DR SARMA'S DERMPATH: Common Spindle Cell Malignant Neoplasms of the Skin Differential Diagnosis and...

8/14/2019 DR SARMA'S DERMPATH: Common Spindle Cell Malignant Neoplasms of the Skin Differential Diagnosis and Review of the Literature. The Internet Journal o

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Clinical Featur es

Desmoplastic melanoma (DM) is a rare variant of spindle cell melanoma and an uncommon form of melanoma,

comprising 4% of all melanomas. DM was first described by Conley et al. in 1971 as an inconspicuous superficial

melanocytic lesion of the head and neck, preceding the development of a bulky dermal and subcutaneous tumor [1].

The tumor presents in older individuals as a flesh-colored or variably pigmented nodule measuring on average 2 cm.

It is usually seen on sun-exposed skin (37%) but also on mucosal and acral sites. Males are affected more often than

women, with the exception of the lower limbs. If prominent neurotropism is present, which occurs in at least 30% of

cases, nerve invasion can produce dysesthesias or nerve palsies. DM often is difficult to detect clinically, since half lack

pigmentation. Pale lesions, in particular, are mistaken clinically for basal cell carcinoma, dermatofibroma, or scar.

Pigmentation often is due to an associated lentigo maligna or superficial spreading melanoma. Unusual presentations

include young age, an erythematous nodule, or alopecia. Ulceration is uncommon.

Histopathology (Figure s 1, 2, 3, 4)

DM is composed of usually non-pigmented fusiform melanocytes which often resemble fibroblasts (Figure 1). The

atypical melanocytes are embedded within collagen bundles and may be associated with mild to marked stromal

fibrosis. Phenotypical heterogeneity is under-recognized and desmoplasia may be seen throughout the tumor or in

combination with conventional melanoma (combined DM) [3, 4]. Ultrastructurally, the desmoplastic component

appears to derive from melanocytes that have undergone adaptive fibroplasia [2]. Most often the spindle cells are

arranged in a haphazard fashion, but are sometimes arranged in parallel bundles or in storiform configurations. The

spindle cells are usually mildly to moderately atypical, although cells with larger, more hyperchromatic nuclei are often

seen. Paucicellular variants of DM, in particular, are easily missed on small biopsy specimens. Junctional components

are sometimes minimal or absent. Mitotic rate is variable but often is low, with abnormal forms in the more cellular

tumors. The overlying epidermis may be thinned or thickened with clusters of lymphocytes located at the tumor

periphery. Neurotropism is a common feature (seen in up to 30%) and neural differentiation with a malignant

peripheral nerve sheath-like histology may be seen [5-8]. Neurotropism may be peri- or intraneural and may extend

beyond the desmoplastic component. An osteogenic variant has been reported [9].

The spindle cells in DM are positive for S-100 protein (Figure 2), although sometimes within only a few nuclei (Table

1). Neuron-specific enolase (NSE) and smooth muscle actin (SMA) may be positive, while HMB45 (Figure 3) and

Melan-A (MART-1) and are usually negative [10-13]. Microphthalmia transcription factor (MITF) may (Figure 4) or

may not be positive No single specific marker is yet available to differentiate desmoplastic melanomas from other

tumors [14].


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Figure 1. Dermal spindle cell neoplasm.

Figure 2. The tumor cells are focally positive for S-100 protein

Figure 3. Tumor cells are negative for HMB-45


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Figure 4. Tumor cells show strongly positive nuclear stain with MITF.

Prognosis and Treatment

Desmoplastic melanoma was reported in the older literature as having a worse prognosis when compared to other

types of melanoma. However, recent findings suggest that prospectively diagnosed and definitively treated lesions

show the same survival rate as the usual forms of melanoma when various histologic parameters and risk factors arecontrolled. Expression of N-cadherin may portend a poorer prognosis, however [15]. Treatment is with wide local

excision.

Spindle Cell (Squam ous Cell) Carcinom a.

