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Absent p53 immunohistochemical staining in a pituitary carcinoma.

机译:垂体癌中缺乏p53免疫组织化学染色。

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BACKGROUND: Carcinomatous transformation of pituitary adenomas is uncommon, and is generally accompanied by nuclear accumulation of p53 protein. Pituitary carcinoma lacking accumulation of p53 protein is very rare, only two such cases being previously reported. METHODS: A patient presented with visual disturbance and cranial nerve palsies and was found to have a suprasellar mass. He underwent both transphenoidal and transfrontal excision of a nonfunctioning pituitary adenoma which recurred several times. The third recurrence was accompanied by multiple dural-based metastases. Despite aggressive surgical management, he continued to develop additional intracranial lesions and died two years after the discovery of metastatic disease. Specimens from 1984, 1995, 1997 and 1998 were available for histological and immunocytochemical analysis. Antibodies recognizing the pituitary hormones (ACTH, PRL, GH, FSH, LH and TSH), as well as cytokeratin, epithelial membrane antigen (EMA), glial fibrillary acidic protein (GFAP) and chromogranin A were applied to investigate the lineage of the neoplasm. Antisera specific for Ki-67 (MIB-1) and p53 protein were also applied to further delineate the biology of the tumour. RESULTS: Although cytokeratin and chromogranin A were detected in neoplastic cells. no expression of pituitary hormones was demonstrable, indicative of a nonfunctioning, null-cell pituitary adenoma. Nuclear pleomorphism and mitotic activity increased with subsequent resections. Abnormal accumulation of p53 protein was not observed, neither in early resections nor in the metastatic deposits. CONCLUSIONS: Failure to demonstrate p53 protein accumulation does not ensure a favourable outcome for pituitary adenoma. Accordingly, pituitary carcinoma may occur in the absence of p53 accumulation. The factors which underlie aggressive behaviour of pituitary neoplasms are uncertain but are under investigation.
机译:背景:垂体腺瘤的癌变并不常见,通常伴有p53蛋白的核积累。缺乏p53蛋白积聚的垂体癌非常罕见,以前仅报道过两例。方法:一名患者出现视觉障碍和颅神经麻痹,并被发现具有鞍上肿块。他经历了无功能的垂体腺瘤的经蝶骨切除和经额叶切除,复发了几次。第三次复发伴有多个基于硬脑膜的转移。尽管采取了积极的外科手术治疗方法,他仍继续发展其他颅内病变,并在发现转移性疾病两年后死亡。 1984、1995、1997和1998年的标本可用于组织学和免疫细胞化学分析。识别垂体激素(ACTH,PRL,GH,FSH,LH和TSH)的抗体,以及细胞角蛋白,上皮膜抗原(EMA),神经胶质纤维酸性蛋白(GFAP)和嗜铬粒蛋白A的抗体被用于研究肿瘤的谱系。对Ki-67(MIB-1)和p53蛋白具有特异性的抗血清也被用于进一步描述肿瘤的生物学特性。结果:尽管在肿瘤细胞中检测到了细胞角蛋白和嗜铬粒蛋白A。没有可证实的垂体激素表达,说明无功能的垂体-空细胞腺瘤。核多态性和有丝分裂活性随随后的切除而增加。在早期切除术和转移性沉积物中均未观察到p53蛋白的异常积累。结论:未能证明p53蛋白积聚不能确保垂体腺瘤的良好预后。因此,在不存在p53蓄积的情况下可能发生垂体癌。垂体肿瘤侵袭行为的基础因素尚不确定,但仍在研究中。

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