Pseudosarcoma of the larynx: the value of ploidy analysis

Abstract

An 82-year-old male presented with a two-month history of hoarseness. A 2 cm pedunculated lesion was removed from the base of his epiglottis. Microscopy showed a polypoid atypical spindle cell lesion. Multiple levels failed to reveal an invasive squamous cell carcinoma. On the basis of haematozylin and eosin stained sections the main differential diagnosis was a pseudosarcoma with an overlying dysplastic squamous mucosa or infiltrating spindle cell carcinoma. Immunohistochemistry showed positive staining for vimentin but no convincing staining with antibodies to cytokeratin and EMA. Ultrastructural analysis also failed to reveal epithelial characteristics. Ploidy analysis by static cytophotometry of the spindle cell proliferation revealed an aneuploid stem line with a DNA index of 1.67. On the basis of this the process was felt unlikely to be reactive and a diagnosis of a spindle cell squamous carcinoma was made. This diagnosis was subsequently supported by a clinical recurrence of the nodule at a six-month follow-up.

Sarcomatoid (Spindle Cell) Carcinoma of the Head and Neck Mucosal Region: A Clinicopathologic Review of 103 Cases from a Tertiary Referral Cancer Centre

“…Sarcomatoid carcinoma contains both a conventional epithelial squamous component and a sarcomatous spindle cell component [2,3,[17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32]. As also noted in our study, epithelial differentiation evident within the tumor is reported to be highly variable with either changes in the overlying epithelium in the form of dysplasia or carcinoma in situ or as part of the infiltrating tumor [1][2][3].…”

“…Both the sarcomatoid as well as conventional squamous carcinoma components have now been proven to arise monoclonally from a single stem cell, and there is further evidence to prove that the sarcomatoid component represents a dedifferentiation and suggests molecular progression of the conventional component [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32]. The clinical behavior of sarcomatoid carcinoma is however reported to parallel that of conventional squamous carcinoma with the outcome being determined by the location and clinical stage [2,3,19].…”

“…As also noted in our study, epithelial differentiation evident within the tumor is reported to be highly variable with either changes in the overlying epithelium in the form of dysplasia or carcinoma in situ or as part of the infiltrating tumor [1][2][3]. The latter may be demonstrable at light microscopy or by the expression of epithelial markers at immunohistochemistry, electron microscopy or at the molecular level [2,3,[17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32]. The degree and intensity of epithelial marker expression is also reported to vary [3] as was observed in our study as well.…”

“…The degree of mesenchymal metaplasia within the tumor may vary widely and may be seen as bony or cartilagenous elements within the tumor or as aberrant immunohistochemical marker expression [2][3][4][5][6][7][8][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32]. Although no aberrant metaplastic elements were observed in any of our cases, we did see aberrant expression of vimentin, calponin, SMA, desmin and S100 protein, which is also well reported in literature [3].…”

“…These tumors have now been proved to be monoclonal, evolving from conventional squamous carcinoma with dedifferentiation associated with sarcomatoid transformation [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32]. They pose a significant diagnostic challenge to the pathologist with remarkable morphological and immunohistochemical overlap with other benign and malignant spindle cell tumors [1,3].…”