PMID- 8919546
OWN - NLM
STAT- MEDLINE
DCOM- 19970106
LR  - 20191101
IS  - 1052-9551 (Print)
IS  - 1052-9551 (Linking)
VI  - 5
IP  - 1
DP  - 1996 Mar
TI  - Papillary renal cell carcinoma: quantitation of chromosomes 7 and 17 by FISH, 
      analysis of chromosome 3p for LOH, and DNA ploidy.
PG  - 53-64
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 
      alpha-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.
FAU - Corless, C L
AU  - Corless CL
AD  - Department of Pathology, Brigham & Women's Hospital, Boston, Massachusetts, USA.
FAU - Aburatani, H
AU  - Aburatani H
FAU - Fletcher, J A
AU  - Fletcher JA
FAU - Housman, D E
AU  - Housman DE
FAU - Amin, M B
AU  - Amin MB
FAU - Weinberg, D S
AU  - Weinberg DS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Diagn Mol Pathol
JT  - Diagnostic molecular pathology : the American journal of surgical pathology, part 
      B
JID - 9204924
SB  - IM
MH  - Adult
MH  - Aged
MH  - Carcinoma, Renal Cell/*genetics/pathology
MH  - *Chromosome Deletion
MH  - *Chromosomes, Human, Pair 17
MH  - *Chromosomes, Human, Pair 3
MH  - *Chromosomes, Human, Pair 7
MH  - Female
MH  - Heterozygote
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Karyotyping
MH  - Kidney Neoplasms/*genetics/pathology
MH  - Male
MH  - Middle Aged
MH  - *Ploidies
EDAT- 1996/03/01 00:00
MHDA- 1996/03/01 00:01
CRDT- 1996/03/01 00:00
PHST- 1996/03/01 00:00 [pubmed]
PHST- 1996/03/01 00:01 [medline]
PHST- 1996/03/01 00:00 [entrez]
AID - 10.1097/00019606-199603000-00009 [doi]
PST - ppublish
SO  - Diagn Mol Pathol. 1996 Mar;5(1):53-64. doi: 10.1097/00019606-199603000-00009.