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Palisading and Verocay body-prominent dermatofibrosarcoma protuberans: A case report
Pathology – Research and Practice 212 (2016) 145–147
Contents lists available at ScienceDirect
Pathology – Research and Practice journal homepage: www.elsevier.com/locate/prp
Teaching Cases
Palisading and Verocay body-prominent dermatofibrosarcoma protuberans: A case report Shuanzeng Wei a,∗ , Alain Dumas b , Paul J. Zhang a , Kumarasen Cooper a a Department of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, 6th Floor Founders Building, Philadelphia, PA 19104, USA b Dianon Pathology, 1 Forest Parkway, Shelton, CT 06484, USA
a r t i c l e
i n f o
Article history: Received 29 August 2015 Received in revised form 27 November 2015 Accepted 30 November 2015 Keywords: Dermatofibrosarcoma protuberans Palisading Verocay body t(17:22) translocation
a b s t r a c t Dermatofibrosarcoma protuberans (DFSP) is a rare cutaneous sarcoma with a tendency for local recurrence, which commonly presents as a slowly growing flesh-colored skin lesion without epidermal invasion but with intracutaneous and subcutaneous spread. Pathologically, the tumor generally presents with an infiltrating dermal mass containing closely packed fibroblasts arranged in a storiform pattern. Several uncommon growth patterns have been described, including sclerosing, atrophic, myxoid, pigmented, giant cell-rich, granular cell, herringbone pattern and palisading/Verocay body-prominent forms. To our knowledge, only five cases of DFSP with nuclear palisading/Verocay body formation have been reported in the literature, and no t(17:22) translocation study has been done on these cases. In this report we describe such a case with negative t(17:22) translocation. © 2015 Elsevier GmbH. All rights reserved.
Introduction Dermatofibrosarcoma protuberans (DFSP) is a rare cutaneous sarcoma with a tendency for local recurrence, which commonly presents as a slowly growing flesh-colored skin lesion without epidermal invasion but with intracutaneous and subcutaneous spread [1]. Pathologically, the tumor presents with an infiltrating dermal mass composed of closely packed fibroblasts arranged in a storiform pattern, and mitoses are rare. The overlying epidermis is generally thinned in contrast to dermatofibroma. Deep extension from the dermis into subcutaneous adipose tissue produces a characteristic “honeycomb” pattern [1,2]. Cytogenetically, DFSP is characterized by the presence of a reciprocal translocation t(17:22)(q22:q13) or supernumerary ring chromosomes derived from t(17:22) [3,4]. Several uncommon growth patterns have been described, including sclerosing [5], atrophic [6], myxoid [7], pigmented [8], giant cell-rich [9], granular cell [10], herringbone pattern [11,12] and palisading/Verocay body-prominent forms [13,14]. DFSP with nuclear palisading/Verocay body formation may be misdiagnosed as schwannoma, perineurioma, neurofibroma,
∗ Corresponding author. Tel.: +1 215 662 3209; fax: +1 215 349 8994. E-mail addresses: [email protected] (S. Wei), [email protected] (A. Dumas), [email protected] (P.J. Zhang), [email protected] (K. Cooper). http://dx.doi.org/10.1016/j.prp.2015.11.020 0344-0338/© 2015 Elsevier GmbH. All rights reserved.
even malignant peripheral nerve sheath tumor. To our knowledge, only five cases of DFSP with nuclear palisading/Verocay body formation have been reported in the literature [13–15], and no t(17:22) translocation study has been done on these cases. In this report we describe such a case with negative t(17:22) translocation. Case report A 28-year-old male presented with a pea sized, painless nodule in the superficial subcutaneous tissue of the anterior right thigh near the groin for four months. The mass was excised and the clinical impression was a lipoma. The specimen grossly was a piece of adipose tissue measuring 1.9 × 1.4 × 0.6 cm. Microscopically there was a markedly infiltrative spindle cell tumor involving the dermis and subcutis with honeycomb pattern (Fig. 1A and B). The tumor comprised spindle cells with slender wavy nuclei and some areas with prominent storiform pattern. Other areas show nuclear palisading, with Verocay bodies formation (Fig. 1B). The tumor cells were CD34 (BD Biosciences) positive (Fig. 1C), S100 (Dako, Z0311), EMA (Dako—M0613) and factor XIII (Lab Vision, MS-1237-P) negative (Fig. 1D and E). Fluorescence in situ hybridization (FISH) for detecting chromosomal translocations of t(17:22) (PDGFB Break Apart FISH Probe Orange & Green, Loci: 22q13, Empire Genomics) was performed and was negative (Fig. 1F). The morphology in conjunction with the immunophenotype supports a diagnosis of dermatofibrosarcoma protuberans (DFSP). Since the resection
146
S. Wei et al. / Pathology – Research and Practice 212 (2016) 145–147
Fig. 1. (A) Tumor involved the adipose tissue showing the classic honeycomb pattern (×200, H&E). (B) Palisading growth pattern and Verocay body (×400, H&E). (C) CD34 is positive in the tumor. (D) S100 highlights the adipose tissue, not the tumor cells. (E) Factor XIII is negative. (F) t(17:22) is negative by FISH.
