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Synonyms and keywords: Sarcoma of fat cells; Malignancy of fat cells; Fat cells cancer

Overview

Liposarcoma is a uncommon cancer of connective tissues. Liposarcoma is a malignant tumor that arises in fat cells in deep soft tissue, such as that inside the thigh or in the retroperitoneum.

They are typically large bulky tumors which tend to have multiple smaller satellites extending beyond the main confines of the tumor.

Historical Perspective

Liposarcoma was first described by Dr. Rudolph Virchow, a German pathologist, in 1857. Virchow reported a “myxoma lipomatoides malignum”, highlighting the malignant nature of the tumor. Between 1954 and 1979, several authors reported cases of liposarcoma and suggested that liposarcoma should be classified according to histopathological analysis into well-differentiated, myxoid, and dedifferentiated subtypes.

Classification

Liposarcoma may be classified into well-differentiated, de-differentiated, myxoid, round cell, or pleomorphic liposarcoma.

Pathophysiology

The pathogenesis of liposarcoma depends on the histological subtype. The role of proto-oncogenes has been implicated in the development of well-differentiated liposarcoma

Causes

There are no established causes for liposarcoma.

Differential Diagnosis

Liposarcoma must be differentiated from other diseases that cause a painless, growing mass such as spindle cell lipoma, neurofibroma, dermatofibrosarcoma protuberans, and malignant peripheral nerve sheath tumor.

Epidemiology and Demographics

Liposarcoma is the second most common type of all soft tissue sarcomas in adults. The annual incidence is 0.25 cases per 100,000 individuals. Men are slightly more affected with liposarcoma than women. It is most frequent in middle-aged and older adults.

Risk Factors

Common risk factors in the development of liposarcoma include chemical carcinogens, radiation, immunodeficiency, genetic disorders, and viral infections.

Natural History, Complications and Prognosis

Common complication of liposarcoma include metastasis. Mass may compress adjacent structures causing different clinical manifestations. Metastasis is the most important aspect to assess in the prognosis of liposarcoma. The prognosis will depend on the histopathological subtype, being the well differentiated liposarcoma the subtype with the best prognosis, and the pleomorphic liposarcoma with the worst prognosis.

Diagnosis

Staging

The staging of liposarcoma is based on the TNM classification, which includes primary tumor spread, lymph node involvement, and presence of metastasis.

History and Symptoms

Liposarcoma usually presents as a painless mass. The most common location of a liposarcoma is the lower extremities. Patients with retroperitoneal liposarcoma remain asymptomatic until the mass invades adjacent structures, which may cause pain or obstructive symptoms.

Physical Examination

Physical examination findings of liposarcoma depend on the location of the tumor. Since most liposarcomas are located in the lower extremities, liposarcoma is commonly associated with the findings of palpable firm nontender mass in one lower extremity. Physical examination of retroperitoneal liposarcomas is usually unremarkable, but other pertinent findings on physical examination of retroperitoneal liposarcomas include palpation of an abdominal mass, abdominal distension, and tenderness.

Laboratory Findings

There are no specific laboratory tests for the diagnosis of liposarcoma. The pertinent laboratory findings of liposarcoma include anemia and elevated BUN due to GI bleeding and elevated creatinine among patients with obstructive nephropathy.

Biopsy

The definitive diagnosis of liposarcoma is made by biopsy, which also provides histopathological classification of the liposarcoma’s subtype.

CT

CT imaging is crucial for the diagnosis of liposarcoma. CT scan may detect regions of lipid and non-lipid components that correlate with histological subtypes of liposarcoma. CT imaging may demonstrate the size, location, and depth of a liposarcoma, as well as lymph node involvement and distant metastasis. CT findings may be correlated with the histopathological subtype.

MRI

MRI is the optimal imaging test for the diagnosis of liposarcoma. MRI findings for a well-differentiated liposarcoma include a mass with at least 75% of adipose content with thin irregular septa. MRI also evaluates the size, location, and depth of the mass. MRI findings help to differentiate between the different subtypes of liposarcoma and help to assess distant metastasis.

Other Imaging Findings

Positron emission tomography (PET) scan is useful in cases where the liposarcoma is firm, deep, and has a size greater than 3 cm.^[1] PET scan may also help evaluate the grade and prognosis of the tumor,as well as its shrinkage following chemotherapy.

Other Diagnostic Studies

Li-Fraumeni syndrome is associated with liposarcoma. Mutations in the TP53 gene that encodes the tumor suppressor gene p53 cause Li-Fraumeni syndrome.^[1]

Treatment

Medical Therapy

Medical therapy for liposarcoma includes Chemotherapy, chemoradiation, immunotherapy and targeted therapy.

