Open Access

Spindle Cell Lipoma and Pleomorphic Lipoma: An Update and Review

OHSHIMA YUKIKO 1
NISHIO JUN 2
NAKAYAMA SHIZUHIDE 1
KOGA KAORI 3
AOKI MIKIKO 3
  &  
YAMAMOTO TAKUAKI 1

1Department of Orthopaedic Surgery, Faculty of Medicine, Fukuoka University, Fukuoka, Japan

2Section of Orthopaedic Surgery, Department of Medicine, Fukuoka Dental College, Fukuoka, Japan

3Department of Pathology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan

Cancer Diagnosis & Prognosis May-June; 3(3): 282-290 DOI: 10.21873/cdp.10213
Received 14 March 2023 | Revised 25 May 2024 | Accepted 04 April 2023
Corresponding author
Jun Nishio, MD, Ph.D., Section of Orthopaedic Surgery, Department of Medicine, Fukuoka Dental College, 2-15-1 Tamura, Sawara-ku, Fukuoka 814-0193, Japan. Tel: +81 928010411, Fax: +81 928010735, email: nishio@fdcnet.ac.jp

Abstract

Spindle cell lipoma (SCL) is a benign adipocytic tumor that primarily occurs in the subcutis of the posterior neck, upper back, and shoulder, particularly of middle-aged males. SCL and pleomorphic lipoma (PL) represent a morphological spectrum of one disease process. The lesion typically presents as a relatively small (<5 cm), mobile, slow-growing, painless mass. Magnetic resonance imaging reveals the lesion to be a well-defined subcutaneous mass with a mixture of adipose and non-adipose components. Intense enhancement of the non-adipose component is seen after contrast administration. Histologically, SCL is composed of variable distributions of mature adipocytes, bland spindle cells and ropey collagen bundles and PL also contains pleomorphic and multinucleated floret-like giant cells. By immunohistochemistry, the spindle and pleomorphic/floret-like giant cells of SCL/PL are diffusely positive for CD34 and show loss of nuclear RB transcriptional corepressor 1 (RB1) expression. Recent cytogenetic and molecular genetic studies have shown heterozygous deletions of 13q14, including the RB1 gene. SCL/PL can be successfully treated with simple excision, with a very low recurrence rate. Knowledge of these peculiar tumors is important because it can mimic a variety of benign and malignant soft-tissue tumors. This review provides an updated overview of the clinical, radiological, histopathological, cytogenetic, and molecular genetic features of SCL/PL.
Keywords: Spindle cell lipoma, pleomorphic lipoma, RB1, cytogenetics, atypical lipomatous tumor, atypical spindle cell/pleomorphic tumor, review

Spindle cell lipoma (SCL) is a relatively rare, benign adipocytic tumor composed of a variable mixture of mature adipocytes, bland spindle cells and ropey collagen bundles. Pleomorphic lipoma (PL) lies on a morphological spectrum with SCL and is characterized by pleomorphic spindle cells and multinucleated floret-like giant cells (1). The etiology of SCL/PL remains unknown. SCL/PL can show a morphological overlap with a variety of soft-tissue tumors, including atypical spindle cell/pleomorphic lipomatous tumor (ASCPLT), atypical lipomatous tumor (ALT), solitary fibrous tumor (SFT), myxoid liposarcoma (MLS) and dedifferentiated liposarcoma (DDLS). In our opinion and experience, the imaging appearance of SCL/PL is not pathognomonic and reflects the histological composition of the lesion which contains variable amounts of adipose and non-adipose tissue. Advances in knowledge of the imaging, histopathology and genetics of SCL/PL are leading to more accurate diagnosis and appropriate treatment. This review highlights the clinical, radiological, histological, immuno-histochemical, cytogenetic and molecular genetic features of SCL/PL. In addition, we will discuss the differential diagnosis of SCL/PL.

Clinical Features

SCL/PL can occur at any age but has a peak incidence in the fifth to seventh decades of life, with a marked male predominance (approximately 90%) (1). It typically presents as a solitary, mobile, slow-growing, painless, subcutaneous mass in the posterior neck, upper back, and shoulder (shawl distribution). Occasional lesions are multifocal or arise in a familial setting (2). Fascial and skeletal muscle involvement is uncommon. In women, SCL is more likely to occur outside the shawl distribution and in a younger age group (3). The diameter ranges from 1.0 to 14.0 cm (usually less than 5 cm) (4). Simple excision is the treatment of choice and prognosis is excellent. There is no metastatic potential and no reports of malignant transformation.

Radiological Features

Various imaging modalities have been applied for the detection of SCL/PL. Although identification of fat within the lesion is the most important clue to make diagnosis of adipocytic tumors on imaging, it is recognized that SCL/PL may have minimal or no visible fat. It is essential to be familiar with the key imaging features of SCL/PL to avoid an unnecessary radical surgery.

Radiographs may be unremarkable or reveal a soft-tissue mass depending on the size and location of the lesion. Although cases of bone erosion have been described (5,6), the underlying bone is typically normal. Ultrasound shows non-specific soft-tissue echogenicity with moderate internal Doppler vascularity in the non-adipose component (7). Computed tomography (CT) reveals a well-defined soft-tissue mass with slightly increased attenuation compared with that of subcutaneous fat in the adipose component and slightly low attenuation compared with that of skeletal muscle in the non-adipose component (8). Contrast-enhanced CT demonstrates significant enhancement in the non-adipose component (7-10). In our experience, the non-adipose component is best detected and evaluated with magnetic resonance imaging (MRI). On MRI, the lesion is usually well-defined and contains variable amounts of adipose and non-adipose components (7-12) (Figure 1). In general, many lesions contain between 25% and 75% fat (10). However, a significant number of SCL/PLs may exhibit a “low-fat” or “fat-free” appearance that can mimic more aggressive tumors such as MLS, DDLS and non-adipocytic sarcomas (7,11,12). The non-adipose component displays isointense relative to skeletal muscle on T1-weighted images and variable signal intensity on T2-weighted images. Contrast-enhanced MRI demonstrates intense enhancement in the non-adipose component (10,12). Recently, Kawaguchi et al. reported that the maximum diameter, the proportion of non-adipose area on T1-weighted images and solid hyperintense area on fat-suppressed T2-weighted images were useful MRI features for differentiating SCL/PL from ALT (13). To date, position-emission tomography (PET) features for SCL/PL have been described in only three cases (7). Integrated PET/CT images show increased uptake in the non-adipose component, with a standardized uptake value (SUV) range of 2.0-8.0. In our opinion, SCL/PL should be considered a possible diagnosis when a well-defined, complex, fatty mass is encountered in the subcutis of a middle-aged man.

