Analysis by comparative genomic hybridization of epithelial and spindle cell components in sarcomatoid carcinoma and carcinosarcoma: histogenetic aspects

Torenbeek, R.; Hermsen, Mario; Meijer, Guido T.; Baak, J. P. A.; Meijer, Chris J.L.M.

doi:10.1002/(sici)1096-9896(199911)189:3<338::aid-path429>3.3.co;2-h

Cited by 22 publications

(30 citation statements)

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“…This clearly separates SC from adenocarcinomas and squamous cell carcinomas, although both are the most frequent found components in SC. In one study, the various parts of SC were investigated separately by CGH, and no influence on the chromosomal aberrations was seen [17].…”

Section: Resultsmentioning

confidence: 99%

“…Comparative genomic hybridization (CGH) [12,20] was essentially done as previously described by Halbwedl et al [7]. We did not separate the histologically different pleomorphic carcinoma components because in a previous report, no genetic differences between the epithelial-and spindle-cell component were found by CGH [17].…”

Section: Dna Isolationmentioning

confidence: 99%

“…It has been proven in the past that the different phenotypically appearing epithelial-and spindle-cell components within some subgroups of SC (urinary bladder and pharynx) might originate from the same clone [17]. Furthermore, epithelial-mesenchymal transition (EMT) could best describe the origin of the sarcoma-like appearing components of the SC [4].…”

Section: Introductionmentioning

confidence: 99%

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Sarcomatoid carcinomas of the lung—are these histogenetically heterogeneous tumors?

et al. 2006

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Sarcomatoid carcinomas (SC) of the lung are a heterogeneous group of nonsmall cell lung carcinomas (NSCLC) containing a sarcoma or sarcoma-like component. SC may represent an epithelial neoplasm undergoing divergent tissue differentiation originating from a single clone. Epithelial-mesenchymal transition (EMT) best describes the origin of the spindle and giant cells. We aimed to define chromosomal aberrations within the subgroups of SC and if EMT does play a role in SC. Twenty-two SC were investigated by chromosomal comparative genomic hybridization (CGH). Immunohistochemical staining was performed with antibodies for E-cadherin, Vimentin, c-Fos, c-Jun, Snail, TGFbeta1, Notch1, beta-catenin, Glycogen synthase kinase 3beta (GSK3beta), and Fascin. Gains occurred more frequently than losses (70.5 vs 29.5%). The shortest regions of overlap were gains on chromosomes 8q and 7 followed by 1q, 3q, and 19, supporting the common origin of the different subtypes of SC. The immunohistochemical staining suggests that the sarcomatoid components of SC might have undergone EMT, not triggered by the signaling pathways Notch1, Snail, and TGFbeta1, but probably initiated by an upregulation of c-Jun and a consecutive overexpression of Vimentin and Fascin. The Wnt-pathway was not deregulated because combined membrane and cytoplasmic reactivity for beta-catenin and GSK3beta was observed.

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Section: Resultsmentioning

confidence: 99%

Section: Dna Isolationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Sarcomatoid carcinomas of the lung—are these histogenetically heterogeneous tumors?

et al. 2006

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“…Carcinosarcomas are rare biphasic malignant tumors with an epithelial and a spindle cell component in which the mesenchymal component does not express any epithelial markers [16]. For the histogenesis of these tumors, two hypotheses have been put forward:…”

Section: Introductionmentioning

confidence: 99%

Immunohistomorphologic and molecular cytogenetic analysis of a carcinosarcoma of the urinary bladder

et al. 2002

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Carcinosarcomas of the urinary bladder are malignant biphasic tumors with an epithelial and a spindle cell component. For the histogenesis of the two components, a biclonal and a monoclonal origin are discussed. We present the immunomorphology and molecular cytogenetics of such a case. The immunohistology of biopsies of the urinary bladder revealed a poorly differentiated urothelial carcinoma (GIII) and a co-existing pleomorphic, spindle cell leiomyosarcoma (GIII). The two components were microdissected and further analyzed for gains and losses of chromosomal material using comparative genomic hybridization. In addition, loss of heterozygosity analyses were included. The tumor components revealed as overlapping core aberrations losses on the short arm of chromosome 9 and on the long arm of chromosome 11. However, both components showed additional aberrations exclusively detected in one of the components. The occurrence of overlapping aberrations strongly argues for a monoclonal origin of this tumor with a common ancestor. The additional aberrations of the components point to an independent and divergent course of tumor progression in both components.

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“…Immunohistochemical [7,13,24,30] and electron microscopic [7,24,25] studies indicated that the SA component carried various degrees of epithelial differentiation. Limited genetic studies on sarcomatoid carcinomas have also found that the same genetic alterations are commonly shared in the SCC and SA components in the uterus, breast, lung, gastrointestinal tract, urinary bladder, pharynx, and the upper respiratory tract [1,3,28,29]. However, although a great deal of progress in histogenetic and genetic studies has been made toward unraveling the monoclonal origins of sarcomatoid carcinomas, few divergent genetic changes responsible for the biphasic differentiation have been identified.…”

Section: Introductionmentioning

confidence: 99%

Extensive and divergent chromosomal losses in squamous and spindle-cell components of esophageal sarcomatoid carcinoma

et al. 2003

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Sarcomatoid carcinoma of the esophagus is an unusual type of squamous cell carcinoma (SCC) with a variable component of sarcomatoid spindle cells (SA). The loss of heterozygosity (LOH) involving multiple cancer-associated chromosomal arms has been reported to have a concerted, rather than an individual, effect on tumor progression. In order to delineate the role of LOH in the evolution of a biphasic tumor, the carcinoma in situ (CIS), invasive squamous cell carcinoma (ISCC), and SA components from a sarcomatoid carcinoma of the esophagus were compared for their clonality and extent of LOH. Forty microsatellite markers on the cancer-associated chromosomes, 3p, 4p, 5q, 8p, 9p, 13q, 17p, and 18q, were used for the polymerase chain reaction-based LOH analysis. All eight sarcomatoid carcinomas tested revealed extensive LOHs, involving an average of seven chromosomal arms. All CIS, ISCC, and SA components carried not only a high-level primary LOH (mean chromosomal involvement, 5.3) in common but also a low-level secondary LOH (mean chromosomal involvement, 1.8) in disparity. Interestingly, more secondary LOHs were always burdened in the CIS (four cases) rather than the matched ISCC. SA had a greater (four cases), equal (one case), or fewer (one case) number of secondary LOHs than ISCC. Given that excessive chromosomal losses may confer a disadvantage for tumor growth or a benefit for a metaplastic transformation, these results suggest that the multidirectional differentiation of a SCC precursor is stimulated by extensive and divergent LOHs acquired at the initial or early stages, and a precursor burdened with excessive LOH either remains in CIS or expands as a SA component.

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Analysis by comparative genomic hybridization of epithelial and spindle cell components in sarcomatoid carcinoma and carcinosarcoma: histogenetic aspects

Cited by 22 publications

References 0 publications

Sarcomatoid carcinomas of the lung—are these histogenetically heterogeneous tumors?

Sarcomatoid carcinomas of the lung—are these histogenetically heterogeneous tumors?

Immunohistomorphologic and molecular cytogenetic analysis of a carcinosarcoma of the urinary bladder

Extensive and divergent chromosomal losses in squamous and spindle-cell components of esophageal sarcomatoid carcinoma

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