Papillary renal cell carcinoma

Quantitation of chromosomes 7 and 17 by FISH, analysis of chromosome 3p for LOH, and DNA ploidy

Christopher L. Corless, Hiroyuki Aburatani, Jonathan A. Fletcher, David E. Housman, Mahul Amin, David S. Weinberg

Research output: Contribution to journalArticle

79 Citations (Scopus)

Abstract

Papillary renal cell carcinoma (papillary RCC) is an uncommon histologic variant of RCC with distinct gross, microscopic, and immunohistochemical features. Recent karyotypic analyses suggest that papillary RCC differs from other types of RCC at the genetic level as well. Whereas nonpapillary (clear cell, granular cell) RCC is characterized by deletions in chromosome 3p, papillary tumors reportedly exhibit a pattern of chromosomal trisomies, typically including chromosomes 7 and 17. To further examine the relationship between overrepresentation of these chromosomes and papillary histology, archival material from 36 papillary tumors was subjected to fluorescence in situ hybridization (FISH) analysis using α-satellite repeat probes specific to 7 and 17. Excess signals for chromosome 17 were detected in 22 of 28 (78%) low-grade papillary tumors (Fuhrman nuclear grades 1 and 2), and in seven of eight (87%) high-grade tumors (grades 3 and 4). Correlation of chromosome 17 FISH signals with karyotypes performed on two low-grade and three high-grade tumors was excellent. Among the cases without evidence of excess chromosome 17 were three unusual papillary tumors with sclerotic and hyalinized fibrovascular cores. In two cases, comparison was made of FISH signals from multiple, separate gross nodules of tumor: concordance for trisomic 17 signals was observed in one case, but not in the other. Chromosome 7 signals were overrepresented in all seven papillary tumors examined. DNA ploidy was determined in 19 of the 36 tumors: a relationship between DNA ploidy and polysomy 7 or 17 was not apparent. To examine the possible role of chromosome 3p deletions in the development of papillary RCC, 11 cases were studied for loss of heterozygosity(LOH) at one or more loci in the region of 3p13-21. Only three of the 11 cases had LOH at these loci. The findings are discussed with respect to the development and progression of papillary RCC.

Original languageEnglish (US)
Pages (from-to)53-64
Number of pages12
JournalDiagnostic Molecular Pathology
Volume5
Issue number1
DOIs
StatePublished - Mar 7 1996
Externally publishedYes

Fingerprint

Chromosomes, Human, Pair 17
Chromosomes, Human, Pair 7
Ploidies
Loss of Heterozygosity
Fluorescence In Situ Hybridization
Renal Cell Carcinoma
Chromosomes
DNA
Neoplasms
Chromosome Deletion
Trisomy
Karyotype
Histology

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology

Cite this

Papillary renal cell carcinoma : Quantitation of chromosomes 7 and 17 by FISH, analysis of chromosome 3p for LOH, and DNA ploidy. / Corless, Christopher L.; Aburatani, Hiroyuki; Fletcher, Jonathan A.; Housman, David E.; Amin, Mahul; Weinberg, David S.

In: Diagnostic Molecular Pathology, Vol. 5, No. 1, 07.03.1996, p. 53-64.

Research output: Contribution to journalArticle

Corless, Christopher L. ; Aburatani, Hiroyuki ; Fletcher, Jonathan A. ; Housman, David E. ; Amin, Mahul ; Weinberg, David S. / Papillary renal cell carcinoma : Quantitation of chromosomes 7 and 17 by FISH, analysis of chromosome 3p for LOH, and DNA ploidy. In: Diagnostic Molecular Pathology. 1996 ; Vol. 5, No. 1. pp. 53-64.
@article{eb64aa07475b474cbe9018e4fdda4d0b,
title = "Papillary renal cell carcinoma: Quantitation of chromosomes 7 and 17 by FISH, analysis of chromosome 3p for LOH, and DNA ploidy",
abstract = "Papillary renal cell carcinoma (papillary RCC) is an uncommon histologic variant of RCC with distinct gross, microscopic, and immunohistochemical features. Recent karyotypic analyses suggest that papillary RCC differs from other types of RCC at the genetic level as well. Whereas nonpapillary (clear cell, granular cell) RCC is characterized by deletions in chromosome 3p, papillary tumors reportedly exhibit a pattern of chromosomal trisomies, typically including chromosomes 7 and 17. To further examine the relationship between overrepresentation of these chromosomes and papillary histology, archival material from 36 papillary tumors was subjected to fluorescence in situ hybridization (FISH) analysis using α-satellite repeat probes specific to 7 and 17. Excess signals for chromosome 17 were detected in 22 of 28 (78{\%}) low-grade papillary tumors (Fuhrman nuclear grades 1 and 2), and in seven of eight (87{\%}) high-grade tumors (grades 3 and 4). Correlation of chromosome 17 FISH signals with karyotypes performed on two low-grade and three high-grade tumors was excellent. Among the cases without evidence of excess chromosome 17 were three unusual papillary tumors with sclerotic and hyalinized fibrovascular cores. In two cases, comparison was made of FISH signals from multiple, separate gross nodules of tumor: concordance for trisomic 17 signals was observed in one case, but not in the other. Chromosome 7 signals were overrepresented in all seven papillary tumors examined. DNA ploidy was determined in 19 of the 36 tumors: a relationship between DNA ploidy and polysomy 7 or 17 was not apparent. To examine the possible role of chromosome 3p deletions in the development of papillary RCC, 11 cases were studied for loss of heterozygosity(LOH) at one or more loci in the region of 3p13-21. Only three of the 11 cases had LOH at these loci. The findings are discussed with respect to the development and progression of papillary RCC.",
author = "Corless, {Christopher L.} and Hiroyuki Aburatani and Fletcher, {Jonathan A.} and Housman, {David E.} and Mahul Amin and Weinberg, {David S.}",
year = "1996",
month = "3",
day = "7",
doi = "10.1097/00019606-199603000-00009",
language = "English (US)",
volume = "5",
pages = "53--64",
journal = "Diagnostic Molecular Pathology",
issn = "1052-9551",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Papillary renal cell carcinoma