Histological and Immunohistochemical Characteristics

Grossly, SCL/PL appears as an oval or discoid, well-circumscribed mass with a yellow or grayish white cut surface (1). Histologically, SCL is composed of variable distributions of mature adipocytes, bland spindle cells and ropey collagen bundles (Figure 2). The ratio of the spindle cells and mature adipocytes is variable, but the great majority of cases have significant amounts of both components. In the other end of the spectrum, PL is characterized by the presence of pleomorphic spindle cells and multinucleated floret-like giant cells. Occasional lipoblasts can be present in a significant subset of cases (14). Mitotic figures are rare, and necrosis is absent. There is relatively sparse vascularity, of small to medium-sized thick-walled, sometimes hyalinized vessels. A variety of variants of SCL have been described including low-fat, fat-free, (pseudo)angiomatous, fibrous, myxoid and plexiform subtypes (1,15-19). Immunohistochemically, the spindle, pleomorphic and multinucleated floret-like cells are diffusely positive for CD34 (Figure 3) and show loss of nuclear RB transcriptional corepressor 1 (RB1) protein expression (20). Immunostainings for S-100 protein, desmin and smooth muscle actin (SMA) are typically negative.

Cytogenetic and Molecular Genetic Features

SCL and PL show similar cytogenetic aberrations which are usually more complex than conventional lipoma (21). SCL/PL displays unbalanced karyotypes, mostly hypodiploid, with multiple partial losses. Structural rearrangements, mainly deletions, of chromosome arm 13q or losses of whole chromosome 13 are the most common cytogenetic aberrations (22). The related region (13q14) contains the RB1 gene. Fluorescence in situ hybridization (FISH) analyses have revealed a heterozygous deletion of RB1 in a subset of SCL/PLs (22,23). Single nucleotide polymorphism array analyses have identified two minimally deleted regions in 13q14 in SCL (24). The first region includes RB1, lysophosphatidic acid receptor 6 (LPAR6), RCC1 and BTB domain containing protein 2 (RCBTB2) and cysteinyl leukotriene receptor 2 (CYSLTR2). The second region lies between the genes fibronectin type III domain containing 3A (FNDC3A) and transmembrane phosphoinositide 3-phosphatase and tensin homolog 2 pseudogene 3 (TPTE2P3, formerly LOC220115) and harbors 34 genes including SPRY domain containing 7 (SPRDY7, formerly C13orf1), dehydrogenase/reductase 12 (DHRS12), ATPase copper transporting beta (ATP7B), ALG11 alpha-1,2-mannosyltransferase (ALG11) and vacuolar protein sorting 36 homolog (VPS36) and the two microRNA genes miR-15a and miR-16-1. Recently, Uehara et al. reported that SCL/PL expressed decreased levels of forkhead box O1 (FOXO1) and RB1 and showed the activation of p38 mitogen-activated protein kinase (MAPK) pathway induced by oxidative stress (25). In addition to 13q deletions, SCL/PL also shows chromosome 16q losses with partial monosomy (26). The involved genes have not been specifically identified in this region. In our extensive experience, SCL/PL lacks amplification of murine double minute 2 (MDM2).

Deletion of RB1 is shared with a group of morphologically similar spindle cell tumors with variable admixed fat and immunohistochemically overlapping features, including SCL/PL, ASCPLT, mammary-type myofibroblastoma and cellular angiofibroma (CAF) (27). RB1 loss has also been described as a recurrent finding in other mesenchymal neoplasms such as pleomorphic fibroma (28) and superficial acral fibromyxoma (29). The current World Health Organization classification of soft-tissue tumors suggests that these lesions are typically benign and are mainly seen in the older adult population. It is of interest that RB1 has been implicated in the regulation of adipocyte differentiation (30,31).

Differential Diagnosis

The differential diagnosis for SCL/PL is broad due to its varying morphology and includes benign, intermediate, and malignant soft-tissue tumors such as ASCPLT, CAF, ALT, fat-forming SFT, MLS and DDLS (Table I).

ASCPLT is a new entity of benign adipocytic neoplasm that usually presents as an enlarging or persistent mass in the extremities and limb girdles, sometimes with tenderness. It can occur at any age but has a peak incidence in the sixth decade of life, with a slight male predominance. The diameter ranges from 0.5 to 28.0 cm (32). ASCPLT has a low rate of non-destructive local recurrence (10-15%) (32). Importantly, there is no risk for dedifferentiation or metastasis. There is only limited description of the imaging appearance of ASCPLT (33-35). On MRI, the lesion displays variable signal intensity on T1- and T2-weighted images. ASCPLT and SCL/PL tend to have similar enhancement patterns on T1-weighted images (33). Preoperative imaging diagnosis is difficult, and histopathological and molecular evaluations are required for a definite diagnosis. Histologically, ASCPLT shows infiltrative margins and demonstrates atypical hyperchromatic spindle cells, pleomorphic lipoblasts and bizarre pleomorphic (multinucleated) cells with mitotic activity in contrast with SCL/PL. ASCPLT typically lacks ropey collagen bundles. ASCPLT and SCL/PL share similar immunohistochemical features such as CD34 positivity and loss of RB1 protein expression (50-70%) (32). In addition, ASCPLT shows variable expression of S100 protein and desmin. Weak and/or focal expression of MDM2 or cyclin-dependent kinase 4 (CDK4) may be seen, but the combination of MDM2 and CDK4 expression is not compatible with a diagnosis of ASCPLT (36). Molecular studies have shown that deletions of 13q14 in ASCPLT are more extensive and complex than in SCL/PL, including multiple functionally important exons of RB1 and its adjacent genes RCBTB2, deleted in lymphocytic leukemia 1 (DLEU1) and integral membrane protein 2B (ITM2B) (37). Moreover, monosomy 7 has been described in a subset of ASCPLTs (36,38). MDM2 or CDK4 amplification is absent in ASCPLT.

