在微小（最小）前列腺腺癌中 TMPRSS2-ERG 基因融合状态。
TMPRSS2-ERG gene fusion status in minute (minimal) prostatic adenocarcinoma.
机构信息
Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
出版信息
Mod Pathol. 2009 Nov;22(11):1415-22. doi: 10.1038/modpathol.2009.121. Epub 2009 Sep 4.
Minute prostatic adenocarcinomas are considered to be of insufficient virulence. Given recent suggestions of TMPRSS2-ERG gene fusion association with aggressive prostatic adenocarcinoma, we evaluated the incidence of TMPRSS2-ERG fusion in minute prostatic adenocarcinomas. A total of 45 consecutive prostatectomies with minute adenocarcinoma were used for tissue microarray construction. A total of 63 consecutive non-minimal, Gleason Score 6 tumors, from a separate PSA Era prostatectomy tissue microarray, were used for comparison. FISH was carried out using ERG break-apart probes. Tumors were assessed for fusion by deletion (Edel) or split (Esplit), duplicated fusions and low-level copy number gain in normal ERG gene locus. Minute adenocarcinomas: Fusion was evaluable in 32/45 tumors (71%). Fifteen out of 32 (47%) tumors were positive for fusion. Six (19%) were of the Edel class and 7 (22%) were classified as combined Edel+Esplit. Non-minute adenocarcinomas (pT2): Fusion was identified in 20/30 tumors (67%). Four (13%) were of Edel class and 5 (17%) were combined Edel+Esplit. Duplicated fusions were encountered in 5 (16%) tumors. Non-minute adenocarcinomas (pT3): Fusion was identified in 19/33 (58%). Fusion was due to a deletion in 6 (18%) tumors. Seven tumors (21%) were classified as combined Edel+Esplit. One tumor showed Esplit alone. Duplicated fusions were encountered in 3 (9%) cases. The incidence of duplicated fusions was higher in non-minute adenocarcinomas (13 vs 0%; P=0.03). A trend for higher incidence of low-level copy number gain in normal ERG gene locus without fusion was noted in non-minute adenocarcinomas (10 vs 0%; P=0.07). We found a TMPRSS2-ERG fusion rate of 47% in minute adenocarcinomas. The latter is not significantly different from that of grade matched non-minute adenocarcinomas. The incidence of duplicated fusion was higher in non-minute adenocarcinomas. Our finding of comparable rate of TMPRSS2-ERG fusion in minute adenocarcinomas may argue against its value as a marker of aggressive prostate carcinoma phenotype.
微小前列腺腺癌被认为侵袭性较弱。鉴于最近 TMPRSS2-ERG 基因融合与侵袭性前列腺腺癌相关的提示，我们评估了微小前列腺腺癌中 TMPRSS2-ERG 融合的发生率。总共使用 45 例连续前列腺切除术的微小腺癌组织进行组织微阵列构建。总共使用来自另一个 PSA 时代前列腺切除术组织微阵列的 63 例连续非最小、Gleason 评分 6 的肿瘤进行比较。使用 ERG 断裂探针进行 FISH。通过缺失（Edel）或分裂（Esplit）、重复融合和正常 ERG 基因座的低水平拷贝数增益评估肿瘤融合。微小腺癌：可评估融合的肿瘤有 32/45 例（71%）。32 例中有 15 例（47%）肿瘤阳性融合。6 例（19%）为 Edel 类，7 例（22%）为 Edel+Esplit 联合类。非微小腺癌（pT2）：融合在 20/30 例肿瘤中（67%）被鉴定。4 例（13%）为 Edel 类，5 例（17%）为 Edel+Esplit 联合类。在 5 例（16%）肿瘤中遇到重复融合。非微小腺癌（pT3）：融合在 19/33 例（58%）中被鉴定。融合是由 6 例（18%）肿瘤的缺失引起的。7 例（21%）肿瘤被归类为 Edel+Esplit 联合类。1 例肿瘤仅表现为 Esplit。在 3 例（9%）病例中遇到重复融合。非微小腺癌中重复融合的发生率较高（13%比 0%；P=0.03）。注意到非微小腺癌中正常 ERG 基因座中融合无低水平拷贝数增益的发生率较高（10%比 0%；P=0.07）。我们发现微小腺癌中的 TMPRSS2-ERG 融合率为 47%。后者与分级匹配的非微小腺癌无显著差异。非微小腺癌中重复融合的发生率较高。我们在微小腺癌中发现 TMPRSS2-ERG 融合率相当，这可能表明其作为侵袭性前列腺癌表型的标志物价值不大。
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