Surgery

The predominant therapy for liposarcoma is surgical resection. Adjunctive chemotherapy and radiation may be required.

References

↑ ^1.0 ^1.1 “NCCN Guidelines for Patients – Soft Tissue Sarcoma”.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [2]; Ammu Susheela, M.D. [3]

Historical Perspective

Overview

Liposarcoma was first described by Rudolph Virchow, a German pathologist, in 1857. Virchow reported a “myxoma lipomatoides malignum”, highlighting the malignant nature of the tumor. Between 1954 and 1979, several authors reported cases of liposarcoma and suggested that liposarcoma should be classified according to histopathological analysis into well-differentiated, myxoid, and dedifferentiated subtypes.

Historical Perspective

Discovery

Liposarcoma was first discovered in 1857 by Rudolph Virchow, a German pathologist, who described a tumor arising from fat tissue. Originally, Virchow called the tumor “myxoma lipomatodes malignum”.^[1]
Virchow demonstrated that the tumor has a malignant nature.
In 1859, Delamater reported a “mammoth” retroperitoneal tumor with lipomatous aspect.^[2]

Several lesions similar to lipoma myxomatodes were reported by Robertson in 1916.^[3]
In 1921, Von Wahlendorf demonstrated that retroperitoneal tumors of the adipose tissue that are dangerous in a collective review of liposarcomas (14%) of 168 collected cases.^[4]
The malignant component of the liposarcoma was described in 1927 by Seids et al., who reported malignant lesions with a myxoid component.^[5]
Ewing described adipose tumors that arise from the embryonal tissue in adults in 1935.^[6]
In 1942 and 1944, liposarcoma was described in different anatomical locations and with different clinical manifestations that were associated with the disease prognosis. ^[7]^[8]
Between 1954 and 1979, several authors reported cases of liposarcoma and suggested that liposarcoma should be classified according to histopathological analysis into well-differentiarted, myxoid, and dedifferentiated subtypes. ^[9]^[10]^[11]

Famous Cases

In 2014, Rob Ford, the mayor of Toronto, was diagnosed with an abdominal pleomorphic liposarcoma.

References

↑ Virchow, Rud (1857). “Ein Fall von bösartigen, zum Theil in der Form des Neuroms auftretenden Fettgeschwülsten”. Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin. 11 (3): 281–288. doi:10.1007/BF01995372. ISSN 0945-6317.
↑ Delamater, J.: Mammoth tumors. Cleveland M. Gaz. 1: 31, 1859
↑ H. E. Robertson (1916). “Lipoma Myxomatodes”. The Journal of medical research. 35 (1): 131–146. PMID 19972316. Unknown parameter |month= ignored (help)
↑ DEWEERD JH, DOCKERTY MB (1952). “Lipomatous retroperitoneal tumors”. Am J Surg. 84 (4): 397–407. PMID 12986048.
↑ Seids JV, McGinnis RS (1927) Malignant tumors of fatty tissues.Surg Gynec Obstet 44:232–243
↑ Ewing, James (1935). “FASCIAL SARCOMA AND INTERMUSCULAR MYXOLIPOSARCOMA”. Archives of Surgery. 31 (4): 507. doi:10.1001/archsurg.1935.01180160003001. ISSN 0004-0010.
↑ Ackerman LV, Wheeler P (1942) Liposarcoma. South Med J 35:156–160
↑ A. P. Stout (1944). “Liposarcoma-the Malignant Tumor of Lipoblasts”. Annals of surgery. 119 (1): 86–107. PMID 17858339. Unknown parameter |month= ignored (help)
↑ G. T. PACK & J. C. PIERSON (1954). “Liposarcoma; a study of 105 cases”. Surgery. 36 (4): 687–712. PMID 13195985. Unknown parameter |month= ignored (help)
↑ H. T. ENTERLINE, J. D. CULBERSON, D. B. ROCHLIN & L. W. BRADY (1960). “Liposarcoma. A clinical and pathological study of 53 cases”. Cancer. 13: 932–950. PMID 13696965. Unknown parameter |month= ignored (help)
↑ H. L. Evans (1979). “Liposarcoma: a study of 55 cases with a reassessment of its classification”. The American journal of surgical pathology. 3 (6): 507–523. PMID 534388. Unknown parameter |month= ignored (help)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [2]

Classification

Overview

Liposarcoma may be classified into well-differentiated, de-differentiated, myxoid, round cell, or pleomorphic liposarcoma.