margins were positive; a wide re-excision was performed with margins being negative. Discussion A palisade is a fence comprising a row of wooden poles. Palisading is used to describe the microscopic findings of certain lesions with arrangements of elongated nuclei stacked in rows [16]. “Verocay bodies” is defined as stacked elongated palisading nuclei alternating with anuclear zones containing cell processes. Although not pathognomonic, palisading and Verocay bodies are often seen in Antoni A area in schwannomas [16]. Occasionally central nervous system tumors, soft-tissue tumors, and even carcinomas may display palisades [13,16]. Reibel suggested that enhanced cell adhesion, as a result of overexpression of laminins, may be responsible for such a peculiar cell alignment [17]. Weiner demonstrated that certain extracellular signaling phospholipids can induce formation of similar cell clusters when applied to Schwann cells in vitro [18]. In dermatopathology, alternating areas of epithelial cell cords and stroma seen in some cutaneous neoplasms has been referred to “rippled pattern”. Histologically, this pattern may be indistinguishable from palisading/Verocay bodies [19]. Llatjos et al reported 3 cases of DFSP characterized by prominent nuclear palisading and Verocay body formation. All 3 lesions were positive for CD34 and negative for S100 [13]. Sylvia reported a case which was initially
reported as neurogenic tumor based on prominent Verocay bodies, myxoid change and increased mitoses [14]. Before this growth pattern was recognized in DFSP, Schwob et al reported 6 cases of dermatofibromas with striking nuclear palisading and named them “palisading cutaneous fibrous histiocytoma [20].” An acral predilection was also noted in 2 other studies [21,22]. Prominent Verocay bodies were also reported in a case of cutaneous angioleiomyoma arising as a subcutaneous nodule on the back of the head of a 31-year-old man [19]. In order to separate this tumor from the mimics including peripheral nerve sheath tumors, immunostains of CD34, S100 and factor XIIIa are recommended [1]. A CD34+S100-XIIIa-immunophenotype supports the diagnosis of DFSP. The infiltrating growth pattern also helps differentiate DFSP from these well-circumscribed tumors, such as schwannoma, perineurioma, neurofibroma and leiomyoma. Cytogenetically, DFSP is characterized by the presence of a reciprocal translocation t(17:22)(q22:q13) or supernumerary ring chromosomes derived from t(17:22) [3,4]. This translocation creates a fusion between the gene for collagen type I alpha 1 (COL1A1) on chromosome 17q and the gene encoding platelet-derived growth factor beta (PDGFß) on chromosome 22q [23,24]. The COL1A1–PDGFß fusion protein can bind to the PDGF receptor and acts as an autocrine factor to stimulate growth of DFSP tumor cells. COL1A1–PDGFß fusion transcripts were present in 90% of cases of DFSP [1,24]. Our case is negative for t(17:22), which should be borne in mind when FISH for t(17:22) is used as an confirmatory test.
