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The architectural arrangements of the neoplastic spindle cells in FLSCC tumors are also variable, ranging from intersecting fascicles to vaguely storiform patterns, haphazard sheetlike growth, individually infiltrating cells, or vascular-acantholytic growth patterns characterized by vessellike gaping spaces lined by spindle cells.
The diagnosis of metaplastic spindle cell carcinoma, including FLSCC, may not be obvious in tumors composed exclusively of spindle cells.
The spindle cells in FLSCC are typically negative for smooth muscle myosin heavy chain and epithelial membrane antigen, but epithelial membrane antigen positivity may be seen in the epithelial components.
As mentioned previously, FLSCC represents a low-grade variant of spindle cell carcinoma, and is essentially a neoplasm composed almost exclusively of cytologically bland spindle cells.
The most important lesion to distinguish from FLSCC is pure fibromatosis.
Exuberant, extensive scars, reactive spindle cell nodules, and nodular fasciitis are reactive entities that may mimic FLSCC. The presence of hemosiderin, fat necrosis, and foreign body multinucleated giant cells favors scar formation.
These lesions may also harbor foci of increased cellularity with myofibroblasts arranged in fascicles, mimicking FLSCC. Pseudoangiomatous stromal hyperplasia has been described in association with many benign and malignant breast lesions, including carcinoma, hamartoma, fibroadenoma, and phyllodes tumor, but it has also been described in a nodular form that was not associated with other breast lesions.
Finally, primary sarcomas in the breast are also rare but represent an extremely important entity to distinguish from FLSCC. Primary sarcomas usually require extensive sampling in order to distinguish them from metaplastic spindle cell carcinomas.
(30) The exception to this generalization is FLSCC. On the spectrum of metaplastic spindle cell carcinomas of the breast, FLSCC represents a low-grade variant with clinically indolent behavior that is similar to pure fibromatosis.
No definitive conclusions regarding the biologic behavior of FLSCC tumors have been made because most case series are limited by small sample sizes, variable clinical follow-up intervals, and differences in treatment regimens.
A definitive diagnosis of FLSCC is aided by identifying areas of epithelial differentiation in the tumor and by using a panel of immunohistochemical stains with antibodies against cytokeratins and myoepithelial markers.
No definitive conclusions can be made about the clinical behavior of FLSCC. Continued studies of FLSCC in addition to close clinical monitoring of patients following removal of these tumors will hopefully shed new light on specifications regarding the biologic behavior and appropriate management of these unusual breast tumors.