CAF is a benign fibroblastic tumor that usually presents as a slow-growing, painless, subcutaneous mass in the vulvovaginal region for women and the inguinoscrotal region for men. It has a peak incidence in the fifth decade of life in women and the seventh in men, with no sex predilection. The diameter ranges from 0.6 to 25.0 cm (39). Simple excision is the treatment of choice and local recurrence is uncommon. On MRI, the lesion is well-defined and displays intermediate or low signal intensity on T1-weighted images and heterogeneous high signal intensity on T2-weighted images (40). Contrast-enhanced MRI demonstrates intense heterogeneous enhancement. The presence of intralesional fat has been reported in up to 56% of CAF (41). CAF has some morphological overlap with SCL/PL. Histologically, the lesion consists of uniform, short spindle-shaped cells in an edematous to fibrous stroma. Mature adipocytes are observed in close to 50% of cases (39). In contrast with SCL/PL, there are numerous small to medium-sized thick-walled blood vessels, often with perivascular fibrosis or hyalinization. CAF and SCL/PL share similar immunohistochemical features such as CD34 positivity (30-60%) and loss of RB1 protein expression (39). Moreover, CAF shows expression for estrogen receptor and progesterone receptor (42). Variable expression of SMA and desmin is seen in a minority of cases (39). Genetically, loss of 13q14, including RB1, is characteristic of CAF as well as SCL/PL (27,43-46).

ALT is an intermediate (locally aggressive) mesenchymal neoplasm that usually presents as a deep-seated, painless mass in the lower extremities, trunk, and retroperitoneum. It most commonly occurs in middle-aged and older adults, with no sex predilection (47). Unlike SCL/PL, ALT shows a significant propensity for local recurrence and can dedifferentiate to DDLS (incidence up to 10%) (48). Radiographs may depict the presence of a soft-tissue mass. Calcification is seen in 10-32% of cases (49). Ultrasound reveals a heterogeneous, multilobulated, typically well-defined mass. The presence of hyperechoic foci suggests fat (49). On CT and MRI, ALT shows a predominantly adipose mass with irregularly thickened, linear, swirled and/or nodular septa. Generally, the lesion contains at least 75% adipose tissue (49). In our experience, the non-adipose component displays non-specific decreased signal intensity on T1-weighted images and variably increased signal intensity on T2-weighted images. Contrast-enhanced MRI usually demonstrates significant enhancement in the non-adipose component (50). Histologically, ALT may be indistinguishable from fat-rich SCL/PL. However, the spindle cells seen in ALT contain more irregular, enlarged, hyperchromatic nuclei. In contrast to SCL/PL, ALT usually lacks ropey collagen bundles. Immunohistochemically, nuclear expression of MDM2 and/or CDK4 is seen in most cases (47). Unlike SCL/PL, ALT is cytogenetically characterized by the presence of one or more supernumerary ring and/or giant marker chromosomes containing amplified chromosome 12 sequences (21). Moreover, MDM2 and/or CDK4 amplification is present in ALT. Detection of MDM2 (and/or CDK4) amplification by fluorescence in situ hybridization (FISH) serves to distinguish ALT from SCL/PL.

SFT is an intermediate (rarely metastasizing) mesenchymal neoplasm that usually presents as a slow-growing, painless mass in the pleura, abdominal cavity, extremities and head and neck. It most commonly occurs in middle-aged adults, with no sex predilection (51). Wide excision is the current treatment mainstay. Local recurrence occurs in 10-40% of cases and distant metastases develop in up to 35-45% of cases (51,52). Dedifferentiation can occur at the end of the transforming histological stage of SFT. Radiographs may reveal a non-specific soft-tissue mass. Calcification is rare, occurring in about 9% of cases (53). Ultrasound generally shows a heterogeneous, well-defined, hypoechoic mass (54). CT reveals a well-defined, occasionally lobulated mass of similar attenuation to that of skeletal muscle. Contrast-enhanced CT demonstrates mild to marked heterogeneous enhancement (54). On MRI, the lesion is well-defined and displays isointense signal intensity on T1-weighted images and variable signal intensity on T2-weighted images (55). Contrast-enhanced MRI demonstrates strong focal or diffuse enhancement. In our experience, the presence of prominent collateral feeding vessels is a useful distinguishing imaging feature of SFT. Histologically, the lesion consists of uniform ovoid to spindle-shaped cells with a patternless architecture embedded in a variably collagenous stroma. Some SFTs contain a component of mature adipose tissue (56). This SFT variant (fat-forming SFT) can be confused with SCL/PL. In contrast with SCL/PL, SFT typically contains branching and hyalinized staghorn-like blood vessels. Immunohistochemically, SFT typically shows diffuse expression of CD34, CD99 and BCL2 (57). Importantly, immunostaining for signal transducer and activator of transcription 6 (STAT6) reliably distinguishes SFT from SCL/PL (58). The discovery of a NGFI-A binding protein 2 (NAB2)-STAT6 fusion gene has recently led to more precise diagnosis of SFT (59). Unlike SCL/PL, SFT is not characterized by deletion of RB1 and corresponding nuclear loss of expression for RB1 (20,60).

