For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
28
views
32
references
 Top references
cited by
17
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      199
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Differential diagnosis of laryngeal spindle cell carcinoma and inflammatory myofibroblastic tumor – report of two cases with similar morphology

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Spindle cell tumors of the larynx are rare. In some cases, the dignity is difficult to determine. We report two cases of laryngeal spindle cell tumors.

          Case presentation

          Case 1 is a spindle cell carcinoma (SPC) in a 55 year-old male patient and case 2 an inflammatory myofibroblastic tumor (IMT) in a 34 year-old female patient. A comprehensive morphological and immunohistochemical analysis was done. Both tumors arose at the vocal folds. Magnified laryngoscopy showed polypoid tumors. After resection, conventional histological investigation revealed spindle cell lesions with similar morphology. We found ulceration, mild atypia, and myxoid stroma. Before immunohistochemistry, the dignity was uncertain. Immunohistochemical investigations led to diagnosis of two distinct tumors with different biological behaviour. Both expressed vimentin. Furthermore, the SPC was positive for pan-cytokeratin AE1/3, CK5/6, and smooth-muscle actin, whereas the IMT reacted with antibodies against ALK-1, and EMA. The proliferation (Ki67) was up to 80% in SPC and 10% in IMT. Other stainings with antibodies against p53, p21, Cyclin D1, or Rb did not result in additional information. After resection, the patient with SPC is free of disease for seven months. The IMT recurred three months after first surgery, but no relapses were found eight months after resurgery.

          Conclusion

          Differential diagnosis can be difficult without immunohistochemistry. Therefore, a comprehensive morphological and immunohistochemical analysis is necessary, but markers of cell cycle (apart from the assessment of proliferation) do not help.

          Related collections

          Most cited references32

          • Record: found
          • Abstract: found
          • Article: not found

          TPM3-ALK and TPM4-ALK oncogenes in inflammatory myofibroblastic tumors.

          Brandon Lawrence, Antonio R Perez-Atayde, Michele Hibbard … (2000)
          Inflammatory myofibroblastic tumors (IMTs) are neoplastic mesenchymal proliferations featuring an inflammatory infiltrate composed primarily of lymphocytes and plasma cells. The myofibroblastic cells in some IMTs contain chromosomal rearrangements involving the ALK receptor tyrosine-kinase locus region (chromosome band 2p23). ALK-which is normally restricted in its expression to neural tissues-is expressed strikingly in the IMT cells with 2p23 rearrangements. We now report a recurrent oncogenic mechanism, in IMTs, in which tropomyosin (TPM) N-terminal coiled-coil domains are fused to the ALK C-terminal kinase domain. We have cloned two ALK fusion genes, TPM4-ALK and TPM3-ALK, which encode approximately 95-kd fusion oncoproteins characterized by constitutive kinase activity and tyrosylphosphorylation. Immunohistochemical and molecular correlations, in other IMTs, implicate non-TPM ALK oncoproteins that are predominantly cytoplasmic or pre- dominantly nuclear, presumably depending on the subcellular localization of the ALK fusion partner. Notably, a TPM3-ALK oncogene was reported recently in anaplastic lymphoma, and TPM3-ALK is thereby the first known fusion oncogene that transforms, in vivo, both mesenchymal and lymphoid human cell lineages.
          Article 0 comments Cited 128 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            ALK1 and p80 expression and chromosomal rearrangements involving 2p23 in inflammatory myofibroblastic tumor.