Clinical Featur es

Squamous cell carcinoma is the second most common cutaneous malignancy after basal cell carcinoma. The uncommon

spindle cell variant occurs commonly on sun-exposed surfaces of elderly patients as a plaque or as an enlarging tan to

red nodule, often with surface ulceration and crusting. The spindle cell (squamous cell) carcinoma (SCSCC) may beassociated with previous skin injury, including trauma and radiotherapy.

Histopathology (Figure s 5, 6, 7, 8)

Four histopathologic categories of squamous cell carcinoma are described: conventional, spindle cell, acantholytic, and

verrucous. In the uncommon spindle cell variant, atypical spindle cells emanate from the epidermis and form whorls

intermingling with strands of collagen (Figures 1, 2). Within the dermis, the cells form intertwining fascicles and

bundles. Individual tumor cells have indistinct borders and contain eosinophilic cytoplasm. Nuclei are hyperchromatic

or vesicular and elongated. Nuclei may be pleomorphic and contain multiple nucleoli. Mitotic activity is brisk and

atypical forms may be seen. With cellular pleomorphism and tumor giant cell formation, the tumors can bear a closeresemblance to atypical fibroxanthoma. In fact, prior to the advent of immunohistochemistry, these lesions were often

misdiagnosed. Connection of malignant tumor cells to the epidermis or foci of more typical squamous differentiation

favor spindle cell carcinoma. Cytokeratin stains (Figure 7) are usually helpful. In addition, SCSCC can stain positively

with mesenchymal markers such as vimentin (Figure 8) and smooth muscle actin.

Recently it has been suggested that p63 may be a useful marker for SCSCC; Dotto et al. reports a series of 13 cases of

SCSCC in which nuclear expression was seen in all cases, while focal labeling was seen in only 2/4 cutaneous

leiomyosarcomas and 2/10 atypical fibroxanthomas [16].


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Figure 5. Ulcerating tumor infiltrates into the dermis and is composed of solid nests of squamoid cells as well as

pleomorphic spindle cells.

Figure 6. The squamoid cells blend into the spindle cells


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Figure 7. Both epithelial and spindle cells are positive for CK AE 1/3 (Cytokeratin).

Figure 8. Both epithelial and spindle cells are positive for Vimentin.


Spindle-cell squamous cell carcinoma is a poorly differentiated variant of squamous cell carcinoma with the potential

for an aggressive clinical course. One-third of cutaneous squamous cell carcinomas that metastasize are of this type.

Treatment is surgical. Metastases usually first occur to the regional lymph nodes.

Spindle Cell Atypical Fibroxan thom a.

Clinical Featur es

Atypical fibroxanthoma (AFX) usually arises in sun-exposed skin of the head and neck in older patients, often on the

nose and cheek. Therapeutic radiation is a predisposing factor, with tumors usually appearing more than a decade

following treatment. AFX usually presents as a nodule, which is sometimes ulcerated. The surface may be reddened

and polypoid, resembling a capillary hemangioma.

Histopathology (Figure s 9, 10)

AFX is a highly cellular mesenchymal tumor. There is an extensive proliferation of spindled to polygonal cells (Figures

9 and 10), which in the usual form closely resemble malignant fibrous histiocytoma (MFH) of the deep soft tissues.

AFX are expansile, dermal nodules that may reach the epidermis causing pressure atrophy. Often there is a

connection to the overlying epidermis. In other cases, an uninvolved portion of overlying dermis, or grenz zone, is

present. In addition, the tumor can compress skin appendages latererally. AFX does not extensively involve the

subcutis and does not invade deeper structures. Areas adjacent to the lesion may show solar elastosis, vascular

dilation, and capillary proliferation. Hemorrhage can be extensive, with the associated presence of hemosiderin-laden

macrophages. Scattered inflammatory cells can be seen. In contrast with the usual type of AFX, the spindle cell

variant is not pleomorphic, although most cases contain scattered giant cells of varying proportion [17, 18]. Sclerosis

may be prominent and the lesion may be active mitotically. This morphology creates diagnostic difficulties because of

its resemblance to other malignant spindle cell tumors. An absence of junctional nesting argues against malignant


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melanoma, although caution must be taken as some spindle cell desmoplastic melanomas lack a junctional component.

