Häussler O, Epstein J I, Amin M B, Heitz P U, Hailemariam S
Institute of Clinical Pathology, Department of Pathology, University of Zurich, Switzerland.
Hum Pathol. 1999 Sep;30(9):1077-86. doi: 10.1016/s0046-8177(99)90226-5.
There is scant information on the cell proliferation, apoptosis, oncogenes, and tumor suppressor genes status in adenosis. Forty-eight foci of adenosis were studied with immunohistochemistry for MIB-1; c-erbB-2, c-erbB-3, bcl-2 oncogenes; and p53. To evaluate apoptosis, the TdT dUTP nick end labeling (TUNEL) method was applied. Results were compared with the same studies on benign prostatic hyperplasia (BPH) (n = 20), low-grade prostatic intraepithelial neoplasia (PIN) (n = 10); high-grade PIN (n = 20), Gleason sum 2 to 6 cancer (n = 16); and Gleason sum 7 to 10 cancer (n = 22). MIB-1 proliferation index was lowest in BPH, followed by adenosis, low-grade prostatic intraepithelial neoplasia (PIN), low-grade cancer, high-grade PIN, and high-grade cancer. The apoptotic rate was generally low in all groups, although it was higher in PIN and cancer. In BPH and adenosis, bcl-2 was absent in luminal cells. In low- and high-grade PIN, both basal and luminal cells expressed bcl-2, whereas in cancer, expression was found in only 1 case (3%). C-erbB-2 showed absent or low values for cancer and adenosis, whereas it was commonly expressed in BPH and low- and high-grade PIN. Low expression in adenosis was also found with c-erbB-3 (6%) compared with all other groups. Expression of p53 was confined to cancer. Despite a significantly higher proliferation index rate compared with BPH, adenosis showed a markedly lower proliferating index when compared with low-grade PIN, high-grade PIN, and cancer. Expression of the oncogenes c-erbB-2 and cerbB-3 was very low in adenosis, and the staining pattern for bcl-2 was similar to that of BPH. These results provide additional evidence to that of prior studies that adenosis is a histological small acinar proliferation more akin to BPH than high-grade PIN or adenocarcinoma.
关于腺病中细胞增殖、凋亡、癌基因和肿瘤抑制基因状态的信息很少。对48个腺病病灶进行了免疫组织化学研究,检测MIB-1、c-erbB-2、c-erbB-3、bcl-2癌基因和p53。为评估细胞凋亡,应用了末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)法。将结果与对良性前列腺增生(BPH)(n = 20)、低级别前列腺上皮内瘤变(PIN)(n = 10)、高级别PIN(n = 20)、Gleason评分2至6分的癌症(n = 16)以及Gleason评分7至10分的癌症(n = 22)的相同研究进行比较。MIB-1增殖指数在BPH中最低,其次是腺病、低级别前列腺上皮内瘤变(PIN)、低级别癌症、高级别PIN和高级别癌症。所有组的凋亡率总体较低,尽管在PIN和癌症中较高。在BPH和腺病中,管腔细胞中不存在bcl-2。在低级别和高级别PIN中,基底细胞和管腔细胞均表达bcl-2,而在癌症中,仅1例(3%)有表达。c-erbB-2在癌症和腺病中表现为无表达或低表达,而在BPH以及低级别和高级别PIN中普遍表达。与所有其他组相比,腺病中c-erbB-3的表达也较低(6%)。p53的表达局限于癌症。尽管与BPH相比,腺病的增殖指数率显著更高,但与低级别PIN、高级别PIN和癌症相比,腺病的增殖指数明显更低。癌基因c-erbB-2和cerbB-3在腺病中的表达非常低,并且bcl-2的染色模式与BPH相似。这些结果为先前的研究提供了更多证据,表明腺病是一种组织学上的小腺泡增殖,与BPH更相似,而不是与高级别PIN或腺癌相似。