T2 - Quantitation of chromosomes 7 and 17 by FISH, analysis of chromosome 3p for LOH, and DNA ploidy

AU - Corless, Christopher L.

AU - Aburatani, Hiroyuki

AU - Fletcher, Jonathan A.

AU - Housman, David E.

AU - Amin, Mahul

AU - Weinberg, David S.

PY - 1996/3/7

Y1 - 1996/3/7

N2 - Papillary renal cell carcinoma (papillary RCC) is an uncommon histologic variant of RCC with distinct gross, microscopic, and immunohistochemical features. Recent karyotypic analyses suggest that papillary RCC differs from other types of RCC at the genetic level as well. Whereas nonpapillary (clear cell, granular cell) RCC is characterized by deletions in chromosome 3p, papillary tumors reportedly exhibit a pattern of chromosomal trisomies, typically including chromosomes 7 and 17. To further examine the relationship between overrepresentation of these chromosomes and papillary histology, archival material from 36 papillary tumors was subjected to fluorescence in situ hybridization (FISH) analysis using α-satellite repeat probes specific to 7 and 17. Excess signals for chromosome 17 were detected in 22 of 28 (78%) low-grade papillary tumors (Fuhrman nuclear grades 1 and 2), and in seven of eight (87%) high-grade tumors (grades 3 and 4). Correlation of chromosome 17 FISH signals with karyotypes performed on two low-grade and three high-grade tumors was excellent. Among the cases without evidence of excess chromosome 17 were three unusual papillary tumors with sclerotic and hyalinized fibrovascular cores. In two cases, comparison was made of FISH signals from multiple, separate gross nodules of tumor: concordance for trisomic 17 signals was observed in one case, but not in the other. Chromosome 7 signals were overrepresented in all seven papillary tumors examined. DNA ploidy was determined in 19 of the 36 tumors: a relationship between DNA ploidy and polysomy 7 or 17 was not apparent. To examine the possible role of chromosome 3p deletions in the development of papillary RCC, 11 cases were studied for loss of heterozygosity(LOH) at one or more loci in the region of 3p13-21. Only three of the 11 cases had LOH at these loci. The findings are discussed with respect to the development and progression of papillary RCC.

AB - Papillary renal cell carcinoma (papillary RCC) is an uncommon histologic variant of RCC with distinct gross, microscopic, and immunohistochemical features. Recent karyotypic analyses suggest that papillary RCC differs from other types of RCC at the genetic level as well. Whereas nonpapillary (clear cell, granular cell) RCC is characterized by deletions in chromosome 3p, papillary tumors reportedly exhibit a pattern of chromosomal trisomies, typically including chromosomes 7 and 17. To further examine the relationship between overrepresentation of these chromosomes and papillary histology, archival material from 36 papillary tumors was subjected to fluorescence in situ hybridization (FISH) analysis using α-satellite repeat probes specific to 7 and 17. Excess signals for chromosome 17 were detected in 22 of 28 (78%) low-grade papillary tumors (Fuhrman nuclear grades 1 and 2), and in seven of eight (87%) high-grade tumors (grades 3 and 4). Correlation of chromosome 17 FISH signals with karyotypes performed on two low-grade and three high-grade tumors was excellent. Among the cases without evidence of excess chromosome 17 were three unusual papillary tumors with sclerotic and hyalinized fibrovascular cores. In two cases, comparison was made of FISH signals from multiple, separate gross nodules of tumor: concordance for trisomic 17 signals was observed in one case, but not in the other. Chromosome 7 signals were overrepresented in all seven papillary tumors examined. DNA ploidy was determined in 19 of the 36 tumors: a relationship between DNA ploidy and polysomy 7 or 17 was not apparent. To examine the possible role of chromosome 3p deletions in the development of papillary RCC, 11 cases were studied for loss of heterozygosity(LOH) at one or more loci in the region of 3p13-21. Only three of the 11 cases had LOH at these loci. The findings are discussed with respect to the development and progression of papillary RCC.

UR - http://www.scopus.com/inward/record.url?scp=0030027790&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030027790&partnerID=8YFLogxK

U2 - 10.1097/00019606-199603000-00009

DO - 10.1097/00019606-199603000-00009

M3 - Article

VL - 5

SP - 53

EP - 64

JO - Diagnostic Molecular Pathology

JF - Diagnostic Molecular Pathology

SN - 1052-9551

IS - 1

ER -