Differentiation from spindle cell melanoma is suggested by lack of an overlying in-situ melanoma component and

absence of S-100 staining in tumor cells. The cells of AFX are HMB-45 negative (Table 1). Spindle cell carcinomas

show positive staining for cytokeratin and often keratinocyte dysplasia or Bowens disease is present at the edge of the

lesion. Leiomyosarcoma can be confused with this variant of AFX. AFX, however, is desmin negative and shows only

focal actin positivity. The neoplastic cells of AFX are positive for vimentin and CD68 (Figure 11). Matthew et al.

reported CK117 positivity in 15/16 AFX, suggesting that c-kit may be a sensitive marker [19].

Figure 9. Diffusely infiltrating dermal tumor.

Figure 10. The tumor is composed of predominantly pleomorphic polygonal cells.


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Figure 11. Tumor cells show positivity with CD68 immunostain.


Although AFX may be indistinguishable from MFH histologically, the prognosis is excellent following conservative

excision. Most authors agree that larger tumors (>2 cm) which extensively invade subcutaneous tissue such as fascia

or muscle, or show necrosis or vascular invasion, should be diagnosed as MFH. Lack of H-ras and K-ras mutations in

AFX but presence in MFH further suggest biologic differences between these two entities [20].

Derm atofibrosarcom a Protuberans.Clinical Featur es

Dermatofibrosarcoma protuberans (DFSP) is a neoplasm regarded as a superficial low-grade sarcoma. The lesion most

commonly presents in young to middle-aged persons on the trunk or proximal extremities as an indurated plaque

with one or more associated gray-white nodules. DFSP presents less often at other body sites, including the head,

neck, and distal extremities [21, 22]. Early lesions are sharply-demarcated or plaque-like, often with peripheral red or

blue discoloration. At this stage, lesions may clinically resemble morpheaform basal cell carcinoma. Advanced lesions

are fungating and ulcerated. Sometimes the tumors contain gelatinous or translucent areas corresponding

microscopically to myxoid change. Hemorrhage and cystic degeneration can occur.

DFSP exhibits slow and persistent growth, often over several years. There is evidence that many tumors develop

during childhood and become clinically apparent later in life. Congenital and childhood forms are known, but may not

come to attention early because of difficulty in clinical detection [23-25].

Histopathology (Figur es 12, 13, 14)

DFSP shows a dense proliferation of monotonous spindle cells that diffusely infiltrate the dermis and subcutis (Figure

12). The center of the tumor is composed of slender fibroblasts which contain moderately-enlarged, tapered nuclei and

are arranged around inconspicuous vessels in a distinctive storiform configuration (Figure 13). Occasional mitoses are

seen but are not abundant. Atypical forms are usually not seen. The tumor may extend to the epidermis or,

alternatively, a grenz zone is seen. Lateral extension of the tumor beyond the dermal component may be marked but

subtle. DFSP has a characteristic pattern of subcutaneous infiltration, including growth along septa and between

lipocytes in a honeycomb configuration or horizontally layered, parallel to the epidermal surface. Other findings in

DSFP are seen rarely, including multinucleated giant cells, hypercellular zones, and myoid or myofibroblastic


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differentiation [26-28]. Occasional tumors contain myxoid areas, and when prominent, the storiform pattern becomes

less apparent. Unusual variants include sclerosing [29, 30] and pigmented types. Histology with a discrete fascicular or

herringbone pattern may suggest fibrosarcomatous transformation. The mitotic rate is usually, but not always,

higher when this occurs, although occasional examples of DFSP demonstrate up to 35 mitotic figures per high power

field [31]. It is currently unclear whether fibrosarcomatous areas are more common in recurrent lesions. Recent

studies have shown this not to be the case.