MLS is a malignant adipocytic neoplasm that typically presents as a large, painless mass in the proximal lower extremities. It has a peak incidence in the fourth to fifth decades of life, with no sex predilection (61). Wide excision with or without radiotherapy is the treatment of choice. Local recurrence occurs in 12-25% of cases and distant metastases develop in about 30-60% of cases (61). The presence of a round cell component is associated with a significant higher rate of metastasis and an overall adverse outcome. Unlike other soft-tissue sarcomas, MLS shows a high incidence of extrapulmonary metastasis to the soft tissues and bones. Radiographs may be normal or reveal a non-specific soft-tissue mass. Calcification is uncommon. Ultrasound shows a heterogeneous, well-defined, hypoechoic but solid, non-cystic mass with posterior acoustic enhancement (49). CT reveals a well-defined, lobular mass with low attenuation compared with that of skeletal muscle (49). On MRI, the lesion is well-defined and displays low to intermediate signal intensity with lacy, linear, or amorphous high signal intensity foci on T1-weight images and predominantly high signal intensity on T2-weight images (62). Contrast-enhanced MRI typically demonstrates avid heterogeneous enhancement. Histologically, MLS consists of uniform ovoid cells and a variable number of small lipoblasts in a prominent myxoid stroma. Unlike SCL/PL, there is a delicate, arborizing capillary vascular network. DNA damage-inducible transcript 3 (DDIT3) positivity by immunohistochemistry is a sensitive marker for MLS and is expected to be negative in SCL/PL (63). MLS is genetically characterized by a FUS RNA binding protein (FUS)-DDIT3 gene fusion, resulting from a balanced translocation t(12;16)(q13;p11). A variant EWS RNA binding protein 1 (EWSR1)-DDIT3 gene fusion has also been identified in approximately 3% of MLS (61). Detection of these fusion transcripts would be helpful in distinguishing MLS from other adipocytic neoplasms including SCL/PL (64).

DDLS is a malignant adipocytic neoplasm showing transition from ALT to non-lipogenic sarcoma of variable histological grades. It usually presents as a large (>10 cm), painless mass in the retroperitoneum, extremities and paratesticular region. DDLS has a peak incidence in the sixth to seventh decades of life, with no sex predilection (65). Wide excision is the standard treatment for DDLS. Local recurrence occurs in about 40% of cases and distant metastases develop in 15-30% of cases (66). The most important prognostic factor for DDLS is anatomical location. DDLS shares radiological features with ALT or SCL/PL, and dedifferentiation is usually suggested by the presence of a focal, nodular, non-lipomatous region greater than 1cm in size (49). Radiographs may reveal a non-specific soft-tissue mass. Calcification is uncommon. Ultrasound shows a solid, heterogeneous mass with both hypo- and hyperechoic areas (49). CT usually reveals a well-circumscribed, round, or lobulated mass with slightly increased attenuation compared with that of subcutaneous fat in the adipose component and tissue attenuation similar to or slightly lower than that of skeletal muscle in the non-adipose component (67). Contrast-enhanced CT demonstrates definite enhancement in the non-adipose component. MRI typically shows the coexistence of adipose (ALT) and juxtaposed non-adipose (dedifferentiated) components (68,69). The non-adipose component usually displays low to intermediate signal intensity on T1-weighted images and intermediate to high signal intensity on T2-weighted images. Hemorrhage and necrosis may be seen within the high-grade non-adipose component. Contrast-enhanced MRI demonstrates variable enhancement in the non-adipose component (66). Recently, Parkes et al. have suggested that PET/CT is a sensitive and specific diagnostic tool to identify the presence of dedifferentiation within the tumor (70). Histologically, DDLS typically shows an abrupt transition between well-differentiated and dedifferentiated components. The well-differentiated component consists of mature adipocytes with a significant variation in size and atypical, hyperchromatic stromal spindle cells. A varying number of monovacuolated or multivacuolated lipoblasts may be seen. The dedifferentiated component exhibits a wide morphological spectrum but most frequently resemble myxofibrosarcoma or undifferentiated pleomorphic sarcoma (71). Immunohistochemically, diffuse nuclear expression of MDM2 and/or CDK4 is seen in the vast majority of DDLSs. In addition, DDLS shows variable expression of CD34, SMA and desmin (48). The combination of p16 with CDK4 and MDM2 is helpful in distinguishing DDLS from other adipocytic neoplasms including SCL/PL (72). DDLS cytogenetically overlaps with ALT and is characterized by the presence of ring and giant marker chromosomes composed mainly of amplified chromosome 12 sequences (66). Unlike ALT, high-level amplifications of 1p32 and 6q23 are found in DDLS and are associated with a worse prognosis (66). Of note, MDM2 and/or CDK4 amplification is typically present in DDLS. DDLS can therefore be distinguished from SCL/PL by FISH for MDM2 (and/or CDK4) amplification.

Conclusion

SCL/PL is a distinctive, benign, adipocytic neoplasm and simple excision is usually curative. The morphologic spectrum of this peculiar neoplasm is surprisingly diverse. SCL/PL should be considered a possible diagnosis when a well-defined, complex, fatty mass is encountered in the subcutis of a middle-aged man. Structural rearrangements, mainly deletions, of 13q are prominent in SCL/PL. Detection of loss of the RB1 gene would be helpful diagnostically for SCL/PL in selected cases. Further investigations are required to better delineate the relationship between SCL/PL and ASCPLT.

Conflicts of Interest

The Authors declare no conflicts of interest associated with this article.

