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. 2005 Nov;58(11):1152-6.
doi: 10.1136/jcp.2005.026278.

Immunohistochemical analysis of desmoid tumours

Affiliations

Immunohistochemical analysis of desmoid tumours

A Leithner et al. J Clin Pathol. 2005 Nov.

Abstract

Background/aims: Although the standard treatment for desmoid tumours is complete surgical resection with wide margins, the optimal adjuvant treatment for recurrent or inoperable disease is unclear, often being based on sporadic immunohistochemical reports with a low number of cases. Therefore, a large immunohistochemical study was performed, to provide a theoretical basis for adjuvant treatment regimens.

Methods: One hundred and sixteen tissue samples from 80 patients (49 female, 31 male; mean age, 34 years; range, 0-83) with desmoid tumours (46 extra-abdominal, 21 abdominal, 13 intra-abdominal) were tested for oestrogen receptors alpha and beta, progesterone and androgen receptors, and somatostatin, in addition to HER2, cathepsin D, Ki-67, and c-KIT by immunohistochemistry.

Results: All samples were negative for oestrogen receptor alpha, HER2, and the progesterone receptor. Positive staining for the androgen receptor was found in six extra-abdominal cases. Staining for oestrogen receptor beta was positive in four extra-abdominal, two abdominal, and one intra-abdominal case. Staining for somatostatin was positive in six extra-abdominal, two abdominal, and one intra-abdominal case, and staining for cathepsin D was positive in all cases. Positive staining for Ki-67 was found in 14 extra-abdominal, three abdominal, and three intra-abdominal cases. C-KIT was detectable in one abdominal case only.

Conclusions: The data from this immunohistochemical study show that the published effects of antioestrogens and imatinib mesylate in the treatment of aggressive fibromatoses may not be attributable to oestrogen receptor alpha or c-KIT expression.

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Figures

Figure 1
Figure 1
Skeletal distribution of 46 extra-abdominal desmoid tumours. The figure design was modified from Pignatti and colleagues, with permission.
Figure 2
Figure 2
Histopathology of desmoid tumours and control samples. (A) Macroscopical view of the whitish cut surface of an extra-abdominal desmoid tumour. (B) Abdominal desmoid tumour showing the typical infiltrative growth pattern of the skeletal muscle (haematoxylin and eosin staining; original magnification, ×200). (C) Staining for androgen receptor showing a positive signal (original magnification, ×600). (D) Section of an extra-abdominal desmoid tumour with more than 90% of the cells showing strong staining for somatostatin (original magnification, ×400). (E) Staining for oestrogen receptor β showing focal positivity (original magnification, ×400). (F) Immunohistochemical analysis for Ki-67 (MIB-1) showing about 10% positive cells (original magnification, ×600). (G) Strong positive expression for c-KIT (CD117) in a gastrointestinal stromal tumour (original magnification, ×200) in contrast to (H) a c-KIT negative desmoid tumour, with two positive mast cells as a further internal positive control (original magnification, ×600).

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