S. Wei et al. / Pathology – Research and Practice 212 (2016) 145–147
In summary, we report a case of Palisading and Verocay body-prominent dermatofibrosarcoma protuberans without COL1A1–PDGF translocation. Funding sources None. Acknowledgment The authors would like to thank Dr. Christopher D. Fletcher (Brigham and Women’s Hospital) for reviewing this case. References [1] P. Saiag, J.J. Grob, C. Lebbe, J. Malvehy, V. Del Marmol, H. Pehamberger, K. Peris, A. Stratigos, M. Middelton, L. Basholt, A. Testori, C. Garbe, Diagnosis and treatment of dermatofibrosarcoma protuberans. European consensus-based interdisciplinary guideline, Eur. J. Cancer. 51 (2015) 2604–2608. [2] V. Kumar, A.K. Abbas, N. Fausto, J.C. Aster, Robbins and cotran pathologic basis of disease, in: Professional Edition: Expert Consult-Online, Elsevier Health Sciences, Philadelphia, PA, 2014, pp. 1158–1159. [3] M.P. Simon, F. Pedeutour, N. Sirvent, J. Grosgeorge, F. Minoletti, J.M. Coindre, M.J. Terrier-Lacombe, N. Mandahl, R.D. Craver, N. Blin, G. Sozzi, C. Turc-Carel, K.P. O’Brien, D. Kedra, I. Fransson, C. Guilbaud, J.P. Dumanski, Deregulation of the platelet-derived growth factor B-chain gene via fusion with collagen gene COL1A1 in dermatofibrosarcoma protuberans and giant-cell fibroblastoma, Nat. Genet. 15 (1997) 95–98. [4] F. Pedeutour, M.P. Simon, F. Minoletti, G. Sozzi, M.A. Pierotti, F. Hecht, C. Turc-Carel, Ring 22 chromosomes in dermatofibrosarcoma protuberans are low-level amplifiers of chromosome 17 and 22 sequences, Cancer Res. 55 (1995) 2400–2403. [5] C. Diaz-Cascajo, W. Weyers, S. Borghi, Sclerosing dermatofibrosarcoma protuberans, J. Cutan. Pathol. 25 (1998) 440–444. [6] B. Zelger, D. Öfner, B. Zelger, Atrophic variants of dermatofibroma and dermatofibrosarcoma protuberans, Histopathology 26 (1995) 519–527. [7] A. Orlandi, L. Bianchi, L.G. Spagnoli, Myxoid dermatofibrosarcoma protuberans: morphological, ultrastructural and immunohistochemical features, J. Cutan. Pathol. 25 (1998) 386–393. [8] J. Ding, H. Hashimoto, T. Sugimoto, M. Tsuneyoshi, M. Enjoji, Bednaˇr tumor (pigmented dermatofibrosarcoma protuberans), Pathol. Int. 40 (1990) 744–754. [9] B.M. Shmookler, F.M. Enzinger, S.W. Weiss, Giant cell fibroblastoma. A juvenile form of dermatofibrosarcoma protuberans, Cancer 64 (1989) 2154–2161.
147
[10] S.S. Banerjee, M. Harris, B.P. Eyden, B. Hamid, Granular cell variant of dermatofibrosarcoma protuberans, Histopathology 17 (1990) 375–378. [11] J. Ding, H. Hashimoto, M. Enjoji, Dermatofibrosarcoma protuberans with fibrosarcomatous areas. A clinicopathologic study of nine cases and a comparison with allied tumors, Cancer 64 (1989) 721–729. [12] T. Mentzel, A. Beham, D. Katenkamp, A.P. Dei Tos, C.D. Fletcher, Fibrosarcomatous (“high-grade”) dermatofibrosarcoma protuberans: clinicopathologic and immunohistochemical study of a series of 41 cases with emphasis on prognostic significance, Am. J. Surg. Pathol. 22 (1998) 576–587. [13] R. Llatjos, M. Fernández-Figueras, C. Díaz-Cascajo, M. Ribera, A. Ariza, Palisading and Verocay body-prominent dermatofibrosarcoma protuberans: a report of three cases, Histopathology 37 (2000) 452–455. [14] M.T. Sylvia, B.A. Badhe, Verocay bodies and myxoid change in fibrosarcomatous variant of dermatofibrosarcoma protuberans: A case report and review of literature, Indian J. Dermatopathol. Diagn. Dermatol. 2 (2015) 14. [15] J. Gong, L. Guo, Dermatofibrosarcoma protuberans with palisaded and Verocay body variants: a case report and review of the literature Chinese, J. Clin. Exp. Pathol. 