Authors’ Contributions

YO collected the data and searched the literature. JN searched the literature and drafted the article. KK and MA performed the histopathological evaluations. SN and TY reviewed the article. All Authors read and approved the final article.

Acknowledgements

This study was supported in part by the Japan Society for the Promotion of Science KAKENHI (21K09336).

References

1 Billings SD & Ud Din N Spindle cell lipoma and pleomorphic lipoma. In: World Health Organization Classification of Tumours: Soft Tissue and Bone Tumours. Lyon, IARC Press. pp. 29 - 30 2020.
2 Fanburg-Smith JC Devaney KO Miettinen M & Weiss SW Multiple spindle cell lipomas: a report of 7 familial and 11 nonfamilial cases. Am J Surg Pathol. 22(1) 40 - 48 1998. PMID: 9422314. DOI: 10.1097/00000478-199801000-00005
3 Ko JS Daniels B Emanuel PO Elson P Khachaturov V McKenney JK Goldblum JR & Billings SD Spindle cell lipomas in women: a report of 53 cases. Am J Surg Pathol. 41(9) 1267 - 1274 2017. PMID: 28719462. DOI: 10.1097/PAS.0000000000000915
4 Van Treeck BJ & Fritchie KJ Updates in spindle cell/pleomorphic lipomas. Semin Diagn Pathol. 36(2) 105 - 111 2019. PMID: 30850230. DOI: 10.1053/j.semdp.2019.02.005
5 Braunschweig IJ Stein IH Dodwad MI Rangwala AF & Lopano A Case report 751: Spindle cell lipoma causing marked bone erosion. Skeletal Radiol. 21(6) 414 - 417 1992. PMID: 1523441. DOI: 10.1007/BF00241825
6 Petit D Menei P & Fournier HD An unusual and spectacular case of spindle cell lipoma of the posterior neck invading the spinal cervical canal and posterior cranial fossa. J Neurosurg Spine. 15(5) 502 - 506 2011. PMID: 21819187. DOI: 10.3171/2011.7.SPINE10820
7 Khashper A Zheng J Nahal A & Discepola F Imaging characteristics of spindle cell lipoma and its variants. Skeletal Radiol. 43(5) 591 - 597 2014. PMID: 24554024. DOI: 10.1007/s00256-014-1834-5
8 Choi JW Kim HJ Kim J Kim HJ Cha JH & Kim ST Spindle cell lipoma of the head and neck: CT and MR imaging findings. Neuroradiology. 55(1) 101 - 106 2013. PMID: 23053001. DOI: 10.1007/s00234-012-1098-5
9 Younan Y Martinez A Reimer N Edgar M Gonzalez F Umpierrez M Subhawong T & Singer AD Combined classical spindle cell/pleomorphic lipoma spectrum imaging and clinical data. Skeletal Radiol. 47(1) 51 - 59 2018. PMID: 28823067. DOI: 10.1007/s00256-017-2751-1
10 Bancroft LW Kransdorf MJ Peterson JJ Sundaram M Murphey MD & O’Connor MI Imaging characteristics of spindle cell lipoma. AJR Am J Roentgenol. 181(5) 1251 - 1254 2003. PMID: 14573414. DOI: 10.2214/ajr.181.5.1811251
11 Kirwadi A Abdul-Halim R Fernando M Highland A & Kotnis N MR imaging features of spindle cell lipoma. Skeletal Radiol. 43(2) 191 - 196 2014. PMID: 24240205. DOI: 10.1007/s00256-013-1765-6
12 Jelinek JS Wu A Wallace M Kumar D Henshaw RM Murphey MJ Van Horn A & Aboulafia AJ Imaging of spindle cell lipoma. Clin Radiol. 75(5) 396.e15 - 396.e21 2020. PMID: 31932047. DOI: 10.1016/j.crad.2019.11.020
13 Kawaguchi M Kato H Kobayashi K Miyazaki T Nagano A Noda Y Hyodo F & Matsuo M Differences in MRI findings of superficial spindle cell lipoma and atypical lipomatous tumor/well-differentiated liposarcoma. Br J Radiol. 96(1143) 20220743 2023. PMID: 36607278. DOI: 10.1259/bjr.20220743
14 Michal M Kazakov DV Hadravsky L Michalova K Grossmann P Steiner P Vanecek T Renda V Suster S & Michal M Lipoblasts in spindle cell and pleomorphic lipomas: a close scrutiny. Hum Pathol. 65 140 - 146 2017. PMID: 28546131. DOI: 10.1016/j.humpath.2017.05.006
15 Billings SD & Folpe AL Diagnostically challenging spindle cell lipomas: a report of 34 “low-fat” and “fat-free” variants. Am J Dermatopathol. 29(5) 437 - 442 2007. PMID: 17890910. DOI: 10.1097/DAD.0b013e31813735df
16 Hawley IC Krausz T Evans DJ & Fletcher CD Spindle cell lipoma – a pseudoangiomatous variant. Histopathology. 24(6) 565 - 569 1994. PMID: 8063285. DOI: 10.1111/j.1365-2559.1994.tb00577.x
17 Diaz-Cascajo C Borghi S & Weyers W Fibrous spindle cell lipoma: report of a new variant. Am J Dermatopathol. 23(2) 112 - 115 2001. PMID: 11285405. DOI: 10.1097/00000372-200104000-00005
18 Wong YP Chia WK Low SF Mohamed-Haflah NH & Sharifah NA Dendritic fibromyxolipoma: a variant of spindle cell lipoma with extensive myxoid change, with cytogenetic evidence. Pathol Int. 64(7) 346 - 351 2014. PMID: 25047505. DOI: 10.1111/pin.12176
19 Zelger BW Zelger BG Plörer A Steiner H & Fritsch PO Dermal spindle cell lipoma: plexiform and nodular variants. Histopathology. 27(6) 533 - 540 1995. PMID: 8838333. DOI: 10.1111/j.1365-2559.1995.tb00324.x
