Papillary renal tumors. Morphologic, cytochemical, and genotypic features

Abstract

Background. Papillary renal tumors lack alterations of chromosome 3 and show trisomy of chromosomes 7 and 17, genotypic features distinct from nonpapillary carcinomas. Methods. The authors examined 39 papillary renal neoplasms to identify morphologic features allowing distinction of high grade from low grade tumors. Twenty‐nine papillary tumors and 13 nonpapillary tumors were examined for the presence of trisomy of chromosome 7 using fluorescence in situ hybridization. Data recorded included tumor size, stage, grade, architectural pattern, and the presence of glycogen, foam cells, and iron. Results. Nineteen tumors were classified as low grade and 20 as high grade. The high grade tumors more often formed tall papillae with solid and tubular areas and had more intracellular glycogen, whereas the low grade tumors were more often trabecular. There was no significant difference in tumor size or iron deposition. High grade tumors were of higher stage. Foam cells more commonly were noted in low grade tumors. Sixty‐seven percent of low grade, 43% of high grade, and none of the non‐papillary tumors showed trisomy of chromosome 7. Metastases developed only in patients with high grade papillary tumors (10/19, 7 within 2 years of diagnosis), all of whom died of disease. Conclusions. Papillary renal carcinomas with high nuclear grade are more likely to behave in an aggressive fashion, whereas those with low nuclear grade may be associated with longer disease free survival. Furthermore, trisomy of chromosome 7 can be identified by fluorescence in situ hybridization and is useful in differentiating true papillary from nonpapillary renal neoplasms. Cancer 1995; 76:669–73.

Renal mucinous tubular and spindle carcinoma lacks the gains of chromosomes 7 and 17 and losses of chromosome Y that are prevalent in papillary renal cell carcinoma

“…17,[23][24][25][26][27][28][34][35][36] The typical gains of chromosome 7 and 17 and loss of Y in papillary renal cell carcinomas have been observed in several FISH-based studies, and FISH analyses with centromeric probes for chromosomes 7, 17 and Y have been previously proposed to have a potential role in the differential diagnosis of papillary renal cell tumors with metanephric adenomas. 25,27,32,35,37 Furthermore, recent studies performed with multicolor FISH confirmed the typical chromosomal abnormalities described in papillary renal cell carcinomas and interphase FISH may be considered as a sensitive and specific technique for a rapid and accurate identification of distinctive genetic abnormalities, that are potentially useful in the distinction of the different histotypes of renal cell carcinomas. 38,39 In conclusion, analysis of chromosomes 7, 17 and Y by FISH with centromeric probes showed that mucinous tubular and spindle cell carcinomas lack the gains of chromosomes 7 and 17 and losses of chromosome Y, that are prevalent in papillary renal cell carcinomas, and may be helpful in the differential diagnosis with classic and sarcomatoid papillary renal cell carcinomas.…”

Metanephric adenoma: the utility of immunohistochemical and cytogenetic analyses in differential diagnosis, including solid variant papillary renal cell carcinoma and epithelial-predominant nephroblastoma

“…Metanephric adenoma, an uncommon benign tumor, can show morphological similarities to some papillary renal cell carcinomas and epithelial-predominant however, compression of the papillary structures can result in more solid architectural patterns. 19 It is in these instances that the differential diagnosis includes metanephric adenoma. Microscopically, most nephroblastomas are triphasic, containing blastemal cells and epithelial and stromal elements.…”

Involvement of adrenomedullin induced by hypoxia in angiogenesis in human renal cell carcinoma

“…Previous studies have demonstrated that the hypovascular papillary renal carcinomas have different biological characteristics compared to hypervascular conventional (clear cell) renal carcinomas. [25][26][27] These results suggest that AM and VEGF may be in concert with the forming histopathologic character and AM may play a role in tumor growth in conjunction with VEGF, which induces tumor angiogenesis in RCC. Zhao et al reported that AM strongly stimulated endothelial cell growth and acted as an angiogenic factor.…”