Microarray-based comparative genomic hybridization of pheochromocytoma cell lines from neurofibromatosis knockout mice reveals genetic alterations similar to those in human pheochromocytomas

James F. Powers, Arthur S. Tischler, Mansoor Mohammed, Rizwan C. Naeem

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Somatic genetic aberrations have been identified in both sporadic pheochromocytomas and those associated with familial tumor syndromes; however, individual variations between human tumors and the absence of in vitro human pheochromocytoma models hinder efforts to understand the roles of those aberrations in tumorigenesis. Pheochromocytomas occur frequently in neurofibromatosis knockout mice and we have recently developed cell lines from those tumors. The availability of multiple tumors from genetically identical animals provides a powerful tool for understanding the pathobiology of pheochromocytomas. For the present investigation, we performed a genomic scanning analysis of four mouse pheochromocytoma cell lines by standard cytogenetics and microarray-based comparative genomic hybridization in order to identify genetic common denominators. All of the lines showed losses of most or all of chromosome 9; three lines lost most or all of chromosome 4. Mouse chromosome 4 is homologous to human chromosome 1p, which is the most frequent deletion in human pheochromocytomas. Mouse chromosome 9 shows large areas of homology to human 3p, 3q, and 11q, which are also frequently deleted. These comparisons suggest that genetic mechanisms in the genesis of pheochromocytomas may be similar across species. Additional changes that may be specific to this model included complete or partial gains of chromosome 12 as seen in 3 of the 4 lines analyzed by array CGH.

Original languageEnglish (US)
Pages (from-to)27-31
Number of pages5
JournalCancer Genetics and Cytogenetics
Volume159
Issue number1
DOIs
StatePublished - May 2005
Externally publishedYes

Fingerprint

Neurofibromatoses
Comparative Genomic Hybridization
PC12 Cells
Pheochromocytoma
Knockout Mice
Chromosomes, Human, Pair 9
Chromosomes, Human, Pair 4
Chromosomes, Human, Pair 12
Neoplasms
Human Chromosomes
Tumor Cell Line
Cytogenetics
Carcinogenesis

ASJC Scopus subject areas

  • Cancer Research
  • Genetics
  • Molecular Biology

Cite this

@article{92b0a4b30d25477d952a13185282d7aa,
title = "Microarray-based comparative genomic hybridization of pheochromocytoma cell lines from neurofibromatosis knockout mice reveals genetic alterations similar to those in human pheochromocytomas",
abstract = "Somatic genetic aberrations have been identified in both sporadic pheochromocytomas and those associated with familial tumor syndromes; however, individual variations between human tumors and the absence of in vitro human pheochromocytoma models hinder efforts to understand the roles of those aberrations in tumorigenesis. Pheochromocytomas occur frequently in neurofibromatosis knockout mice and we have recently developed cell lines from those tumors. The availability of multiple tumors from genetically identical animals provides a powerful tool for understanding the pathobiology of pheochromocytomas. For the present investigation, we performed a genomic scanning analysis of four mouse pheochromocytoma cell lines by standard cytogenetics and microarray-based comparative genomic hybridization in order to identify genetic common denominators. All of the lines showed losses of most or all of chromosome 9; three lines lost most or all of chromosome 4. Mouse chromosome 4 is homologous to human chromosome 1p, which is the most frequent deletion in human pheochromocytomas. Mouse chromosome 9 shows large areas of homology to human 3p, 3q, and 11q, which are also frequently deleted. These comparisons suggest that genetic mechanisms in the genesis of pheochromocytomas may be similar across species. Additional changes that may be specific to this model included complete or partial gains of chromosome 12 as seen in 3 of the 4 lines analyzed by array CGH.",
author = "Powers, {James F.} and Tischler, {Arthur S.} and Mansoor Mohammed and Naeem, {Rizwan C.}",
year = "2005",
month = "5",
doi = "10.1016/j.cancergencyto.2004.09.018",
language = "English (US)",
volume = "159",
pages = "27--31",
journal = "Cancer Genetics and Cytogenetics",
issn = "0165-4608",
publisher = "Elsevier Inc.",
number = "1",

}

TY - JOUR

T1 - Microarray-based comparative genomic hybridization of pheochromocytoma cell lines from neurofibromatosis knockout mice reveals genetic alterations similar to those in human pheochromocytomas

AU - Powers, James F.

AU - Tischler, Arthur S.

AU - Mohammed, Mansoor

AU - Naeem, Rizwan C.

PY - 2005/5

Y1 - 2005/5

N2 - Somatic genetic aberrations have been identified in both sporadic pheochromocytomas and those associated with familial tumor syndromes; however, individual variations between human tumors and the absence of in vitro human pheochromocytoma models hinder efforts to understand the roles of those aberrations in tumorigenesis. Pheochromocytomas occur frequently in neurofibromatosis knockout mice and we have recently developed cell lines from those tumors. The availability of multiple tumors from genetically identical animals provides a powerful tool for understanding the pathobiology of pheochromocytomas. For the present investigation, we performed a genomic scanning analysis of four mouse pheochromocytoma cell lines by standard cytogenetics and microarray-based comparative genomic hybridization in order to identify genetic common denominators. All of the lines showed losses of most or all of chromosome 9; three lines lost most or all of chromosome 4. Mouse chromosome 4 is homologous to human chromosome 1p, which is the most frequent deletion in human pheochromocytomas. Mouse chromosome 9 shows large areas of homology to human 3p, 3q, and 11q, which are also frequently deleted. These comparisons suggest that genetic mechanisms in the genesis of pheochromocytomas may be similar across species. Additional changes that may be specific to this model included complete or partial gains of chromosome 12 as seen in 3 of the 4 lines analyzed by array CGH.

AB - Somatic genetic aberrations have been identified in both sporadic pheochromocytomas and those associated with familial tumor syndromes; however, individual variations between human tumors and the absence of in vitro human pheochromocytoma models hinder efforts to understand the roles of those aberrations in tumorigenesis. Pheochromocytomas occur frequently in neurofibromatosis knockout mice and we have recently developed cell lines from those tumors. The availability of multiple tumors from genetically identical animals provides a powerful tool for understanding the pathobiology of pheochromocytomas. For the present investigation, we performed a genomic scanning analysis of four mouse pheochromocytoma cell lines by standard cytogenetics and microarray-based comparative genomic hybridization in order to identify genetic common denominators. All of the lines showed losses of most or all of chromosome 9; three lines lost most or all of chromosome 4. Mouse chromosome 4 is homologous to human chromosome 1p, which is the most frequent deletion in human pheochromocytomas. Mouse chromosome 9 shows large areas of homology to human 3p, 3q, and 11q, which are also frequently deleted. These comparisons suggest that genetic mechanisms in the genesis of pheochromocytomas may be similar across species. Additional changes that may be specific to this model included complete or partial gains of chromosome 12 as seen in 3 of the 4 lines analyzed by array CGH.

UR - http://www.scopus.com/inward/record.url?scp=18144397194&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=18144397194&partnerID=8YFLogxK

U2 - 10.1016/j.cancergencyto.2004.09.018

DO - 10.1016/j.cancergencyto.2004.09.018

M3 - Article

VL - 159

SP - 27

EP - 31

JO - Cancer Genetics and Cytogenetics

JF - Cancer Genetics and Cytogenetics

SN - 0165-4608

IS - 1

ER -