20 Chen BJ Mariño-Enríquez A Fletcher CD & Hornick JL Loss of retinoblastoma protein expression in spindle cell/pleomorphic lipomas and cytogenetically related tumors: an immunohistochemical study with diagnostic implications. Am J Surg Pathol. 36(8) 1119 - 1128 2012. PMID: 22790852. DOI: 10.1097/PAS.0b013e31825d532d
21 Nishio J Contributions of cytogenetics and molecular cytogenetics to the diagnosis of adipocytic tumors. J Biomed Biotechnol. 2011 524067 2011. PMID: 21274402. DOI: 10.1155/2011/524067
22 Panagopoulos I Gorunova L Lund-Iversen M Andersen K Andersen HK Lobmaier I Bjerkehagen B & Heim S Cytogenetics of spindle cell/pleomorphic lipomas: Karyotyping and FISH analysis of 31 tumors. Cancer Genomics Proteomics. 15(3) 193 - 200 2018. PMID: 29695401. DOI: 10.21873/cgp.20077
23 Chen S Huang H He S Wang W Zhao R Li L Cui Z & Zhang R Spindle cell lipoma: clinicopathologic characterization of 40 cases. Int J Clin Exp Pathol. 12(7) 2613 - 2621 2019. PMID: 31934089.
Pubmed |
24 Bartuma H Nord KH Macchia G Isaksson M Nilsson J Domanski HA Mandahl N & Mertens F Gene expression and single nucleotide polymorphism array analyses of spindle cell lipomas and conventional lipomas with 13q14 deletion. Genes Chromosomes Cancer. 50(8) 619 - 632 2011. PMID: 21563233. DOI: 10.1002/gcc.20884
25 Uehara K Ikehara F Shibuya R Nakazato I Oshiro M Kiyuna M Tanabe Y Toyoda Z Kurima K Kina S Hisaoka M & Kinjo T Molecular signature of tumors with monoallelic 13q14 deletion: a case series of spindle cell lipoma and genetically-related tumors demonstrating a link between FOXO1 status and p38 MAPK pathway. Pathol Oncol Res. 24(4) 861 - 869 2018. PMID: 28887603. DOI: 10.1007/s12253-017-0303-6
26 Mandahl N Mertens F Willén H Rydholm A Brosjö O & Mitelman F A new cytogenetic subgroup in lipomas: loss of chromosome 16 material in spindle cell and pleomorphic lipomas. J Cancer Res Clin Oncol. 120(12) 707 - 711 1994. PMID: 7798294. DOI: 10.1007/BF01194267
27 Libbrecht S Van Dorpe J & Creytens D The rapidly expanding group of RB1-deleted soft tissue tumors: an updated review. Diagnostics (Basel). 11(3) 430 2021. PMID: 33802620. DOI: 10.3390/diagnostics11030430
28 Hinds B Agulló Pérez AD LeBoit PE McCalmont TH & North JP Loss of retinoblastoma in pleomorphic fibroma: An immunohistochemical and genomic analysis. J Cutan Pathol. 44(8) 665 - 671 2017. PMID: 28543636. DOI: 10.1111/cup.12965
29 Agaimy A Michal M Giedl J Hadravsky L & Michal M Superficial acral fibromyxoma: clinicopathological, immunohistochemical, and molecular study of 11 cases highlighting frequent Rb1 loss/deletions. Hum Pathol. 60 192 - 198 2017. PMID: 27825811. DOI: 10.1016/j.humpath.2016.10.016
30 Calo E Quintero-Estades JA Danielian PS Nedelcu S Berman SD & Lees JA Rb regulates fate choice and lineage commitment in vivo. Nature. 466(7310) 1110 - 1114 2010. PMID: 20686481. DOI: 10.1038/nature09264
31 Hansen JB te Riele H & Kristiansen K Novel function of the retinoblastoma protein in fat: regulation of white versus brown adipocyte differentiation. Cell Cycle. 3(6) 774 - 778 2004. PMID: 15197340.
Pubmed |
32 Creytens D & Marino-Enriquez A Atypical spindle cell lipoma/pleomorphic lipomatous tumour. In: World Health Organization Classification of Tumours: Soft Tissue and Bone Tumours.. Lyon, IARC Press. pp. 34 - 35 2020.
33 Ichikawa J Kawasaki T Imada H Kanno S Taniguchi N Ashizawa T & Haro H Case report: Atypical spindle cell/pleomorphic lipomatous tumor masquerading as a myxoid liposarcoma or intramuscular myxoma. Front Oncol. 12 1033114 2022. PMID: 36439417. DOI: 10.3389/fonc.2022.1033114
34 Sugita S Sugawara T Emori M Aoyama T Hosaka M Segawa K Fujita H & Hasegawa T Atypical spindle cell/pleomorphic lipomatous tumor with a sarcomatous component showing high mitotic activity and Ki-67 labeling index: report of a unique case mimicking dedifferentiated liposarcoma. Med Mol Morphol. 55(4) 323 - 328 2022. PMID: 35779129. DOI: 10.1007/s00795-022-00327-8
35 Cheng YW Chen YY Kuo CH Liao WC & Kwan AL Lumbar paraspinal atypical spindle cell/pleomorphic lipomatous tumor: A report of a rare case. Clin Case Rep. 11(1) e6868 2023. PMID: 36726691. DOI: 10.1002/ccr3.6868
36 Mariño-Enriquez A Nascimento AF Ligon AH Liang C & Fletcher CD Atypical spindle cell lipomatous tumor: Clinicopathologic characterization of 232 cases demonstrating a morphologic spectrum. Am J Surg Pathol. 41(2) 234 - 244 2017. PMID: 27879515. DOI: 10.1097/PAS.0000000000000770