1 (2008) 023. [16] F. Wippold, M. Lämmle, F. Anatelli, J. Lennerz, A. Perry, Neuropathology for the neuroradiologist: palisades and pseudopalisades, Am. J. Neuroradiol. 27 (2006) 2037–2041. [17] J. Reibel, U. Wewer, R. Albrechtsen, The pattern of distribution of laminin in neurogenic tumors, granular cell tumors, and nevi of the oral mucosa, Acta Pathol. Microbiol. Scand. Ser. A: Pathol. 93 (1985) 41–47. [18] J.A. Weiner, N. Fukushima, J.J. Contos, S.S. Scherer, J. Chun, Regulation of Schwann cell morphology and adhesion by receptor-mediated lysophosphatidic acid signaling, J. Neurosci. 21 (2001) 7069–7078. [19] A. Biswas, N. Setia, J. Bhawan, Cutaneous neoplasms with prominent Verocay body-like structures: the so-called “Rippled Pattern”, Am. J. Dermatopathol. 33 (2011) 539–550. [20] V. Schwob, D. Santa Cruz, Palisading cutaneous fibrous histiocytoma, J. Cutan. Pathol. 13 (1986) 403–407. [21] H. Kamino, V. Reddy, Unusual benign fibrous and fibrohistiocytic tumors of the skin, Dermatol. Clin. 10 (1992) 203–217. [22] K.F. Helm, T. Helm, F. Helm, Palisading cutaneous fibrous histiocytoma: an immunohistochemical study demonstrating differentiation from dermal dendrocytes, Am. J. Dermatopathol. 15 (1993) 559–561. [23] M.J. Terrier-Lacombe, L. Guillou, G. Maire, P. Terrier, D.R. Vince, N. de Saint Aubain Somerhausen, F. Collin, F. Pedeutour, J.M. Coindre, Dermatofibrosarcoma protuberans, giant cell fibroblastoma, and hybrid lesions in children: clinicopathologic comparative analysis of 28 cases with molecular data—a study from the French Federation of Cancer Centers Sarcoma Group, Am. J. Surg. Pathol. 27 (2003) 27–39. [24] B. Llombart, O. Sanmartin, J.A. Lopez-Guerrero, C. Monteagudo, C. Serra, C. Requena, A. Poveda, J.L. Vistos, S. Almenar, A. Llombart-Bosch, C. Guillen, Dermatofibrosarcoma protuberans: clinical, pathological, and genetic (COL1A1–PDGFB) study with therapeutic implications, Histopathology 54 (2009) 860–872.
Contents lists available at ScienceDirect
Pathology – Research and Practice journal homepage: www.elsevier.com/locate/prp
Teaching Cases
Palisading and Verocay body-prominent dermatofibrosarcoma protuberans: A case report Shuanzeng Wei a,∗ , Alain Dumas b , Paul J. Zhang a , Kumarasen Cooper a a Department of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, 6th Floor Founders Building, Philadelphia, PA 19104, USA b Dianon Pathology, 1 Forest Parkway, Shelton, CT 06484, USA
a r t i c l e
i n f o
Article history: Received 29 August 2015 Received in revised form 27 November 2015 Accepted 30 November 2015 Keywords: Dermatofibrosarcoma protuberans Palisading Verocay body t(17:22) translocation
a b s t r a c t Dermatofibrosarcoma protuberans (DFSP) is a rare cutaneous sarcoma with a tendency for local recurrence, which commonly presents as a slowly growing flesh-colored skin lesion without epidermal invasion but with intracutaneous and subcutaneous spread. Pathologically, the tumor generally presents with an infiltrating dermal mass containing closely packed fibroblasts arranged in a storiform pattern. Several uncommon growth patterns have been described, including sclerosing, atrophic, myxoid, pigmented, giant cell-rich, granular cell, herringbone pattern and palisading/Verocay body-prominent forms. To our knowledge, only five cases of DFSP with nuclear palisading/Verocay body formation have been reported in the literature, and no t(17:22) translocation study has been done on these cases. In this report we describe such a case with negative t(17:22) translocation. © 2015 Elsevier GmbH. All rights reserved.
