Year : 2008 | Volume
: 51 | Issue : 2 | Page : 234--236
Spindle cell lipoma breast
Reema Jaffar1, Sufian Zaheer2, Shaista M Vasenwala2, Shaham Beg2,
1 Department of Pathology, UMASS Memorial Medical Center, Biotech 3, One Innovation drive, Worcester, Massachusetts, USA
2 Department of Pathology, J.N.M.C.H., A.M.U., Aligarh, India
4/1129, Sir Syed Nagar, Aligarh - 202 002, Uttar Pradesh
Spindle cell lipoma, which usually arises in the soft tissues, is rare in breast and is difficult to differentiate from primary mammary spindle cell tumor. Here, we present the case of a 48-year-old woman with a 3-cm, solitary, well-circumscribed and nontethered mass lying deep within the tissue of left breast, incidentally detected on routine mammography. The spindle cells proved to be immunoreactive to CD 34, but nonreactive to desmin and smooth muscle actin.
|How to cite this article:|
Jaffar R, Zaheer S, Vasenwala SM, Beg S. Spindle cell lipoma breast.Indian J Pathol Microbiol 2008;51:234-236
|How to cite this URL:|
Jaffar R, Zaheer S, Vasenwala SM, Beg S. Spindle cell lipoma breast. Indian J Pathol Microbiol [serial online] 2008 [cited 2020 Sep 24 ];51:234-236
Available from: http://www.ijpmonline.org/text.asp?2008/51/2/234/41666
Originally described by Enzinger and Harvey in 1975,  spindle cell lipoma (SCL) is a rare variant of benign lipomas characterized by an admixture of mature fat, collagen-forming spindle cells and varying degrees of myxoid change. It usually occurs in the subcutaneous tissue of the upper back, posterior neck and shoulder of males older than 40 years.  It rarely occurs at several other sites including the oral cavity, scalp, extremities, deep-seated muscles and breast. 
SCLs vary in appearance depending on the relative amounts of mature fat and spindle cells. Classically, there is a relatively equal mixture of mature fat and spindle cells. Breast SCL on fine needle aspirate (FNA), sometimes presents a worrisome picture on account of occasional atypical cells and myxoid stromal background. 
A 48-year-old woman presented to a breast surgeon for the work-up of a vague density seen on her screening mammography. On physical examination, there was no obvious change to the skin, nipple, or areola bilaterally. Palpation confirmed the presence of a solitary, well-circumscribed, nontethered 3-cm mass at 12 O' clock position in the left breast, 5.5 cm above the left nipple. No nipple discharge or retraction of the overlying skin was noted. There were no other palpable abnormalities and no supraclavicular or axillary lymphadenopathy. She gave no family history of breast cancer and no history of previously excised lipoma or family history of fatty tumors or Madelung's disease (multiple symmetrical lipomatosis) was elicited. None of the features of Gardener's syndrome or familial multicentric fibromatosis was identified. There was no history of previous injury to the breast, trauma, FNA, or breast surgery. Her menarche was at the age of 13 years and her first of three full-term pregnancies occurred at age 17. She used oral contraceptives for about a year, beginning at age 18, but discontinued the same. Real-time ultrasound of the left breast in the area of mammographically detected mass showed an oval 33 × 13 mm transversly oriented hypoechoic mass which appeared primarily solid with a low echogenicity shell. It demonstrated some characteristics of a hamartoma. The FNA biopsy showed benign-appearing spindle cells and adipose tissue. A few scattered atypical cells and myxoid background were also visualized. An excision was recommended for definitive diagnosis. The patient underwent needle localization and excision of mass.
The resected surgical specimen consisted of a 4.7 × 2.8 × 2.4 cm unoriented ovoid mass of fibrofatty tissue containing a discrete, thinly encapsulated 3.3 cm, yellow-to-gray pink rubbery mass. No hemorrhage or necrosis was seen. Subsequent microscopic examination of the paraffin sections revealed a poorly circumscribed lesion consisting of fascicles and micronodules of monomorphic spindle cells associated with collagen bundles admixed with adipose tissue [Figure 1]. Focal myxoid areas were also present. The spindle cells were uniform, with short fusiform nuclei, small nucleoli and narrow, bipolar cytoplasmic processes. No cellular atypia, necrosis, or mitotic activity was identified. Fat necrosis was noted. Periodic acid Schiff stain was noncontributory. Immunoperoxidase stains CD 34 [Figure 2] and vimentin stained the spindle cells. Desmin [Figure 3] and smooth muscle actin [Figure 4] were negative/noncontributory.
The patient is alive and well at follow-up, 6 months postoperatively. No local tumor recurrence or de novo breast masses were found on examination.
SCL, a rare variant of benign lipoma, comprises 1.5% of all adipocytic neoplasm. It was first described by Enzinger and Harvey  in 1975, as a benign lesion in which mature fat is replaced by collagen-forming spindle cells. Spindle cell lipoma has a tendency to occur in the subcutaneous tissue of the posterior neck, shoulder and back.  It rarely occurs at other sites, including breast. 
Mammary spindle cell lipomas are reported to occur with equal frequency in males and females, although the overall incidence of SCLs is 100 - fold greater in men than in women.  Although some tumors are large (up to 14 cm), most are 3-5 cm. Grossly, the nodule is soft to firm in consistency and either reddish pink, as in our case, or yellowish white to gray in color depending upon the relative proportions of collagen, spindle cells, fat and blood vessels.  The microscopic appearance of this case was of classic SCL: a lesion of variable cellularity, comprising intermixed collagen fibers, unevenly distributed spindle cells of benign appearance, mature adipocytes and foci of myxoid matrix. The vascular pattern was inconspicuous and consists of a few small or intermediate-size thick-walled vessels.
In cases of SCL of breast, if resection is incomplete, a false impression may be obtained of neoplastic cells aggressively infiltrating normal fat. The process is that of the spindle cells transforming into fat cells. This erroneous interpretation is due to passive adipocyte encirclement which simulates the "aggressive" fat entrapment found in more sinister spindle cell lesions of the breast. 
In our case, the spindle cells were positive for CD 34 and vimentin; and negative for desmin and smooth muscle actin. Immunohistochemically, the spindle cells stain strongly for vimentin and CD34 and very occasionally focally for S-100. Cytokeratin, desmin, smooth muscle actin and factor VIII are negative. 
The histogenesis of SCLs is controversial and previous ultrastructural studies have excluded a Schwann cell origin and current opinion favors an origin from adipocytes and/or nonfat storing, immature mesenchymal cells.  Another hypothesis proposes that SCLs belong to a broad category of mesenchymal tumors capable of differentiating along diverse myofibroblastic, fibroblastic, leiomyomatous and lipomatous lines. 
Differential diagnosis of mammary spindle cell lesions includes a wide range of reactive, benign and malignant proliferations of the epithelium, myoepithelium and stroma; some common to the dermis, subcutis but others unique to breast tissues.
To conclude, spindle cell lesions of the breast include a range of pathological entities, often with minimal or subtle morphological differences but great diversity in local recurrence. SCL should enter differential diagnosis of mammary spindle cell lesions. Although confirmatory cytogenetic analysis was not performed in our case of SCL, representative microscopic examination and a benign clinical course have both excluded both an atypical lipoma and a spindle cell liposarcoma.
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