37 Creytens D van Gorp J Savola S Ferdinande L Mentzel T & Libbrecht L Atypical spindle cell lipoma: a clinicopathologic, immunohistochemical, and molecular study emphasizing its relationship to classical spindle cell lipoma. Virchows Arch. 465(1) 97 - 108 2014. PMID: 24659226. DOI: 10.1007/s00428-014-1568-8
38 Italiano A Chambonniere ML Attias R Chibon F Coindre JM & Pedeutour F Monosomy 7 and absence of 12q amplification in two cases of spindle cell liposarcomas. Cancer Genet Cytogenet. 184(2) 99 - 104 2008. PMID: 18617058. DOI: 10.1016/j.cancergencyto.2008.04.004
39 Iwasa Y Fletcher CDM & Flucke U Cellular fibroma. In: World Health Organization Classification of Tumours: Soft Tissue and Bone Tumours. Lyon, IARC Press. pp. 80 - 81 2020.
40 Figueiredo G O’Shea A Neville GM & Lee SI Rare mesenchymal tumors of the pelvis: Imaging and pathologic correlation. Radiographics. 42(1) 143 - 158 2022. PMID: 34797733. DOI: 10.1148/rg.210049
41 Ntorkou AA Tsili AC Giannakis D Batistatou A Stavrou S Sofikitis N & Argyropoulou MI Magnetic resonance imaging findings of cellular angiofibroma of the tunica vaginalis of the testis: a case report. J Med Case Rep. 10 71 2016. PMID: 27029567. DOI: 10.1186/s13256-016-0861-3
42 Iwasa Y & Fletcher CD Cellular angiofibroma: clinicopathologic and immunohistochemical analysis of 51 cases. Am J Surg Pathol. 28(11) 1426 - 1435 2004. PMID: 15489646. DOI: 10.1097/01.pas.0000138002.46650.95
43 Hameed M Clarke K Amer HZ Mahmet K & Aisner S Cellular angiofibroma is genetically similar to spindle cell lipoma: a case report. Cancer Genet Cytogenet. 177(2) 131 - 134 2007. PMID: 17854668. DOI: 10.1016/j.cancergencyto.2007.05.016
44 Maggiani F Debiec-Rychter M Vanbockrijck M & Sciot R Cellular angiofibroma: another mesenchymal tumour with 13q14 involvement, suggesting a link with spindle cell lipoma and (extra)-mammary myofibroblastoma. Histopathology. 51(3) 410 - 412 2007. PMID: 17727484. DOI: 10.1111/j.1365-2559.2007.02775.x
45 Flucke U van Krieken JH & Mentzel T Cellular angiofibroma: analysis of 25 cases emphasizing its relationship to spindle cell lipoma and mammary-type myofibroblastoma. Mod Pathol. 24(1) 82 - 89 2011. PMID: 20852591. DOI: 10.1038/modpathol.2010.170
46 Panagopoulos I Gorunova L Bjerkehagen B Andersen K Lund-Iversen M & Heim S Loss of chromosome 13 material in cellular angiofibromas indicates pathogenetic similarity with spindle cell lipomas. Diagn Pathol. 12(1) 17 2017. PMID: 28193293. DOI: 10.1186/s13000-017-0607-6
47 Sbaraglia M Dei Tos AP & Pedeutour F Atypical lipomatous tumour/well-differentiated liposarcoma. In: World Health Organization Classification of Tumours: Soft Tissue and Bone Tumours. Lyon, IARC Press. pp. 36 - 38 2020.
48 Thway K Well-differentiated liposarcoma and dedifferentiated liposarcoma: An updated review. Semin Diagn Pathol. 36(2) 112 - 121 2019. PMID: 30852045. DOI: 10.1053/j.semdp.2019.02.006
49 Murphey MD Arcara LK & Fanburg-Smith J From the archives of the AFIP: imaging of musculoskeletal liposarcoma with radiologic-pathologic correlation. Radiographics. 25(5) 1371 - 1395 2005. PMID: 16160117. DOI: 10.1148/rg.255055106
50 Nishio J Iwasaki H Nabeshima K Kamachi Y & Naito M Atypical lipomatous tumor with structural rearrangements involving chromosomes 3 and 8. Anticancer Res. 34(6) 3073 - 3076 2014. PMID: 24922675.
Pubmed |
51 Demicco MG Fritchie KJ & Han A Solitary fibrous tumor. In: World Health Organization Classification of Tumours: Soft Tissue and Bone Tumours.. Lyon, IARC Press. pp. 104 - 108 2020.
52 Martin-Broto J Mondaza-Hernandez JL Moura DS & Hindi N A comprehensive review on solitary fibrous tumor: new insights for new horizons. Cancers (Basel). 13(12) 2913 2021. PMID: 34200924. DOI: 10.3390/cancers13122913
53 Wignall OJ Moskovic EC Thway K & Thomas JM Solitary fibrous tumors of the soft tissues: review of the imaging and clinical features with histopathologic correlation. AJR Am J Roentgenol. 195(1) W55 - W62 2010. PMID: 20566782. DOI: 10.2214/AJR.09.3379
54 Papathanassiou ZG Alberghini M Picci P Staals E Gambarotti M Garaci FG & Vanel D Solitary fibrous tumors of the soft tissues: imaging features with histopathologic correlations. Clin Sarcoma Res. 3(1) 1 2013. PMID: 23351922. DOI: 10.1186/2045-3329-3-1
55 Nishio J Iwasaki H Aoki M Nabeshima K & Naito M FDG PET/CT and MR imaging of CD34-negative soft-tissue solitary fibrous tumor with NAB2-STAT6 fusion gene. Anticancer Res. 35(2) 967 - 971 2015. PMID: 25667482.
Pubmed |