Introduction Dermatofibrosarcoma protuberans (DFSP) is a rare cutaneous sarcoma with a tendency for local recurrence, which commonly presents as a slowly growing flesh-colored skin lesion without epidermal invasion but with intracutaneous and subcutaneous spread [1]. Pathologically, the tumor presents with an infiltrating dermal mass composed of closely packed fibroblasts arranged in a storiform pattern, and mitoses are rare. The overlying epidermis is generally thinned in contrast to dermatofibroma. Deep extension from the dermis into subcutaneous adipose tissue produces a characteristic “honeycomb” pattern [1,2]. Cytogenetically, DFSP is characterized by the presence of a reciprocal translocation t(17:22)(q22:q13) or supernumerary ring chromosomes derived from t(17:22) [3,4]. Several uncommon growth patterns have been described, including sclerosing [5], atrophic [6], myxoid [7], pigmented [8], giant cell-rich [9], granular cell [10], herringbone pattern [11,12] and palisading/Verocay body-prominent forms [13,14]. DFSP with nuclear palisading/Verocay body formation may be misdiagnosed as schwannoma, perineurioma, neurofibroma,
∗ Corresponding author. Tel.: +1 215 662 3209; fax: +1 215 349 8994. E-mail addresses: [email protected] (S. Wei), [email protected] (A. Dumas), [email protected] (P.J. Zhang), [email protected] (K. Cooper). http://dx.doi.org/10.1016/j.prp.2015.11.020 0344-0338/© 2015 Elsevier GmbH. All rights reserved.
even malignant peripheral nerve sheath tumor. To our knowledge, only five cases of DFSP with nuclear palisading/Verocay body formation have been reported in the literature [13–15], and no t(17:22) translocation study has been done on these cases. In this report we describe such a case with negative t(17:22) translocation. Case report A 28-year-old male presented with a pea sized, painless nodule in the superficial subcutaneous tissue of the anterior right thigh near the groin for four months. The mass was excised and the clinical impression was a lipoma. The specimen grossly was a piece of adipose tissue measuring 1.9 × 1.4 × 0.6 cm. Microscopically there was a markedly infiltrative spindle cell tumor involving the dermis and subcutis with honeycomb pattern (Fig. 1A and B). The tumor comprised spindle cells with slender wavy nuclei and some areas with prominent storiform pattern. Other areas show nuclear palisading, with Verocay bodies formation (Fig. 1B). The tumor cells were CD34 (BD Biosciences) positive (Fig. 1C), S100 (Dako, Z0311), EMA (Dako—M0613) and factor XIII (Lab Vision, MS-1237-P) negative (Fig. 1D and E). Fluorescence in situ hybridization (FISH) for detecting chromosomal translocations of t(17:22) (PDGFB Break Apart FISH Probe Orange & Green, Loci: 22q13, Empire Genomics) was performed and was negative (Fig. 1F). The morphology in conjunction with the immunophenotype supports a diagnosis of dermatofibrosarcoma protuberans (DFSP). Since the resection
146
S. Wei et al. / Pathology – Research and Practice 212 (2016) 145–147
Fig. 1. (A) Tumor involved the adipose tissue showing the classic honeycomb pattern (×200, H&E). (B) Palisading growth pattern and Verocay body (×400, H&E). (C) CD34 is positive in the tumor. (D) S100 highlights the adipose tissue, not the tumor cells. (E) Factor XIII is negative. (F) t(17:22) is negative by FISH.
margins were positive; a wide re-excision was performed with margins being negative. Discussion A palisade is a fence comprising a row of wooden poles. Palisading is used to describe the microscopic findings of certain lesions with arrangements of elongated nuclei stacked in rows [16]. “Verocay bodies” is defined as stacked elongated palisading nuclei alternating with anuclear zones containing cell processes. Although not pathognomonic, palisading and Verocay bodies are often seen in Antoni A area in schwannomas [16]. Occasionally central nervous system tumors, soft-tissue tumors, and even carcinomas may display palisades [13,16]. Reibel suggested that enhanced cell adhesion, as a result of overexpression of laminins, may be responsible for such a peculiar cell alignment [17]. Weiner demonstrated that certain extracellular signaling phospholipids can induce formation of similar cell clusters when applied to Schwann cells in vitro [18]. In dermatopathology, alternating areas of epithelial cell cords and stroma seen in some cutaneous neoplasms has been referred to “rippled pattern”. Histologically, this pattern may be indistinguishable from palisading/Verocay bodies [19]. Llatjos et al reported 3 cases of DFSP characterized by prominent nuclear palisading and Verocay body formation. All 3 lesions were positive for CD34 and negative for S100 [13]. Sylvia reported a case which was initially