The tumor cells in DSFP stain immunohistochemically with CD34 (Figure 14), the human progenitor cell antigen, in a

significant proportion of its cells, making CD34 a highly sensitive marker for this entitiy. Care should be taken not to

interpret entrapped CD34 + dermal dendritic cells as tumor cells.

Almost all cases of DFSP express the chromosomal translocation t (17:22) when investigated with the newest

molecular techniques, including multiplex reverse transcription polymerase chain reaction (RT-PCR) and fluorescence

in situ hybridization (FISH) [32]. The translocation results in a fusion of the collagen type I I (COL1A1) gene on

chromosome 17 with the platelet-derived growth factor beta (PDGF) on chromosome 22 and is most commonly

located on a ring chromosome. The fusion transcript leads to constitutive activation of the PFGR protein tyrosine

kinase, resulting in uncontrolled tumor growth. DFSP has been found to differ from other soft tissue tumors with

similar histology by the expression of this distinct set of genes. In addition, PDGFBR, the receptor for PDGF, is highly

expressed in DFSP, suggesting an autocrine stimulatory loop that may contribute to tumorigenesis [33].

Figure 12. Diffuse monotonous spindle cell infiltration in dermis.


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Figure 13. Storiform pattern

Figure 14. The tumor cells are strongly positive for CD34.

Prognosis and Treatment.

While generally indolent, the tumor possesses a tendency for progressive growth, recurrence, and rarely distant

metastasis. With wide excision and careful pathologic examination of surgical margins, even local recurrence is

extremely low [34]. In one large study of 218 DFSP patients, there was no significant difference in crude cumulative

incidence of local relapses between primary and recurrent disease and in cases with positive and negative margins

[35].

Fibrosarcomatous or malignant fibrous histiocytomatous transformation can occur, although the effect on the biologic

behavior of such a transformation is controversial. Adequacy of wide excision may be more important to prognosis

than the presence of the sarcomatous component per se [36-40]. Transformation to a fibrosarcomatous component

has been associated with microsatellite instability [41] and p53 mutations [41, 42].

Cutaneous Leiomyosarcoma.

Clinical Featur es

Primary leiomyosarcomas (LMS) of the skin are relatively rare sarcomas, reported infrequently in the literature. LMS

of the skin are divided into dermal and subcutaneous types. The dermal type is discussed here and tends to develop in

adults of middle to older age. It arises as one or several dermal or subcutaneous nodules, most often on the hip, thigh,

or knee [43]. Other locations, including the face and scrotum, are reported[44]. Many tumors are present for years


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Figure 16. Higher magnification of the dermal spindle cell tumor.

Figure 17. The tumor cells are positive for SMA (smooth muscle antigen) on immunostain


In a series of 65 primary cutaneous LMS reported by Fields et al. and in smaller series reported by other authors [46,

48], LMS can recur, sometimes due to incomplete surgical excision [51]. None metastasize, despite high mitotic

activity and marked cytologic atypia [53] in some cases. Recurrent tumors may be more atypical and located deeply

[51]. Reported cases of metastases appear in the older literature [54].

Summary

Spindle cell malignancies of the skin, some of which are not particularly common, are nevertheless seen by the

practicing dermatologists and pathologists. Such tumors are not always easily differentiated on histologic findings alone

and many, if not all, must be confirmed with immunohistochemical staining (Table 1). A thorough familiarity with

these lesions is a necessity, as prognosis and treatment may be different.


