Subcellular Distribution of Cytokeratin and Vimentin in Malignant Rhabdoid Tumor: Three-Dimensional Imaging with Confocal Laser Scanning Microscopy and Double Immunofluorescence

Itakura, Eijun; Tamiya, Sadafumi; Morita, Kenichi; Shiratsuchi, Hideki; Kinoshita, Yoshiaki; Oshiro, Yumi; Oda, Yoshinao; Ohta, Shigeru; Furue, Masutaka; Tsuneyoshi, Masazumi

doi:10.1038/modpathol.3880401

Cited by 13 publications

(9 citation statements)

References 26 publications

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“…4). These findings confirm the similarity of MRTs in Snf5 +/À mice and in human patients (46). Moreover, the distinct staining patterns of CPCs +/À mice were assessed for vimentin, S100h, and CK8/18 expression by immunohistochemistry as described in Materials and Methods.…”

Section: Resultssupporting

confidence: 78%

Tumor-Specific Cooperation of Retinoblastoma Protein Family and Snf5 Inactivation

Chai

Lu²,

Godfrey³

et al. 2007

Cancer Research

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Malignant rhabdoid tumors (MRT) are rare aggressive cancers that occur in young children. Seventy-five percent of sporadic MRTs harbor inactivating SNF5 mutations, and mice heterozygous for an Snf5-null allele develop MRTs with partial penetrance. The diagnosis of choroid plexus carcinomas (CPC) in addition to MRTs in families with a single mutant SNF5 allele prompted us to assess the role of SNF5 loss in CPC in genetically engineered mice. With high frequency, TgT 121 mice develop CPCs that are initiated by inactivation of retinoblastoma protein (pRb) and related proteins p107 and p130. However, CPC penetrance and latency were not significantly affected by Snf5 heterozygosity, consistent with recent evidence that CPCs in SNF5 families were, in many cases, misdiagnosed MRTs. Surprisingly, although the CPC phenotype was unaffected, TgT 121 ;Snf5 +/À mice developed MRTs with increased penetrance and decreased latency compared with TgT 121 ;Snf5 +/+ littermates. MRTs expressed the T 121 protein with a concomitant increase in mitotic activity. The predominant appearance of TgT 121 ;Snf5 +/À MRTs in the spinal cord led to the discovery that these tumors likely arose from a subset of spinal cord neural progenitor cells expressing T 121 rather than from transdifferentiation of CPC. Significantly, the target cell type(s) for MRT is unknown. Hence, this study not only shows that pRb f and SNF5 inactivation cooperate to induce MRTs but also provides new insight into the MRT target population. [Cancer Res 2007;67(7):3002-9]

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Section: Resultssupporting

confidence: 78%

Tumor-Specific Cooperation of Retinoblastoma Protein Family and Snf5 Inactivation

Chai

Lu²,

Godfrey³

et al. 2007

Cancer Research

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“…[3][4][5][6] The present case simulated ERT morphologically but was negative for vimentin with looser aggregates of intermediate filaments, and had a favorable outcome. The subcellular coexpression of vimentin and keratin has been reported to be diffuse for the former and showing a paranuclear globular pattern for the latter, 7 as was seen in some of the cells in the present case. Expression of these molecules may be dependent on the tight whorls of intermediate filaments in RT, and keratin alone may be expressed when the loose aggregates are present instead of whorls, as was seen here.…”

Section: A Rhabdoid-mimicking Intrahepatic Cholangiocarcinomasupporting

confidence: 76%

“…5 Ultrastructurally, RT cells show coexpresson of vimentin and low-molecularweight cytokeratin with characteristic whorls of intermediate filaments. 7 Although many ERTs with exceptional clinical features have been reported, i.e., those affecting adults 4 and not necessarily showing a poor outcome, 6 they may not show the same immunohistochemical phenotype, or have not been studied ultrastructurally. [3][4][5][6] The present case simulated ERT morphologically but was negative for vimentin with looser aggregates of intermediate filaments, and had a favorable outcome.…”

Section: A Rhabdoid-mimicking Intrahepatic Cholangiocarcinomamentioning

confidence: 99%

A rhabdoid‐mimicking intrahepatic cholangiocarcinoma

Sugano

Hayashi

Okaya

et al. 2013

Pathology International

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“…Most commonly, these are keratin filaments and can be highlighted by low and high molecular weight keratin immunohistochemical stains [24,25]. In rare instances, such as this case, the intermediate filaments are highlighted by neurofilament markers [9,26].…”

Section: Case Reportmentioning

confidence: 91%

Malignant Rhabdoid Tumor of the Floor of Mouth: First Reported Case in the Oral Cavity of an Adult

Wetzel

Kerpel

Reich

et al. 2014

Head and Neck Pathol

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Malignant rhabdoid tumors (MRTs) are exceedingly rare lesions. To our knowledge, only 2 cases have been reported in the oral cavity, with both examples occurring in infants. The current case is the third reported case of MRT of the oral cavity and the first reported case to occur in an adult at this location. The following report describes the clinical, histologic and immunohistochemical features of this tumor.

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Subcellular Distribution of Cytokeratin and Vimentin in Malignant Rhabdoid Tumor: Three-Dimensional Imaging with Confocal Laser Scanning Microscopy and Double Immunofluorescence

Abstract: Malignant rhabdoid tumor (MRT) is a highly aggres-

Cited by 13 publications

References 26 publications

Tumor-Specific Cooperation of Retinoblastoma Protein Family and Snf5 Inactivation

Tumor-Specific Cooperation of Retinoblastoma Protein Family and Snf5 Inactivation

A rhabdoid‐mimicking intrahepatic cholangiocarcinoma

Malignant Rhabdoid Tumor of the Floor of Mouth: First Reported Case in the Oral Cavity of an Adult

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