56 Nielsen GP Dickersin GR Provenzal JM & Rosenberg AE Lipomatous hemangiopericytoma. A histologic, ultrastructural and immunohistochemical study of a unique variant of hemangiopericytoma. Am J Surg Pathol. 19(7) 748 - 756 1995. PMID: 7793472. DOI: 10.1097/00000478-199507000-00002
57 Thway K Ng W Noujaim J Jones RL & Fisher C The current status of solitary fibrous tumor: diagnostic features, variants, and genetics. Int J Surg Pathol. 24(4) 281 - 292 2016. PMID: 26811389. DOI: 10.1177/1066896915627485
58 Cheah AL Billings SD Goldblum JR Carver P Tanas MZ & Rubin BP STAT6 rabbit monoclonal antibody is a robust diagnostic tool for the distinction of solitary fibrous tumour from its mimics. Pathology. 46(5) 389 - 395 2014. PMID: 24977739. DOI: 10.1097/PAT.0000000000000122
59 Robinson DR Wu YM Kalyana-Sundaram S Cao X Lonigro RJ Sung YS Chen CL Zhang L Wang R Su F Iyer MK Roychowdhury S Siddiqui J Pienta KJ Kunju LP Talpaz M Mosquera JM Singer S Schuetze SM Antonescu CR & Chinnaiyan AM Identification of recurrent NAB2-STAT6 gene fusions in solitary fibrous tumor by integrative sequencing. Nat Genet. 45(2) 180 - 185 2013. PMID: 23313952. DOI: 10.1038/ng.2509
60 Fritchie KJ Carver P Sun Y Batiouchko G Billings SD Rubin BP Tubbs RR & Goldblum JR Solitary fibrous tumor: is there a molecular relationship with cellular angiofibroma, spindle cell lipoma, and mammary-type myofibroblastoma. Am J Clin Pathol. 137(6) 963 - 970 2012. PMID: 22586056. DOI: 10.1309/AJCPQEG6YNN6CNAL
61 Thway K & Nielsen TO Myxoid liposarcoma. In: World Health Organization Classification of Tumours: Soft Tissue and Bone Tumours. Lyon, IARC Press. pp. 42 - 44 2020.
62 Saifuddin A Andrei V Rajakulasingam R Oliveira I & Seddon B Magnetic resonance imaging of trunk and extremity myxoid liposarcoma: diagnosis, staging, and response to treatment. Skeletal Radiol. 50(10) 1963 - 1980 2021. PMID: 33792747. DOI: 10.1007/s00256-021-03769-w
63 Scapa JV Cloutier JM Raghavan SS Peters-Schulze G Varma S & Charville GW DDIT3 immunohistochemistry is a useful tool for the diagnosis of myxoid liposarcoma. Am J Surg Pathol. 45(2) 230 - 239 2021. PMID: 32815829. DOI: 10.1097/PAS.0000000000001564
64 Iwasaki H Ishiguro M Nishio J Aoki M Yokoyama R Yokoyama K Taguchi K & Nabeshima K Extensive lipoma-like changes of myxoid liposarcoma: morphologic, immunohistochemical, and molecular cytogenetic analyses. Virchows Arch. 466(4) 453 - 464 2015. PMID: 25650275. DOI: 10.1007/s00428-015-1721-z
65 Dei TOS AP Marino-Enriquez A & Pedeutour F Dedifferentiated liposarcoma. In: World Health Organization Classification of Tumours: Soft Tissue and Bone Tumours. Lyon, IARC Press. pp. 39 - 41 2020.
66 Nishio J Nakayama S Nabeshima K & Yamamoto T Biology and management of dedifferentiated liposarcoma: state of the art and perspectives. J Clin Med. 10(15) 3230 2021. PMID: 34362013. DOI: 10.3390/jcm10153230
67 Hong SH Kim KA Woo OH Park CM Kim CH Kim MJ Chung JJ Han JK & Rha SE Dedifferentiated liposarcoma of retroperitoneum: spectrum of imaging findings in 15 patients. Clin Imaging. 34(3) 203 - 210 2010. PMID: 20416485. DOI: 10.1016/j.clinimag.2009.12.025
68 Nishio J Aoki M Nabeshima K Iwasaki H & Naito M Cytogenetic and molecular cytogenetic findings in giant dedifferentiated liposarcoma of the thigh. Oncol Rep. 27(3) 764 - 768 2012. PMID: 22160092. DOI: 10.3892/or.2011.1584
69 Nishio J Iwasaki H Nabeshima K & Naito M Immunohistochemical, cytogenetic, and molecular cytogenetic characterization of both components of a dedifferentiated liposarcoma: implications for histogenesis. Anticancer Res. 35(1) 345 - 350 2015. PMID: 25550570.
Pubmed |
70 Parkes A Urquiola E Bhosale P Lin H Watson K Wang WL Feig B Torres K Roland CL Conley AP Zarzour M Livingston JA Ratan R Ludwig J Araujo DM Ravi V Benjamin RS Patel S & Somaiah N PET/CT imaging as a diagnostic tool in distinguishing well-differentiated versus dedifferentiated liposarcoma. Sarcoma. 2020 8363986 2020. PMID: 32565716. DOI: 10.1155/2020/8363986
71 Mori T Yamada Y Kinoshita I Kohashi K Yamamoto H Ito Y Susuki Y Kawaguchi K Nakashima Y & Oda Y Clinicopathological and histopathological review of dedifferentiated liposarcoma: a comprehensive study of 123 primary tumours. Histopathology. 80(3) 538 - 557 2022. PMID: 34699612. DOI: 10.1111/his.14588
72 Thway K Flora R Shah C Olmos D & Fisher C Diagnostic utility of p16, CDK4, and MDM2 as an immunohistochemical panel in distinguishing well-differentiated and dedifferentiated liposarcomas from other adipocytic tumors. Am J Surg Pathol. 36(3) 462 - 469 2012. PMID: 22301498. DOI: 10.1097/PAS.0b013e3182417330