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Genome-Wide Analysis of Gene Expression in Synovial Sarcomas Using a Cdna Microarray1

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Genome-Wide Analysis of Gene Expression in Synovial Sarcomas Using a Cdna Microarray1 [CANCER RESEARCH 62, 5859–5866, October 15, 2002] Genome-wide Analysis of Gene Expression in Synovial Sarcomas Using a cDNA Microarray1 Satoshi Nagayama, Toyomasa Katagiri, Tatsuhiko Tsunoda, Taisuke Hosaka, Yasuaki Nakashima, Nobuhito Araki, Katsuyuki Kusuzaki, Tomitaka Nakayama, Tadao Tsuboyama, Takashi Nakamura, Masayuki Imamura, Yusuke Nakamura,2 and Junya Toguchida Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan [S. N., T. K., Yu. N.]; Laboratory for Medical Informatics, SNP Research Center, RIKEN (Institute of Physical and Chemical Research), Tokyo 108-8639, Japan [Tat. T.]; Department of Tissue Regeneration, Institute for Frontier Medical Sciences [S. N., T. H., J. T.], and Departments of Orthopaedic Surgery [T. H., To. N., Ta. N.], Pathology [Ya. N], and Surgery and Surgical Basic Science [S. N., M. I.], Graduate School of Medicine, College of Medical Technology [Tad. T.], Kyoto University, Kyoto 606-8507, Japan; Department of Orthopedic Surgery, Osaka Medical Center for Cancer and Cardiovascular Diseases [N. A.], Osaka 537-8511, Japan; Department of Orthopedic Surgery, Kyoto Prefectural University of Medicine [K. K.], Kyoto 602-0841, Japan ABSTRACT (10). These data support the hypothesis that SS may originate from cells that are widely distributed in a variety of tissues. Among a histologically heterogeneous group of soft tissue sarcomas, Among several histological findings, the most distinctive feature of synovial sarcoma (SS) is regarded as a “miscellaneous” entity of uncertain SS is epithelial differentiation. On the basis of the presence or absence origin. Although recent molecular analysis has disclosed involvement of a of an epithelial component, SS is classified into two major subtypes: specific chromosomal translocation in the pathogenesis of SS, its genetic features remain largely unclear. In the work reported here we examined biphasic, which is composed of distinct epithelial and spindle tumor genome-wide gene expression profiles of 13 SS cases and 34 other spindle- cells; and monophasic, which is composed of fibrosarcoma-like spin- cell sarcoma cases by cDNA microarray consisting of 23,040 genes. A dle tumor cells and no detectable epithelial components (1). However, hierarchical clustering analysis grouped SS and malignant peripheral because the proportion and features of the epithelial component vary nerve sheath tumor into the same category, and these two types of tumor significantly among biphasic tumors, transition from one to the other shared expression patterns of numerous genes relating to neural differ- subtype may be gradual rather than abrupt. entiation. Several genes were up-regulated in almost all SS cases, and the Although the histogenesis of SS remains unclear, molecular anal- presumed functions of known genes among them were related to migra- ysis of the mechanisms underlying tumorigenesis of SS progressed tion or differentiation of neural crest cells, suggesting the possibility of markedly with the discovery that a SYT-SSX fusion gene is a SS- neuroectodermal origin of SS. Moreover, we identified a set of genes that specific genetic alteration (11, 12). The SYT-SSX fusion product divided SS cases into two putative subclasses, a feature that may shed light contains both activator and repressor elements for transcription, and on novel biological aspects of SS in addition to those having to do with the net result seems to be transcriptional repression of certain genes in epithelial differentiation. These data have provided clues for understand- precursors of SS (13, 14). Target genes of the SYT-SSX protein seem ing the origin and tumorigenesis of SS. to be related not only to oncogenesis, but also to epithelial differen- tiation, because the SYT-SSX2 fusion protein has been found only in tumors with monophasic morphology, whereas biphasic tumors con- INTRODUCTION tain only the SYT-SSX1 subtype (15, 16). Therefore, identifying the STSs3 are difficult diseases to both diagnose and treat. STSs are target genes for the SYT-SSX protein will require determination of generally classified according to their histological resemblance to what the precursor cells are. mature, normal tissues (1). However, some sarcomas have no histo- In this study we analyzed the gene expression profiles of a panel of logical counterparts in normal tissues and therefore are grouped SS cases, using a genome-wide cDNA microarray containing 23,040 together as “miscellaneous soft tissue tumors” in the latest edition of genes. This approach has been useful for clarifying molecular mech- the WHO Soft Tissue Tumor Classification (2). A prototype of such anisms that underlie disease progression, for identifying novel cancer- tumors is SS, which predominantly affects the lower extremities of related genes, and for classifying human cancers at the molecular level adolescents and young adults 15–40 years of age (1). The clinico- (17–22). In addition to SS, we