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Table 1. Immunohistochemical Staining in Spindle Cell Malignancies of the Skin

Correspondence

Deba P Sarma, MD

Department of Pathology

Creighton University Medical Center

Omaha, Nebraska USA 68131

debasarma@creighton .edu

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http://scholar.google.ca/scholar?q=Szollosi%2C%2BZ.%2Band%2BZ.%2BNemes%2C%2BTransformed%2Bdermatofibrosarcoma%2Bprotuberans%3A%2Ba%2Bclinicopathological%2Bstudy%2Bof%2Beight%2Bcases.%2BJ%2BClin%2BPathol%2C%2B2005.%2B58%287%29%3A%2Bp.%2B751-6.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Diaz-Cascajo%2C%2BC.%2C%2Bet%2Bal.%2C%2BDermatofibrosarcoma%2Bprotuberans%2Bwith%2Bfibrosarcomatous%2Bareas%3A%2Ba%2Bclinico-pathologic%2Band%2Bimmunohistochemic%2Bstudy%2Bin%2Bfour%2Bcases.%2BAm%2BJ%2BDermatopathol%2C%2B1997.%2B19%286%29%3A%2Bp.%2B562-7.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Takahira%2C%2BT.%2C%2Bet%2Bal.%2C%2BMicrosatellite%2Binstability%2Band%2Bp53%2Bmutation%2Bassociated%2Bwith%2Btumor%2Bprogression%2Bin%2Bdermatofibrosarcoma%2Bprotuberans.%2BHum%2BPathol%2C%2B2004.%2B35%282%29%3A%2Bp.%2B240-5.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Swanson%2C%2BP.E.%2C%2Bet%2Bal.%2C%2BPrimary%2Bcutaneous%2Bleiomyosarcoma.%2BA%2Bhistological%2Band%2Bimmunohistochemical%2Bstudy%2Bof%2B9%2Bcases%2C%2Bwith%2Bultrastructural%2Bcorrelation.%2BJ%2BCutan%2BPathol%2C%2B1988.%2B15%283%29%3A%2Bp.%2B129-41.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Bellezza%2C%2BG.%2C%2Bet%2Bal.%2C%2BPrimary%2Bcutaneous%2Bleiomyosarcoma%3A%2Ba%2Bclinicopathological%2Band%2Bimmunohistochemical%2Bstudy%2Bof%2B7%2Bcases.%2BInt%2BJ%2BSurg%2BPathol%2C%2B2004.%2B12%281%29%3A%2Bp.%2B39-44.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Choy%2C%2BC.%2C%2BA.%2BCooper%2C%2Band%2BS.%2BKossard%2C%2BPrimary%2Bcutaneous%2Bdiffuse%2Bleiomyosarcoma%2Bwith%2Bdesmoplasia.%2BAustralas%2BJ%2BDermatol%2C%2B2006.%2B47%284%29%3A%2Bp.%2B291-5.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Berzal-Cantalejo%2C%2BF.%2C%2Bet%2Bal.%2C%2BDesmoplastic%2Bcutaneous%2Bleiomyosarcoma%3A%2Bcase%2Breport%2Band%2Breview%2Bof%2Bthe%2Bliterature.%2BJ%2BCutan%2BPathol%2C%2B2006.%2B33%2BSuppl%2B2%3A%2Bp.%2B29-31.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Valeriani%2C%2BM.%2C%2Bet%2Bal.%2C%2BRecurrent%2Bcutaneous%2Bleiomyosarcoma.%2BJ%2BExp%2BClin%2BCancer%2BRes%2C%2B1998.%2B17%281%29%3A%2Bp.%2B83-5.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Karroum%2C%2BJ.E.%2C%2BE.G.%2BZappi%2C%2Band%2BC.J.%2BCockerell%2C%2BSclerotic%2Bprimary%2Bcutaneous%2Bleiomyosarcoma.%2BAm%2BJ%2BDermatopathol%2C%2B1995.%2B17%283%29%3A%2Bp.%2B292-6.