            C M Coffin, A. Patel, S. Perkins … (2001)
            Inflammatory myofibroblastic tumor (IMT) is an uncommon tumor of extrapulmonary and pulmonary tissues with an unpredictable clinical course, occasional recurrences, and rare malignant transformation. Clonal abnormalities with rearrangements of chromosome of 2p23 and the ALK gene have been reported in a few cases. The purpose of this study is to investigate whether these are consistent abnormalities among IMTs or represent a distinct subset. Formalin-fixed, paraffin-embedded archival tissue sections from 47 IMTs in 40 patients were immunostained with monoclonal antibodies against ALK and p80. Fluorescence in situ hybridization for ALK rearrangements was done on 22 IMTs from 19 patients. Findings were correlated with clinical features and outcome. ALK positivity was observed in 17 of 47 IMTs (36%) and p80 positivity in 16 of 47 IMTs (34%). Fluorescence in situ hybridization showed ALK rearrangements in nine cases (47%), aneuploidy in three cases (16%), and no rearrangement in seven cases (37%). IMTs with ALK abnormalities by immunohistochemistry and/or fluorescence in situ hybridization originated in the abdomen/pelvis/retroperitoneum, chest, and extremities. The mean age was 6.6 years, with a male/female ratio of 1.3. 64% of patients had no evidence of disease at last follow-up, 45% had one or more recurrences, and 18% displayed histologic evidence of malignant transformation. The IMTs without ALK abnormalities occurred in older children, were more frequent in females, and had fewer recurrences. However, in this group of 40 patients, the differences between the groups with and without ALK abnormalities did not have statistical significance. Aneuploidy without ALK abnormalities was associated with malignant transformation in three of five cases. Abnormalities of ALK and p80 and evidence of chromosomal rearrangements of 2p23 occur in a significant proportion of IMTs. These changes are most frequent in abdominal and pulmonary IMTs in the first decade of life and are associated with a higher frequency of recurrence. These findings confirm the neoplastic nature of a subset IMT with ALK abnormalities and suggest that aneuploid IMT is a subset with more aggressive clinical behavior.
            Article 0 comments Cited 125 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Fusion of ALK to the Ran-binding protein 2 (RANBP2) gene in inflammatory myofibroblastic tumor.

              Frank H Collins, János Sümegi, D. Hill … (2003)
              Inflammatory myofibroblastic tumor (IMT) is a rare mesenchymal proliferation of transformed myofibroblasts, with a prominent inflammatory cell component, that can mimic other spindle cell processes such as nodular fasciitis, desmoid tumor, and gastrointestinal stromal tumor. Genetic analyses have recently demonstrated rearrangements of anaplastic lymphoma kinase (ALK), located at 2p23, in a subset of IMTs. Molecular characterizations have identified ALK fusions involving tropomyosin-3 and -4 (TPM-3 and -4), the clathrin heavy chain (CLTC), and the cysteinyl-tRNA synthetase (CARS) genes as fusion partners. Here we describe two IMTs with a novel ALK fusion that involves the Ran-binding protein 2 (RANBP2) gene at 2q13, which normally encodes a large (358-kDa) nucleopore protein localized at the cytoplasmic side of the nuclear pore complex. The N-terminal 867 residues of RANBP2 are fused to the cytoplasmic segment of ALK in the 1,430-amino acid RANBP2-ALK chimeric protein. Myofibroblasts that express RANBP2-ALK exhibit nuclear membrane-associated ALK staining that is unique compared to the subcellular localization observed with other ALK fusions in IMT, presumably attributable to heteroassociation of the fusion with normal RANBP2 at the nuclear pore. These findings expand the spectrum of ALK abnormalities observed in IMT and further confirm the clonal, neoplastic nature of these lesions. Copyright 2003 Wiley-Liss, Inc.
              Article 0 comments Cited 56 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Diagn Pathol
                Title: Diagnostic Pathology
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1746-1596
                Publication date Collection: 2007
                Publication date (Electronic): 9 January 2007
                Volume: 2
                Page: 1
                Affiliations
                [1 ]Institute of Pathology, University, Josef-Schneider-Str.2, 97080 Würzburg, Germany
                [2 ]Department of Otorhinolaryngology, University, Josef-Schneider-Str.2, 97080 Würzburg, Germany
                Article
                Publisher ID: 1746-1596-2-1
                DOI: 10.1186/1746-1596-2-1
                PMC ID: 1779261
                PubMed ID: 17212821
                SO-VID: 74ce1563-4fe5-41e8-9570-d787a63ab449
                Copyright © Copyright © 2007 Völker et al; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 4 December 2006
                Date accepted : 9 January 2007
                Categories
                Subject: Case Report

                ScienceOpen disciplines: Pathology
                Data availability:
                ScienceOpen disciplines: Pathology

                Comments

                Comment on this article

                scite_

                Similar content199

                See all similar

                Cited by16

                See all cited by

                Most referenced authors285

                See all reference authors