Classification

Liposarcoma is a type of soft tissue sarcoma, which accounts for approximately 20% of the mesenchymal malignancies. Liposarcomas may be classified into different subtypes, according to their histologic, cytogenetic, biologic, and molecular features. The World Health Organization proposed the following classification of liposarcomas:^[1]^[2]^[3]


WHO Classification of Liposarcoma^[3]
Well-diferentiated liposarcoma: Adipocytic or lipoma-like Inflammatory Sclerosing De-differentiated liposarcoma Myxoid-round cell liposarcoma (MRCLS) Pleomorphic liposarcoma Liposarcoma, not otherwise specified

References

↑ Weiss, Sharon (1994). Histological typing of soft tissue tumours. Berlin New York: Springer-Verlag. ISBN 3540567941.
↑ Dei Tos AP (2000). “Liposarcoma: new entities and evolving concepts”. Ann Diagn Pathol. 4 (4): 252–66. doi:10.1053/adpa.2000.8133. PMID 10982304.
↑ ^3.0 ^3.1 “WHO Classification of Soft Tissue Tumors” (PDF). WHO. WHO. Retrieved Sep 25 2014. Check date values in: |accessdate= (help)}}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Pathophysiology

Overview

Liposarcoma is the most common sarcoma of soft tissue. The pathogenesis of liposarcoma depends on the histological sub-type. The two sub-types, well differentiated and dedifferentiated, are the two most commonly occurring liposarcomas. The majority of well differentiated liposarcomas arise in the retroperitoneum. The chromosome region 12q13-15, is rich in protooncogenes, including the CHOP, CDK4, MDM2, HMGI-C, GLI, SAS, OS1, and the OS9, all of which play an important role in the pathogenesis of many neoplasms. Liposarcoma is associated with genetic conditions like Li-Fraumeni syndrome. Liposarcoma usually presents as a mass which often resembles lipoma and is multinodular. Microscopic pathological findings of liposarcoma depend on the sub-type.

Pathophysiology

Pathogenesis

Liposarcoma is the most common sarcoma of soft tissue.^[1]
The two sub-types, well differentiated and dedifferentiated, are the two most commonly occurring liposarcomas.^[2]
The majority of well differentiated liposarcomas arise in the retroperitoneum.^[3]^[4]

The tumor can also arise in the deep soft tissue of the thigh, mediastinum, and paratesticular area.^[5]^[6]

Retroperitoneal tumors are more likely to recur.^[7]^[8]
The dedifferentiated sub-type arises as a primary or de novo lesion in majority of the cases.^[9]^[10]^[11]^[12]

The dedifferentiated sub-type is clinically more aggressive than the well differentiated liposarcoma.^[13]^[14]^[15]^[16]

Genetics

Well-Differentiated Liposarcoma

The chromosome region 12q13-15, is rich in protooncogenes, including the CHOP, CDK4, MDM2, HMGI-C, GLI, SAS, OS1, and the OS9, all of which play an important role in the pathogenesis of many neoplasms.
Amplification of some of these regions, with concomitant amplification of their proteins, has clearly been demonstrated in liposarcoma.^[17]
The difference between malignant and benign masses resides in the amount of rearranged gene present in each tissue.^[17]

Associated Conditions

Liposarcoma is associated with genetic conditions like Li-Fraumeni syndrome.

Gross Pathology

Liposarcoma usually presents as a mass which often resembles lipoma and is multinodular.
Cut surface may be soft or firm and is yellow in color.
Focal mucinous area may be seen.
Areas of necrosis may be noted.

Microscopic Pathology

Each liposarcoma sub-type has specific characteristics:

Well-Differentiated Liposarcoma

Sclerosing Liposarcoma

The particular histological finding in this type of well differentiated liposarcoma is the identification of distinctive stromal cells distributed across the tissue, which are associated with lipoblasts filled with multiple vacuoles.
This association forms a collagenous background of fibrillary appearance.
In certain cases, the fibrous component of the neoplasm may occupy most of its mass.^[18]

Adipocytic Liposarcoma

Frequently composed by adipocytes with different cell sizes, hyperchromasia, and nuclear atypia.
Fibrous septa may be identified surrounding adipocytes, containing hyperchromatic stromal cells.
Besides these two types of cells, mono- or multi-vacuolated lipoblasts may also be identified.
Lipoblasts are characterized by the presence of single (mono) or multiple (multi) peripheral cytoplasmic vacuoles that press on the hyperchromatic nucleus.^[18]
In general, adipocytic neoplasms are often identified by the presence of these lipoblasts.
Additionally, lipoblasts may infrequently be absent, which makes the diagnosis of adipocytic neoplasm more difficult but possible with the help of other histological features.^[18]