reported as neurogenic tumor based on prominent Verocay bodies, myxoid change and increased mitoses [14]. Before this growth pattern was recognized in DFSP, Schwob et al reported 6 cases of dermatofibromas with striking nuclear palisading and named them “palisading cutaneous fibrous histiocytoma [20].” An acral predilection was also noted in 2 other studies [21,22]. Prominent Verocay bodies were also reported in a case of cutaneous angioleiomyoma arising as a subcutaneous nodule on the back of the head of a 31-year-old man [19]. In order to separate this tumor from the mimics including peripheral nerve sheath tumors, immunostains of CD34, S100 and factor XIIIa are recommended [1]. A CD34+S100-XIIIa-immunophenotype supports the diagnosis of DFSP. The infiltrating growth pattern also helps differentiate DFSP from these well-circumscribed tumors, such as schwannoma, perineurioma, neurofibroma and leiomyoma. Cytogenetically, DFSP is characterized by the presence of a reciprocal translocation t(17:22)(q22:q13) or supernumerary ring chromosomes derived from t(17:22) [3,4]. This translocation creates a fusion between the gene for collagen type I alpha 1 (COL1A1) on chromosome 17q and the gene encoding platelet-derived growth factor beta (PDGFß) on chromosome 22q [23,24]. The COL1A1–PDGFß fusion protein can bind to the PDGF receptor and acts as an autocrine factor to stimulate growth of DFSP tumor cells. COL1A1–PDGFß fusion transcripts were present in 90% of cases of DFSP [1,24]. Our case is negative for t(17:22), which should be borne in mind when FISH for t(17:22) is used as an confirmatory test.
S. Wei et al. / Pathology – Research and Practice 212 (2016) 145–147
In summary, we report a case of Palisading and Verocay body-prominent dermatofibrosarcoma protuberans without COL1A1–PDGF translocation. Funding sources None. Acknowledgment The authors would like to thank Dr. Christopher D. Fletcher (Brigham and Women’s Hospital) for reviewing this case. References [1] P. Saiag, J.J. Grob, C. Lebbe, J. Malvehy, V. Del Marmol, H. Pehamberger, K. Peris, A. Stratigos, M. Middelton, L. Basholt, A. Testori, C. Garbe, Diagnosis and treatment of dermatofibrosarcoma protuberans. European consensus-based interdisciplinary guideline, Eur. J. Cancer. 51 (2015) 2604–2608. [2] V. Kumar, A.K. Abbas, N. Fausto, J.C. Aster, Robbins and cotran pathologic basis of disease, in: Professional Edition: Expert Consult-Online, Elsevier Health Sciences, Philadelphia, PA, 2014, pp. 1158–1159. [3] M.P. Simon, F. Pedeutour, N. Sirvent, J. Grosgeorge, F. Minoletti, J.M. Coindre, M.J. Terrier-Lacombe, N. Mandahl, R.D. Craver, N. Blin, G. Sozzi, C. Turc-Carel, K.P. O’Brien, D. Kedra, I. Fransson, C. Guilbaud, J.P. Dumanski, Deregulation of the platelet-derived growth factor B-chain gene via fusion with collagen gene COL1A1 in dermatofibrosarcoma protuberans and giant-cell fibroblastoma, Nat. Genet. 15 (1997) 95–98. [4] F. Pedeutour, M.P. Simon, F. Minoletti, G. Sozzi, M.A. Pierotti, F. Hecht, C. Turc-Carel, Ring 22 chromosomes in dermatofibrosarcoma protuberans are low-level amplifiers of chromosome 17 and 22 sequences, Cancer Res. 55 (1995) 2400–2403. [5] C. Diaz-Cascajo, W. Weyers, S. Borghi, Sclerosing dermatofibrosarcoma protuberans, J. Cutan. Pathol. 25 (1998) 440–444. [6] B. Zelger, D. Öfner, B. Zelger, Atrophic variants of dermatofibroma and dermatofibrosarcoma protuberans, Histopathology 26 (1995) 519–527. [7] A. Orlandi, L. Bianchi, L.G. Spagnoli, Myxoid dermatofibrosarcoma protuberans: morphological, ultrastructural and immunohistochemical features, J. Cutan. Pathol. 25 (1998) 386–393. [8] J. Ding, H. Hashimoto, T. Sugimoto, M. Tsuneyoshi, M. Enjoji, Bednaˇr tumor (pigmented dermatofibrosarcoma protuberans), Pathol. Int. 40 (1990) 744–754. [9] B.M. Shmookler, F.M. Enzinger, S.W. Weiss, Giant cell fibroblastoma. A juvenile form of dermatofibrosarcoma protuberans, Cancer 64 (1989) 2154–2161.
