Fan K, Dao D D, Schutz M, Fink L M
Department of Pathology and Laboratory Medicine, John L. McClellan Memorial Veterans Hospital, Little Rock, AK 72205.
Diagn Mol Pathol. 1994 Dec;3(4):265-70. doi: 10.1097/00019606-199412000-00009.
We have examined the loss of heterozygosity (LOH) of codon 72 and evaluated the overexpression of the tumor suppressor gene p53 in 43 primary human prostatic adenocarcinomas (PC). DNA from tumors and normal tissues were extracted from radical prostatectomy specimens. LOH was determined by restriction fragment length polymorphism analysis (RFLP) of the codon-specific endonuclease-digested polymerase chain reaction (PCR) products. Results showed 17 heterozygous cases (39%) among this patient group. Seven of the heterozygous cases displayed LOH. Six of the seven LOH cases were high-grade PCs with Gleason's combined score of > or = 7 and showed capsular invasion. One of the LOH cases, however, displayed an intermediate morphological score of 6 but also with evidence of capsular invasion. The 43 primary PCs were also examined for overexpression of p53 by a monoclonal antibody-mediated immunofluorescence reaction. Overexpression of nuclear p53 as detected by antibody was demonstrable only in tumors with combined morphological Grade > or = 7. No significant overexpression of p53 was noted in lower-grade tumors. In addition, 10 cases of benign prostatic hyperplasia (BPH) were evaluated for p53 expression. All 10 cases showed no detectable p53 overexpression.
我们检测了密码子72的杂合性缺失（LOH），并评估了43例原发性人类前列腺腺癌（PC）中肿瘤抑制基因p53的过表达情况。肿瘤组织和正常组织的DNA取自根治性前列腺切除术标本。通过对密码子特异性内切酶消化的聚合酶链反应（PCR）产物进行限制性片段长度多态性分析（RFLP）来确定LOH。结果显示，该患者组中有17例杂合病例（39%）。其中7例杂合病例出现了LOH。7例LOH病例中有6例为高级别PC，Gleason综合评分为≥7分，且有包膜侵犯。然而，其中1例LOH病例的形态学评分为中等的6分，但也有包膜侵犯的证据。通过单克隆抗体介导的免疫荧光反应，还对43例原发性PC进行了p53过表达检测。仅在形态学分级≥7分的肿瘤中检测到抗体介导的核p53过表达。在低级别肿瘤中未发现p53的明显过表达。此外，对10例良性前列腺增生（BPH）病例进行了p53表达评估。所有10例病例均未检测到p53过表达。