Inflammatory Liposarcoma

Its adipocytic nature may be misidentified due to the heavy chronic inflammatory infiltrate.
The inflammatory component is frequently composed of different lympho–plasmacytic aggregates. These tend to be predominantly formed by a specific type of B-cell, or less commonly T-cells may populate the inflammatory aggregate.^[18]^[19]^[20]

Spindle Cell Lipocarcinoma

This is a rare adult-type of well-differentiated liposarcoma.
It results from the proliferation of neural-like spindle cells, which are organized in a fibrous structure, that contains lipoblasts.^[21]^[22]

De-differentiated Liposarcoma

In this form of liposarcoma, there is a transition from a low-grade differentiation to a high-grade differentiation within the same mass of well-differentiated liposarcoma.^[18]^[23]^[24]
90% of dedifferentiation from well-differentiated liposarcomas occur in primary tumors, while the remaining 10% occur in recurrent neoplasms.^[25]^[26]^[27]^[28]

Myxoid Liposarcoma

They have a non-homogenous appearance with cystic and solid components.

Round Cell Liposarcoma

It is a high-grade liposarcoma which is a poorly differentiated form of myxoid sarcoma.
It has a very poor prognosis and often metastasizes to the retroperitoneum, pleural cavity, soft tissue, or pelvis and very rarely to the lungs.
Microscopically, it consists of small, round, or spindle cells with sparse eosinophilic and granular cytoplasm and large nuclei.
It may have scattered lipoblasts and areas of necrosis.

Pleiomorphic Liposarcoma

Pleomorphic cells may be identified with enlarged round to bizarre nuclei.

Images

Well Differentiated Liposarcoma. Image courtesy of Wikimedia Commons	Dedifferentiated Liposarcoma. Image courtesy of Wikimedia Commons	Dedifferentiated Liposarcoma. Image courtesy of Wikimedia Commons
Dedifferentiated Liposarcoma. Image courtesy of Wikimedia Commons	Dedifferentiated Liposarcoma. Image courtesy of Wikimedia Commons

