peritoneal cavity, invasion of fat or of organ walls is again the most reliable indicator of malignancy, but entrapment of benign cells in organizing granulation tissue or between fat lobules is frequent and confusing. Proliferations confined to the pleural or peritoneal space, particularly linear arrays of atypical mesothelial cells on the free surface, should not be called malignant in the absence of unequivocal invasion. Cytologic atypia is often not helpful in separating benign from malignant reactions, because benign processes are commonly atypical and mesotheliomas are often deceptively monotonous. Densely packed mesothelial cells within the pleural space are frequent in benign reactions, but densely packed mesothelial cells within the stroma favor a diagnosis of malignancy. Organizing effusions (fibrous pleurisy) typically show zonation with high cellularity and cytologic atypia toward the pleural space and increasing fibrosis with decreasing cellularity and lesser atypia toward the chest wall, whereas sarcomatous (including desmoplastic) mesotheliomas do not demonstrate this type of zonation. Elongated capillaries perpendicular to the pleural surface are seen in organizing effusions but are not a feature of sarcomatous mesotheliomas. The combination of a paucicellular storiform pattern, plus invasion of the stroma (including fat and adjacent tissues), or bland necrosis, overtly sarcomatous foci, or distant metastases, is required for the diagnosis of desmoplastic mesothelioma. Necrosis is usually a sign of malignancy but is occasionally seen in benign mesothelial reactions. Keratin staining is useful in indicating the distribution of mesothelial cells, and particularly in demonstrating penetration of mesothelial cells into the stroma or adjacent structures, but is of no help in separating benign and malignant proliferations because both are keratin-positive. Although both p53 and EMA staining have been proposed as markers of mesothelial malignancy, in our experience they are not helpful for the individual case.