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Kaddu%2C%2BS.%2C%2Bet%2Bal.%2C%2BCutaneous%2Bleiomyosarcoma.%2BAm%2BJ%2BSurg%2BPathol%2C%2B1997.%2B21%289%29%3A%2Bp.%2B979-87.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Chow%2C%2BJ.%2C%2Bet%2Bal.%2C%2BCutaneous%2Bleiomyosarcoma%3A%2Bcase%2Breports%2Band%2Breview%2Bof%2Bthe%2Bliterature.%2BAnn%2BPlast%2BSurg%2C%2B1987.%2B18%284%29%3A%2Bp.%2B319-22.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Limaiem%2C%2BF.%2C%2Bet%2Bal.%2C%2BPrimary%2Bcutaneous%2Bleiomyosarcoma%3A%2Ba%2Bhistological%2Band%2Bimmunohistochemical%2Bstudy%2Bof%2B4%2Bcases.%2BPathologica%2C%2B2007.%2B99%286%29%3A%2Bp.%2B415-9.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Jensen%2C%2BM.L.%2C%2Bet%2Bal.%2C%2BIntradermal%2Band%2Bsubcutaneous%2Bleiomyosarcoma%3A%2Ba%2Bclinicopathological%2Band%2Bimmunohistochemical%2Bstudy%2Bof%2B41%2Bcases.%2BJ%2BCutan%2BPathol%2C%2B1996.%2B23%285%29%3A%2Bp.%2B458-63.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Sasaki%2C%2BM.%2C%2Bet%2Bal.%2C%2BDermatofibrosarcoma%2Bprotuberans%3A%2Ban%2Banalysis%2Bof%2Bproliferative%2Bactivity%2C%2BDNA%2Bflow%2Bcytometry%2Band%2Bp53%2Boverexpression%2Bwith%2Bemphasis%2Bon%2Bits%2Bprogression.%2BPathol%2BInt%2C%2B1999.%2B49%289%29%3A%2Bp.%2B799-806.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Takahira%2C%2BT.%2C%2Bet%2Bal.%2C%2BMicrosatellite%2Binstability%2Band%2Bp53%2Bmutation%2Bassociated%2Bwith%2Btumor%2Bprogression%2Bin%2Bdermatofibrosarcoma%2Bprotuberans.%2BHum%2BPathol%2C%2B2004.%2B35%282%29%3A%2Bp.%2B240-5.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Mentzel%2C%2BT.%2C%2Bet%2Bal.%2C%2BFibrosarcomatous%2B%28%22high-grade%22%29%2Bdermatofibrosarcoma%2Bprotuberans%3A%2Bclinicopathologic%2Band%2Bimmunohistochemical%2Bstudy%2Bof%2Ba%2Bseries%2Bof%2B41%2Bcases%2Bwith%2Bemphasis%2Bon%2Bprognostic%2Bsignificance.%2BAm%2BJ%2BSurg%2BPathol%2C%2B1998.%2B22%285%29%3A%2Bp.%2B576-87.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Diaz-Cascajo%2C%2BC.%2C%2Bet%2Bal.%2C%2BDermatofibrosarcoma%2Bprotuberans%2Bwith%2Bfibrosarcomatous%2Bareas%3A%2Ba%2Bclinico-pathologic%2Band%2Bimmunohistochemic%2Bstudy%2Bin%2Bfour%2Bcases.%2BAm%2BJ%2BDermatopathol%2C%2B1997.%2B19%286%29%3A%2Bp.%2B562-7.%0A&hl=en&lr=&btnG=Searchhttp://scholar.google.ca/scholar?q=Szollosi%2C%2BZ.%2C%2Bet%2Bal.%2C%2BTransformed%2Bdermatofibrosarcoma%2Bprotuberans%3A%2Breal%2Btime%2Bpolymerase%2Bchain%2Breaction%2Bdetection%2Bof%2BCOL1A1-PDGFB%2Bfusion%2Btranscripts%2Bin%2Bsarcomatous%2Bareas.%2BJ%2BClin%2BPa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DR SARMA'S DERMPATH: Common Spindle Cell Malignant Neoplasms of the Skin Differential Diagnosis and...

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