147
[10] S.S. Banerjee, M. Harris, B.P. Eyden, B. Hamid, Granular cell variant of dermatofibrosarcoma protuberans, Histopathology 17 (1990) 375–378. [11] J. Ding, H. Hashimoto, M. Enjoji, Dermatofibrosarcoma protuberans with fibrosarcomatous areas. A clinicopathologic study of nine cases and a comparison with allied tumors, Cancer 64 (1989) 721–729. [12] T. Mentzel, A. Beham, D. Katenkamp, A.P. Dei Tos, C.D. Fletcher, Fibrosarcomatous (“high-grade”) dermatofibrosarcoma protuberans: clinicopathologic and immunohistochemical study of a series of 41 cases with emphasis on prognostic significance, Am. J. Surg. Pathol. 22 (1998) 576–587. [13] R. Llatjos, M. Fernández-Figueras, C. Díaz-Cascajo, M. Ribera, A. Ariza, Palisading and Verocay body-prominent dermatofibrosarcoma protuberans: a report of three cases, Histopathology 37 (2000) 452–455. [14] M.T. Sylvia, B.A. Badhe, Verocay bodies and myxoid change in fibrosarcomatous variant of dermatofibrosarcoma protuberans: A case report and review of literature, Indian J. Dermatopathol. Diagn. Dermatol. 2 (2015) 14. [15] J. Gong, L. Guo, Dermatofibrosarcoma protuberans with palisaded and Verocay body variants: a case report and review of the literature Chinese, J. Clin. Exp. Pathol. 1 (2008) 023. [16] F. Wippold, M. Lämmle, F. Anatelli, J. Lennerz, A. Perry, Neuropathology for the neuroradiologist: palisades and pseudopalisades, Am. J. Neuroradiol. 27 (2006) 2037–2041. [17] J. Reibel, U. Wewer, R. Albrechtsen, The pattern of distribution of laminin in neurogenic tumors, granular cell tumors, and nevi of the oral mucosa, Acta Pathol. Microbiol. Scand. Ser. A: Pathol. 93 (1985) 41–47. [18] J.A. Weiner, N. Fukushima, J.J. Contos, S.S. Scherer, J. Chun, Regulation of Schwann cell morphology and adhesion by receptor-mediated lysophosphatidic acid signaling, J. Neurosci. 21 (2001) 7069–7078. [19] A. Biswas, N. Setia, J. Bhawan, Cutaneous neoplasms with prominent Verocay body-like structures: the so-called “Rippled Pattern”, Am. J. Dermatopathol. 33 (2011) 539–550. [20] V. Schwob, D. Santa Cruz, Palisading cutaneous fibrous histiocytoma, J. Cutan. Pathol. 13 (1986) 403–407. [21] H. Kamino, V. Reddy, Unusual benign fibrous and fibrohistiocytic tumors of the skin, Dermatol. Clin. 10 (1992) 203–217. [22] K.F. Helm, T. Helm, F. Helm, Palisading cutaneous fibrous histiocytoma: an immunohistochemical study demonstrating differentiation from dermal dendrocytes, Am. J. Dermatopathol. 15 (1993) 559–561. [23] M.J. Terrier-Lacombe, L. Guillou, G. Maire, P. Terrier, D.R. Vince, N. de Saint Aubain Somerhausen, F. Collin, F. Pedeutour, J.M. Coindre, Dermatofibrosarcoma protuberans, giant cell fibroblastoma, and hybrid lesions in children: clinicopathologic comparative analysis of 28 cases with molecular data—a study from the French Federation of Cancer Centers Sarcoma Group, Am. J. Surg. Pathol. 27 (2003) 27–39. [24] B. Llombart, O. Sanmartin, J.A. Lopez-Guerrero, C. Monteagudo, C. Serra, C. Requena, A. Poveda, J.L. Vistos, S. Almenar, A. Llombart-Bosch, C. Guillen, Dermatofibrosarcoma protuberans: clinical, pathological, and genetic (COL1A1–PDGFB) study with therapeutic implications, Histopathology 54 (2009) 860–872.