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      Variable Ki67 proliferative index in 65 cases of nodular fasciitis, compared with fibrosarcoma and fibromatosis

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          Abstract

          Abstract

          Nodular fasciitis is the most common pseudosarcomatous lesion of soft tissue. Ki67 was considered as a useful marker for distinguishing some benign and malignant lesions. To study the usefulness of Ki67 in diagnosis of nodular fasciitis, the expression of Ki67 was examined by using immunostaining in 65 nodular fasciitis specimens, 15 desmoid fibromatosis specimens and 20 fibrosarcoma specimens. The results showed that there was a variable Ki67 index in all 65 cases of nodular fasciitis, and the mean labeling index was 23.71±15.01%. In majority (70.77%) of all cases,the index was ranged from 10% to 50%, in 6.15% (4/65) of cases the higher Ki67 index (over 50%) could be seen. The Ki67 proliferative index was closely related to duration of lesion, but not to age distribution, lesion size, sites of lesions and gender. Moreover, the mean proliferative index in desmoid fibromatosis and fibrosarcoma was 3.20±1.26% and 26.15±3.30% respectively. The mean Ki67 index of nodular fasciitis was not significantly lower than fibrosarcoma, but higher than desmoid fibromatosis. The variable and high Ki67 index in nodular fasciitis may pose a diagnostic challenge. We should not misdiagnose nodular fasciitis as a sarcoma because of its high Ki67 index. The recurrence of nodular fasciitis is rare; and the utility of Ki67 immunostaining may be not suitable for recurrence assessment in nodular fasciitis.

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          Nodular fasciitis: a novel model of transient neoplasia induced by MYH9-USP6 gene fusion.

          Nodular fasciitis (NF) is a relatively common mass-forming and self-limited subcutaneous pseudosarcomatous myofibroblastic proliferation of unknown pathogenesis. Due to its rapid growth and high mitotic activity, NF is often misdiagnosed as a sarcoma. While studying the USP6 biology in aneurysmal bone cyst and other mesenchymal tumors, we identified high expression levels of USP6 mRNA in two examples of NF. This finding led us to further examine the mechanisms underlying USP6 overexpression in these lesions. Upon subsequent investigation, genomic rearrangements of the USP6 locus were found in 92% (44 of 48) of NF. Rapid amplification of 5'-cDNA ends identified MYH9 as the translocation partner. RT-PCR and direct sequencing revealed the fusion of the MYH9 promoter region to the entire coding region of USP6. Control tumors and tissues were negative for this fusion. Xenografts of cells overexpressing USP6 in nude mice exhibited clinical and histological features similar to human NF. The identification of a sensitive and specific abnormality in NF holds the potential to be used diagnostically. Considering the self-limited nature of the lesion, NF may represent a model of 'transient neoplasia', as it is, to our knowledge, the first example of a self-limited human disease characterized by a recurrent somatic gene fusion event. © 2011 USCAP, Inc All rights reserved
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            Subcutaneous pseudosarcomatous fibromatosis (fasciitis).

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              Nodular (pseudosarcomatous) fasciitis, a nonrecurrent lesion: clinicopathologic study of 134 cases.

              Clinicopathologic review of 134 patients originally diagnosed as having nodular (pseudosarcomatous) fasciitis is presented. In 114 patients with 116 lesions, no recurrence of the lesion was noted. Of the 114 patients, 85% were younger than 50 years of age, and the forearm and arm were the most common sites of presentation. Nonrecurrent lesions rarely exceed 4 cm and 71% were smaller than 2 cm. In at least six instances, incompletely resected lesions never recurred. Though all lesions were histologically reminiscent of reparative mesenchymal tissue, four subtypes--the reactive type, the densely cellular type, those with osteoid or cartilaginous metaplasia, and the so-called proliferative fasciitis--were distinguished from the majority of lesions that conform to the description given by Kornwaler. Recurrence of the tumor was noted in 18 patients. Fifteen of 18 lesions recurred within two years, and two more recurred at 30 months following initial excision. In all these cases, review of the histology and clinical course led to a revision of the original diagnosis. The greatest number of errors was made in incorrectly classifying of inflammatory fibrous histiocytoma. Recurrence of a lesion originally diagnosed as nodular fasciitis should lead to a careful reappraisal of the pathologic findings.
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                Author and article information

                Journal
                Diagn Pathol
                Diagn Pathol
                Diagnostic Pathology
                BioMed Central
                1746-1596
                2013
                26 March 2013
                : 8
                : 50
                Affiliations
                [1 ]Department of Pathology, the First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang 110001, China
                [2 ]Institute of pathology and pathophysiology, China Medical University, Shenyang 110001, China
                Article
                1746-1596-8-50
                10.1186/1746-1596-8-50
                3622623
                23531088
                5e8f1b17-434f-4c8c-9fd5-7bf091c5881b
                Copyright ©2013 Lin et al.; licensee BioMed Central Ltd.

                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
                : 7 January 2013
                : 21 March 2013
                Categories
                Research

                Pathology
                desmoid fibromatosis,fibrosarcoma,ki67,nodular fasciitis
                Pathology
                desmoid fibromatosis, fibrosarcoma, ki67, nodular fasciitis

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