Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka, 812-8582, Japan.
Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Virchows Arch. 2024 Aug;485(2):299-306. doi: 10.1007/s00428-024-03840-6. Epub 2024 Jun 14.
In papillary renal neoplasm with reverse polarity (PRNRP), the status of chromosomal copy number alterations, especially chromosomes 7/17 gain and chromosome Y loss, has remained controversial. In the literatures, there is a discrepancy among the results of chromosomal alteration in PRNRP depending on the analytical methods. Here, we comprehensively analyzed the status of chromosomal abnormalities in PRNRP. Nineteen PRNRP cases were analyzed by fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC), five of which were additionally subjected to array-based comparative genomic hybridization (aCGH) analysis. Fifteen cases of PRCC were used as controls. From the aCGH results, no genome copy number abnormalities were found in the five PRNRP cases. By FISH, numbers of nuclei with abnormal chromosomal signals in PRNRP (centromere 7 gain: 11-21% of nuclei, centromere 17 gain: 11% of nuclei, centromere Y loss: 14-31% of nuclei) were similar to those in non-neoplastic tubular cells (centromere 7 gain: 11-15% of nuclei, centromere 17 gain: 12-15% of nuclei, centromere Y loss: 13-45% of nuclei). c-MET immunohistochemical overexpression, a substitute marker for chromosome 7 trisomy, was observed in 0 of 19 PRNRP cases, consistent with the analyses by aCGH and NGS regarding chromosome 7 gain. Taken together, the frequency of chromosomal alterations in PRNRP is similar to that in non-neoplastic tubular cells, and lower than that in PRCC. Our data suggest that PRNRP has a different tumorigenesis and is a distinct entity from PRCC.
在反向极性肾肿瘤(PRNRP)中,染色体拷贝数改变的状态,尤其是染色体 7/17 获得和染色体 Y 丢失,一直存在争议。在文献中,PRNRP 中的染色体改变结果因分析方法而异。在这里,我们全面分析了 PRNRP 中染色体异常的状态。通过荧光原位杂交(FISH)和免疫组织化学(IHC)分析了 19 例 PRNRP 病例,其中 5 例还进行了基于阵列的比较基因组杂交(aCGH)分析。15 例 PRCC 作为对照。从 aCGH 结果来看,5 例 PRNRP 中未发现基因组拷贝数异常。通过 FISH,PRNRP 中异常染色体信号核的数量(着丝粒 7 获得:11-21%的核,着丝粒 17 获得:11%的核,着丝粒 Y 丢失:14-31%的核)与非肿瘤管状细胞相似(着丝粒 7 获得:11-15%的核,着丝粒 17 获得:12-15%的核,着丝粒 Y 丢失:13-45%的核)。c-MET 免疫组织化学过表达,染色体 7 三体的替代标志物,在 19 例 PRNRP 病例中均未观察到,与 aCGH 和 NGS 对染色体 7 获得的分析一致。综上所述,PRNRP 的染色体改变频率与非肿瘤管状细胞相似,低于 PRCC。我们的数据表明,PRNRP 的肿瘤发生机制不同,是一种与 PRCC 不同的实体。