Riddle Nicole D, Gorden Lemuel, Rojiani Mumtaz V, Hakam Ardeshir, Rojiani Amyn M
Department of Pathology and Cell Biology, University of South Florida, Tampa, FL 33610, USA.
Int J Clin Exp Pathol. 2010 Jun 12;3(5):515-21.
Neurofibromatosis type 1 (NF1) provides a unique system to evaluate the complete range of neoplastic expressions, from encapsulated benignity to invasiveness and malignancy. This study was aimed at determining whether CD44 and p53 may serve as indicators of malignant progression of neurofibroma. CD44, a transmembrane glycoprotein receptor for hyaluronic acid, and participates in cell-extracellular matrix interactions and migration. CD44 may play a vital role, either through under or overexpression, with invasion and metastases of tumors, altering their ability to infiltrate the adjacent tissue. The tumor suppressor gene, p53, has also been implicated in malignant progression of various human tumors including malignant peripheral nerve sheath tumors (MPNST). A total of 44 tumors from 33 patients with NF1 were evaluated with an anti-human CD44H, CD44 splice variant v6 and anti-p53 monoclonal antibodies. Morphologic expression patterns of expression were evaluated for CD44 while semiquantitative criteria were applied to assess, p53 nuclear positivity. Immunoexpression of p53 was markedly higher in 12 of 16 MPNST (75%). Thirteen of 28 (46%) benign neurofibroma also had some expression of p53 above 'normal level', although much lower than the MPNST. Plexiform neurofibroma did not differ from other benign lesions in their expression of p53. Our results suggest that p53 mutation as evidenced by immunohistochemical overexpression is a factor in malignant transformation and progression of neurofibroma. 70% of benign neurofibroma demonstrated some, usually focal, CD44 positivity. The pattern of CD44 expression in plexiform neurofibroma was revealing, as it was maximal in the 'nonencapsulated' portions of the tumors. Eight of 11 (72%) locally infiltrative cutaneous neurofibroma and 13 of 16 (81%) MPNST exhibited diffuse CD44 positivity. CD44v6 expression was positive in control tissues but was not identified in any of tumor samples. Also, within the confines of encapsulated tumors CD44 expression is limited, while in poorly circumscribed neurofibroma CD44 expression is upregulated. This is interpreted as a reflection of the interaction of CD44+ tumor cells with extracellular matrix, hence facilitating infiltrative behavior.
1型神经纤维瘤病(NF1)提供了一个独特的系统,可用于评估从包膜性良性肿瘤到侵袭性和恶性肿瘤的完整肿瘤表达范围。本研究旨在确定CD44和p53是否可作为神经纤维瘤恶性进展的指标。CD44是一种透明质酸跨膜糖蛋白受体,参与细胞与细胞外基质的相互作用和迁移。CD44可能通过低表达或高表达在肿瘤的侵袭和转移中发挥重要作用,改变其浸润相邻组织的能力。肿瘤抑制基因p53也与包括恶性外周神经鞘瘤(MPNST)在内的各种人类肿瘤的恶性进展有关。用抗人CD44H、CD44剪接变体v6和抗p53单克隆抗体对33例NF1患者的44个肿瘤进行了评估。评估CD44的形态学表达模式,同时应用半定量标准评估p53核阳性情况。16例MPNST中有12例(75%)p53的免疫表达明显更高。28例(46%)良性神经纤维瘤中有13例p53表达也高于“正常水平”,尽管远低于MPNST。丛状神经纤维瘤在p53表达方面与其他良性病变无差异。我们的结果表明,免疫组化高表达所证明的p53突变是神经纤维瘤恶性转化和进展的一个因素。70%的良性神经纤维瘤表现出一些通常为局灶性的CD44阳性。丛状神经纤维瘤中CD44的表达模式具有启示意义,因为在肿瘤的“无包膜”部分表达最高。11例局部浸润性皮肤神经纤维瘤中有8例(72%)和16例MPNST中有13例(81%)表现出弥漫性CD44阳性。CD44v6在对照组织中表达阳性,但在任何肿瘤样本中均未检测到。此外,在包膜性肿瘤范围内,CD44表达受限,而在边界不清的神经纤维瘤中,CD44表达上调。这被解释为CD44+肿瘤细胞与细胞外基质相互作用的反映,从而促进浸润行为。