analyzed gene expression profiles pathological designation was originally given because SS occurs among four other types of STS: MFH, LMS, PLS and DLS, and primarily in the vicinity of large joints and histologically resembles MPNST. These tumors sometimes exhibit histological features that developing synovium (3). However, subsequent immunohistochemi- closely resemble those of SS. Although differential diagnosis among cal and ultrastructural studies (4, 5) have revealed significant differ- these other tumors and SS is now feasible through analysis for the ences between the SS tumor cells and synovial cells. In addition, SS SYT-SSX fusion gene (23), we judged that comparison of expression can arise where synovial structures are rare or absent, including the profiles among the various STSs should provide information about the lung (6), heart (7), kidney (8), digestive tract (9), and bone marrow histogenesis of SS. We report here that SS most closely resembles MPNST in terms of gene expression profiles, sharing differential expression of several Received 1/18/02; accepted 8/19/02. The costs of publication of this article were defrayed in part by the payment of page genes characteristic of neural crest-derived cells. This suggests a charges. This article must therefore be hereby marked advertisement in accordance with neuroectodermal origin of SS. Our results also indicate that SS can be 18 U.S.C. Section 1734 solely to indicate this fact. classified into two subgroups irrespective of the histological classifi- 1 This work was supported in part by Research for the Future Program Grant No. 00L01402 from the Japan Society for the Promotion of Science. cation. We also identified several genes expressed commonly in SS, 2 To whom requests for reprints should be addressed, at Laboratory of Molecular whose products should be suitable targets for development of novel Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan. Phone: 81-3-5449-5372; Fax: therapeutic drugs. 81-3-5449-5433; E-mail: [email protected]. 3 The abbreviations used are: STS, soft tissue sarcoma; SS, synovial sarcoma; MFH, MATERIALS AND METHODS malignant fibrous histiocytoma; LMS, leiomyosarcoma; PLS, pleomorphic liposarcoma, DLS; dedifferentiated liposarcoma; MPNST, malignant peripheral nerve sheath tumor; MSC, mesenchymal stem cell; RT-PCR, reverse transcription-PCR; EST, expressed Tissue Samples. Primary or recurrent STS tissues were obtained from 47 sequence tag. patients who underwent surgical resection, including 13 with SS and 34 with 5859 Downloaded from cancerres.aacrjournals.org on September 27, 2021. © 2002 American Association for Cancer Research. GENOME-WIDE ANALYSIS OF GENE EXPRESSION IN SS spindle cell sarcomas (14 with MFH, 10 with LMS, 3 with PLS, 3 with DLS, list of selected genes, we then chose those showing slight or no expression and 4 with MPNST). Among the four MPNSTs, three had developed in (category D) in Ͼ80% of non-SS cases. patients with a clinical diagnosis of type 1 neurofibromatosis (patients Cluster Analysis of 13 SS Cases According to Gene Expression Profiles. MPNST248, MPNST397, and MPNST558). Tumor samples were snap-frozen To clarify the nature of the histological heterogeneity within the SS group, we in liquid nitrogen immediately after resection and stored at Ϫ80°C until focused on differences in expression patterns of 23,040 genes among the 13 preparation of RNA. Tissue specimens were obtained in the same manner from original SS cases. From the overall expression profiles of the SS group, we 15 additional SS patients to verify the expression patterns. All samples were chose 1405 genes for which data were present in 75% of the cases and that had approved for our analysis by the ethics committee of the Faculty of Medicine, expression ratios that varied by SDs Ͼ1.0. Clustering analysis was performed Kyoto University. Part of each tumor sample was fixed in 10% formalin and in the manner described above. routinely processed for H&E staining to establish a pathological diagnosis by Identification of Candidate Genes for Discriminating between SS Sub- two of us (Y. T. and J. T.). Histological subclassification of SS, either classes. We selected 7067 genes for which data were present in Ͼ10 of 13 SS monophasic or biphasic, was determined by the standard criteria, mainly based cases, and the mean (␮) and SD (␴) were calculated from the relative expres- on the presence of an epithelial component (1). Nine of the 13 cases were thus sion ratios of each gene in one of the two subclasses. A discrimination score ϭ ␮ Ϫ ␮ ␴ ϩ ␴ classified as monophasic, and the remaining 4 were classified as biphasic. At (DS) for each gene was defined as: DS 1 2/( 1 2), where the least 90% of the viable cells in each specimen were identified as tumor cells; subscripts refer to the same groups (26). A large DS indicates that a gene’s contamination with normal elements such as inflammatory cells was consid- expression varies greatly between the two groups but little within its own ered to be minimal. group. We invoked a permutation test to calculate the ability of individual RNA Preparation and T7-based RNA Amplification.
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