Tumor size-related DNA copy number changes occur in solitary fibrous tumors but not in hemangiopericytomas

Markku M. Miettinen, Wael El-Rifai, Maarit Sarlomo-Rikala, Leif C. Andersson, Sakari Knuutila

Research output: Contribution to journalArticle

77 Citations (Scopus)

Abstract

Solitary fibrous tumor (SFT) presenting in the pleura and other soft tissue sites and hemangiopericytoma (HPC) presenting at various soft tissue sites are mesenchymal tumors that share many histologic and immunohistochemical features. This raises the questions of whether these tumors are related and whether they belong within the spectrum of a single biologic entity. The behavior of both SFTs and HPCs is difficult to predict histologically. The genetic background of both SFTs and HPCs is poorly known, but it could be helpful in the evaluation of malignancy and could give clues to their possible relationship. In this study, we analyzed 15 SFTs and 11 HPCs by comparative genomic hybridization (CGH), a powerful molecular cytogenetic tool that can be applied to DNA extracted from formaldehyde- fixed and paraffin-embedded tissue. All of these tumors were immunohistochemically similar and showed reactivity for CD34-antigen but not for keratins, desmin, or muscle actins. Only 1 SFT smaller than 10 cm showed DNA copy number changes (a single loss in chromosome 13), but 7 of 8 SFTs larger than 10 cm (including all 4 tumors with more than 4 mitoses per 10 high power fields) showed changes, mostly chromosomal gains in 5q 7, 8, 12, and 18. Four cases showed losses, two of them in chromosome 13 and two others in 20q. These findings suggest that CGH might be useful in the evaluation of malignant transformation in SFT. The most common change, gain of the entire chromosome 8, seen in two cases as the only change, suggests trisomy 8 and parallels a similar finding previously described in other fibrous tumors, such as subsets of desmoid fibromatosis and infantile fibrosarcoma. In contrast, HPCs, including large and mitotically active tumors, showed no DNA copy number changes on CGH. This suggests that HPC is genetically different from SFT.

Original languageEnglish (US)
Pages (from-to)1194-1200
Number of pages7
JournalModern Pathology
Volume10
Issue number12
StatePublished - Dec 1 1997
Externally publishedYes

Fingerprint

DNA Copy Number Variations
Solitary Fibrous Tumors
Hemangiopericytoma
Comparative Genomic Hybridization
Neoplasms
Chromosomes, Human, Pair 13
CD34 Antigens
Aggressive Fibromatosis
Chromosomes, Human, Pair 8
Chromosomes, Human, Pair 7
Desmin
Fibroma
Pleura
Fibrosarcoma
Keratins
Mitosis
Cytogenetics
Paraffin
Formaldehyde
Actins

Keywords

  • Amplification
  • Comparative genomic hybridization
  • Deletion

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Miettinen, M. M., El-Rifai, W., Sarlomo-Rikala, M., Andersson, L. C., & Knuutila, S. (1997). Tumor size-related DNA copy number changes occur in solitary fibrous tumors but not in hemangiopericytomas. Modern Pathology, 10(12), 1194-1200.

Tumor size-related DNA copy number changes occur in solitary fibrous tumors but not in hemangiopericytomas. / Miettinen, Markku M.; El-Rifai, Wael; Sarlomo-Rikala, Maarit; Andersson, Leif C.; Knuutila, Sakari.

In: Modern Pathology, Vol. 10, No. 12, 01.12.1997, p. 1194-1200.

Research output: Contribution to journalArticle

Miettinen, MM, El-Rifai, W, Sarlomo-Rikala, M, Andersson, LC & Knuutila, S 1997, 'Tumor size-related DNA copy number changes occur in solitary fibrous tumors but not in hemangiopericytomas', Modern Pathology, vol. 10, no. 12, pp. 1194-1200.
Miettinen MM, El-Rifai W, Sarlomo-Rikala M, Andersson LC, Knuutila S. Tumor size-related DNA copy number changes occur in solitary fibrous tumors but not in hemangiopericytomas. Modern Pathology. 1997 Dec 1;10(12):1194-1200.
Miettinen, Markku M. ; El-Rifai, Wael ; Sarlomo-Rikala, Maarit ; Andersson, Leif C. ; Knuutila, Sakari. / Tumor size-related DNA copy number changes occur in solitary fibrous tumors but not in hemangiopericytomas. In: Modern Pathology. 1997 ; Vol. 10, No. 12. pp. 1194-1200.
@article{e1381cddc6ca4df18b5a25435b1a4a4b,
title = "Tumor size-related DNA copy number changes occur in solitary fibrous tumors but not in hemangiopericytomas",
abstract = "Solitary fibrous tumor (SFT) presenting in the pleura and other soft tissue sites and hemangiopericytoma (HPC) presenting at various soft tissue sites are mesenchymal tumors that share many histologic and immunohistochemical features. This raises the questions of whether these tumors are related and whether they belong within the spectrum of a single biologic entity. The behavior of both SFTs and HPCs is difficult to predict histologically. The genetic background of both SFTs and HPCs is poorly known, but it could be helpful in the evaluation of malignancy and could give clues to their possible relationship. In this study, we analyzed 15 SFTs and 11 HPCs by comparative genomic hybridization (CGH), a powerful molecular cytogenetic tool that can be applied to DNA extracted from formaldehyde- fixed and paraffin-embedded tissue. All of these tumors were immunohistochemically similar and showed reactivity for CD34-antigen but not for keratins, desmin, or muscle actins. Only 1 SFT smaller than 10 cm showed DNA copy number changes (a single loss in chromosome 13), but 7 of 8 SFTs larger than 10 cm (including all 4 tumors with more than 4 mitoses per 10 high power fields) showed changes, mostly chromosomal gains in 5q 7, 8, 12, and 18. Four cases showed losses, two of them in chromosome 13 and two others in 20q. These findings suggest that CGH might be useful in the evaluation of malignant transformation in SFT. The most common change, gain of the entire chromosome 8, seen in two cases as the only change, suggests trisomy 8 and parallels a similar finding previously described in other fibrous tumors, such as subsets of desmoid fibromatosis and infantile fibrosarcoma. In contrast, HPCs, including large and mitotically active tumors, showed no DNA copy number changes on CGH. This suggests that HPC is genetically different from SFT.",
keywords = "Amplification, Comparative genomic hybridization, Deletion",
author = "Miettinen, {Markku M.} and Wael El-Rifai and Maarit Sarlomo-Rikala and Andersson, {Leif C.} and Sakari Knuutila",
year = "1997",
month = "12",
day = "1",
language = "English (US)",
volume = "10",
pages = "1194--1200",
journal = "Modern Pathology",
issn = "0893-3952",
publisher = "Nature Publishing Group",
number = "12",

