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PTEN在蕈样肉芽肿中的表达及其与杂合性缺失的相关性。

Expression of PTEN in mycosis fungoides and correlation with loss of heterozygosity.

作者信息

Katona Terrence M, Smoller Bruce R, Webb Alden L, Hattab Eyas M, Khalil Ahmed, Hiatt Kim M

机构信息

Department of Pathology, Division of Dermatopathology, University of Arkansas for Medical Sciences, Little Rock, AR, USA.

出版信息

Am J Dermatopathol. 2013 Jul;35(5):555-60. doi: 10.1097/DAD.0b013e318276cc68.

DOI:10.1097/DAD.0b013e318276cc68
PMID:23715078
Abstract

BACKGROUND

Mycosis fungoides (MF) exhibits a variety of underlying molecular defects including aberrations involving the PTEN tumor suppressor gene. Specifically, loss of heterozygosity of PTEN has been previously demonstrated. We hypothesize that abnormalities of PTEN may result in altered immunohistochemical expression of its protein product.

METHODS

Thirty-six MF specimens were stained with monoclonal antibody against PTEN protein. The percentage of nuclei retaining PTEN expression and the staining intensity was recorded.

RESULTS

Average percentage of lymphoma cells retaining expression of the PTEN protein was 92% within patch-stage lesions, 81.4% in plaque-stage lesions, and 81.1% in tumor-stage lesions. Average intensity of staining for patch-stage lesions was 2.90, 2.50 for plaque lesions and 2.44 for tumor lesions. Cases lacking loss of heterozygozity at PTEN (n = 6) had an average expression of 81% and an average intensity of staining of 2.42. Whereas, cases with loss of heterozygozity at PTEN (n = 6) had an average expression of 75% of cells with an average staining intensity of 2.33.

CONCLUSIONS

The percentage of cells retaining PTEN and staining intensity decrease from patch- to plaque-stage lesions, whereas both parameters show mild diminution in tumor lesions compared with plaque lesions. PTEN expression in a small sample seems to correlate with previous demonstration of loss of heterozygosity at the molecular level. Although a trend for loss of PTEN expression exists with histologic progression of MF, the effect is modest and may not represent the pivotal defect in MF pathogenesis.

摘要

背景

蕈样肉芽肿(MF)存在多种潜在的分子缺陷,包括涉及PTEN肿瘤抑制基因的畸变。具体而言,先前已证实PTEN杂合性缺失。我们推测PTEN异常可能导致其蛋白产物免疫组化表达改变。

方法

36例MF标本用抗PTEN蛋白单克隆抗体染色。记录保留PTEN表达的细胞核百分比及染色强度。

结果

在斑片期病变中,保留PTEN蛋白表达的淋巴瘤细胞平均百分比为92%,斑块期病变为81.4%,肿瘤期病变为81.1%。斑片期病变的平均染色强度为2.90,斑块期病变为2.50,肿瘤期病变为2.44。PTEN无杂合性缺失的病例(n = 6)平均表达率为81%,平均染色强度为2.42。而PTEN有杂合性缺失的病例(n = 6)平均细胞表达率为75%,平均染色强度为2.33。

结论

从斑片期到斑块期病变,保留PTEN的细胞百分比和染色强度降低,而与斑块期病变相比,肿瘤期病变的这两个参数均有轻度降低。小样本中的PTEN表达似乎与分子水平上先前证实的杂合性缺失相关。虽然随着MF的组织学进展存在PTEN表达缺失的趋势,但这种影响较小,可能不代表MF发病机制中的关键缺陷。

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