Pim-I expression in prostatic intraepithelial neoplasia and human prostate cancer
Pim-I expression in prostatic intraepithelial neoplasia and human prostate cancer
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DOI：
10.1002/pros.20064
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发表时间：
2004-09-01
期刊：
影响因子：
2.8
通讯作者：
Egevad, L
中科院分区：
文献类型：
--
作者：
Valdman, A;Fang, XL;Egevad, L
背景PIM-1是丝氨酸/苏氨酸激酶的癌基因产物，已发现其通过磷酸化参与这些过程的靶蛋白而在诱导/抑制细胞凋亡、细胞周期进展和转录调节中起重要作用。最近，PIM-1的表达已被证明与前列腺癌临床结果的测量显著相关。采用免疫组织化学方法分析121例前列腺癌根治术患者中PIM-1在高级别前列腺上皮内瘤变（HGPIN）和前列腺癌中的表达模式。在68%的癌症中观察到中度至强烈的细胞质染色，12%也呈现核阳性。在Gleason评分（GS）7或更高的肿瘤中观察到中度至强表达，而在GS 6或更低的肿瘤中为58%（P = 0.04）。在97%的HGPIN病变中，染色强度为中度或重度。在65%的病例中，与癌症相比，PIM-1在HGPIN中过表达。在良性腺体中表达阴性或弱阳性。我们的数据表明，PIM-1在HGPIN过表达可能是前列腺恶性肿瘤发展的早期事件。此外，PIM-1表达为区分HGPIN与良性上皮提供了补充信息。(C)2004 Wiley-Liss，Inc.
BACKGROUND. PIM-1, an oncogene product of serine/threonine kinase, has been found to play an important role in induction/suppression of apoptosis, cell cycle progression, and transcriptional regulation by phosphorylating the target proteins involved in these processes. Recently, the expression of PIM-1 has been shown to correlate significantly with measures of prostate cancer clinical outcome.METHODS. Immunohistochemical analysis was used to characterize the patterns of PIM-1 expression in high grade prostatic intraepithelial neoplasia (HGPIN) and cancer in 121 radical prostatectomy specimens.RESULTS. Moderate to strong cytoplasmic staining was observed in 68% of cancers, 12% presented nuclear positivity as well. Moderate to strong expression was seen in 76% of tumors with Gleason score (GS) 7 or higher compared to 58% in tumors with GS 6 or lower (P = 0.04). The staining intensity was moderate or strong in 97% of HGPIN lesions. PIM-1 was overexpressed in HGPIN compared to cancer in 65% of cases. Expression in benign glands was negative or only weakly positive.CONCLUSION. Our data suggest that PIM-1 overexpression in HGPIN may be an early event in the development of prostate malignancy. Additionally, PIM-1 expression provides supplementary information for distinguishing HGPIN from benign epithelium. (C) 2004 Wiley-Liss, Inc.