}

TY - JOUR

T1 - Tumor size-related DNA copy number changes occur in solitary fibrous tumors but not in hemangiopericytomas

AU - Miettinen, Markku M.

AU - El-Rifai, Wael

AU - Sarlomo-Rikala, Maarit

AU - Andersson, Leif C.

AU - Knuutila, Sakari

PY - 1997/12/1

Y1 - 1997/12/1

N2 - Solitary fibrous tumor (SFT) presenting in the pleura and other soft tissue sites and hemangiopericytoma (HPC) presenting at various soft tissue sites are mesenchymal tumors that share many histologic and immunohistochemical features. This raises the questions of whether these tumors are related and whether they belong within the spectrum of a single biologic entity. The behavior of both SFTs and HPCs is difficult to predict histologically. The genetic background of both SFTs and HPCs is poorly known, but it could be helpful in the evaluation of malignancy and could give clues to their possible relationship. In this study, we analyzed 15 SFTs and 11 HPCs by comparative genomic hybridization (CGH), a powerful molecular cytogenetic tool that can be applied to DNA extracted from formaldehyde- fixed and paraffin-embedded tissue. All of these tumors were immunohistochemically similar and showed reactivity for CD34-antigen but not for keratins, desmin, or muscle actins. Only 1 SFT smaller than 10 cm showed DNA copy number changes (a single loss in chromosome 13), but 7 of 8 SFTs larger than 10 cm (including all 4 tumors with more than 4 mitoses per 10 high power fields) showed changes, mostly chromosomal gains in 5q 7, 8, 12, and 18. Four cases showed losses, two of them in chromosome 13 and two others in 20q. These findings suggest that CGH might be useful in the evaluation of malignant transformation in SFT. The most common change, gain of the entire chromosome 8, seen in two cases as the only change, suggests trisomy 8 and parallels a similar finding previously described in other fibrous tumors, such as subsets of desmoid fibromatosis and infantile fibrosarcoma. In contrast, HPCs, including large and mitotically active tumors, showed no DNA copy number changes on CGH. This suggests that HPC is genetically different from SFT.

AB - Solitary fibrous tumor (SFT) presenting in the pleura and other soft tissue sites and hemangiopericytoma (HPC) presenting at various soft tissue sites are mesenchymal tumors that share many histologic and immunohistochemical features. This raises the questions of whether these tumors are related and whether they belong within the spectrum of a single biologic entity. The behavior of both SFTs and HPCs is difficult to predict histologically. The genetic background of both SFTs and HPCs is poorly known, but it could be helpful in the evaluation of malignancy and could give clues to their possible relationship. In this study, we analyzed 15 SFTs and 11 HPCs by comparative genomic hybridization (CGH), a powerful molecular cytogenetic tool that can be applied to DNA extracted from formaldehyde- fixed and paraffin-embedded tissue. All of these tumors were immunohistochemically similar and showed reactivity for CD34-antigen but not for keratins, desmin, or muscle actins. Only 1 SFT smaller than 10 cm showed DNA copy number changes (a single loss in chromosome 13), but 7 of 8 SFTs larger than 10 cm (including all 4 tumors with more than 4 mitoses per 10 high power fields) showed changes, mostly chromosomal gains in 5q 7, 8, 12, and 18. Four cases showed losses, two of them in chromosome 13 and two others in 20q. These findings suggest that CGH might be useful in the evaluation of malignant transformation in SFT. The most common change, gain of the entire chromosome 8, seen in two cases as the only change, suggests trisomy 8 and parallels a similar finding previously described in other fibrous tumors, such as subsets of desmoid fibromatosis and infantile fibrosarcoma. In contrast, HPCs, including large and mitotically active tumors, showed no DNA copy number changes on CGH. This suggests that HPC is genetically different from SFT.

KW - Amplification

KW - Comparative genomic hybridization

KW - Deletion

UR - http://www.scopus.com/inward/record.url?scp=0344301857&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0344301857&partnerID=8YFLogxK

M3 - Article

VL - 10

SP - 1194

EP - 1200

JO - Modern Pathology

JF - Modern Pathology

SN - 0893-3952

IS - 12

ER -