References

↑ Kate Lynn J. Bill, Lucia Casadei, Bethany C. Prudner, Hans Iwenofu, Anne M. Strohecker & Raphael E. Pollock (2016). “Liposarcoma: molecular targets and therapeutic implications”. Cellular and molecular life sciences : CMLS. 73 (19): 3711–3718. doi:10.1007/s00018-016-2266-2. PMID 27173057. Unknown parameter |month= ignored (help)
↑ Kate Lynn J. Bill, Lucia Casadei, Bethany C. Prudner, Hans Iwenofu, Anne M. Strohecker & Raphael E. Pollock (2016). “Liposarcoma: molecular targets and therapeutic implications”. Cellular and molecular life sciences : CMLS. 73 (19): 3711–3718. doi:10.1007/s00018-016-2266-2. PMID 27173057. Unknown parameter |month= ignored (help)
↑ N. Azumi, J. Curtis, R. L. Kempson & M. R. Hendrickson (1987). “Atypical and malignant neoplasms showing lipomatous differentiation. A study of 111 cases”. The American journal of surgical pathology. 11 (3): 161–183. PMID 3826477. Unknown parameter |month= ignored (help)
↑ Emily Z. Keung, Jason L. Hornick, Monica M. Bertagnolli, Elizabeth H. Baldini & Chandrajit P. Raut (2014). “Predictors of outcomes in patients with primary retroperitoneal dedifferentiated liposarcoma undergoing surgery”. Journal of the American College of Surgeons. 218 (2): 206–217. doi:10.1016/j.jamcollsurg.2013.10.009. PMID 24315890. Unknown parameter |month= ignored (help)
↑ N. Azumi, J. Curtis, R. L. Kempson & M. R. Hendrickson (1987). “Atypical and malignant neoplasms showing lipomatous differentiation. A study of 111 cases”. The American journal of surgical pathology. 11 (3): 161–183. PMID 3826477. Unknown parameter |month= ignored (help)
↑ Emily Z. Keung, Jason L. Hornick, Monica M. Bertagnolli, Elizabeth H. Baldini & Chandrajit P. Raut (2014). “Predictors of outcomes in patients with primary retroperitoneal dedifferentiated liposarcoma undergoing surgery”. Journal of the American College of Surgeons. 218 (2): 206–217. doi:10.1016/j.jamcollsurg.2013.10.009. PMID 24315890. Unknown parameter |month= ignored (help)
↑ N. Azumi, J. Curtis, R. L. Kempson & M. R. Hendrickson (1987). “Atypical and malignant neoplasms showing lipomatous differentiation. A study of 111 cases”. The American journal of surgical pathology. 11 (3): 161–183. PMID 3826477. Unknown parameter |month= ignored (help)
↑ Elizabeth Fabre-Guillevin, Jean-Michel Coindre, Nicolas de Saint Aubain Somerhausen, Francoise Bonichon, Eberhard Stoeckle & Nguyen Binh Bui (2006). “Retroperitoneal liposarcomas: follow-up analysis of dedifferentiation after clinicopathologic reexamination of 86 liposarcomas and malignant fibrous histiocytomas”. Cancer. 106 (12): 2725–2733. doi:10.1002/cncr.21933. PMID 16688768. Unknown parameter |month= ignored (help)
↑ Ghadimi, Markus P.; Al-Zaid, Tariq; Madewell, John; Peng, Tingsheng; Colombo, Chiara; Hoffman, Aviad; Creighton, Chad J.; Zhang, Yiqun; Zhang, Anna; Lazar, Alexander J.; Pollock, Raphael E.; Lev, Dina (2011). “Diagnosis, Management, and Outcome of Patients with Dedifferentiated Liposarcoma Systemic Metastasis”. Annals of Surgical Oncology. 18 (13): 3762–3770. doi:10.1245/s10434-011-1794-0. ISSN 1068-9265.
↑ G. Lahat, D. A. Anaya, X. Wang, D. Tuvin, D. Lev & R. E. Pollock (2008). “Resectable well-differentiated versus dedifferentiated liposarcomas: two different diseases possibly requiring different treatment approaches”. Annals of surgical oncology. 15 (6): 1585–1593. doi:10.1245/s10434-007-9805-x. PMID 18398663. Unknown parameter |month= ignored (help)
↑ H. L. Evans, K. K. Khurana, B. L. Kemp & A. G. Ayala (1994). “Heterologous elements in the dedifferentiated component of dedifferentiated liposarcoma”. The American journal of surgical pathology. 18 (11): 1150–1157. PMID 7943536. Unknown parameter |month= ignored (help)
↑ W. H. Henricks, Y. C. Chu, J. R. Goldblum & S. W. Weiss (1997). “Dedifferentiated liposarcoma: a clinicopathological analysis of 155 cases with a proposal for an expanded definition of dedifferentiation”. The American journal of surgical pathology. 21 (3): 271–281. PMID 9060596. Unknown parameter |month= ignored (help)
↑ Singer, Samuel; Antonescu, Cristina R.; Riedel, Elyn; Brennan, Murray F. (2003). “Histologic Subtype and Margin of Resection Predict Pattern of Recurrence and Survival for Retroperitoneal Liposarcoma”. Transactions of the … Meeting of the American Surgical Association. 121: 52–65. doi:10.1097/01.sla.0000086542.11899.38. ISSN 0066-0833.
↑ G. Lahat, D. A. Anaya, X. Wang, D. Tuvin, D. Lev & R. E. Pollock (2008). “Resectable well-differentiated versus dedifferentiated liposarcomas: two different diseases possibly requiring different treatment approaches”. Annals of surgical oncology. 15 (6): 1585–1593. doi:10.1245/s10434-007-9805-x. PMID 18398663. Unknown parameter |month= ignored (help)
↑ Emily Z. Keung, Jason L. Hornick, Monica M. Bertagnolli, Elizabeth H. Baldini & Chandrajit P. Raut (2014). “Predictors of outcomes in patients with primary retroperitoneal dedifferentiated liposarcoma undergoing surgery”. Journal of the American College of Surgeons. 218 (2): 206–217. doi:10.1016/j.jamcollsurg.2013.10.009. PMID 24315890. Unknown parameter |month= ignored (help)
↑ Khin Thway, Robin L. Jones, Jonathan Noujaim, Shane Zaidi, Aisha B. Miah & Cyril Fisher (2016). “Dedifferentiated Liposarcoma: Updates on Morphology, Genetics, and Therapeutic Strategies”. Advances in anatomic pathology. 23 (1): 30–40. doi:10.1097/PAP.0000000000000101. PMID 26645460. Unknown parameter |month= ignored (help)
↑ ^17.0 ^17.1 Dei Tos AP, Doglioni C, Piccinin S, Sciot R, Furlanetto A, Boiocchi M; et al. (2000). “Coordinated expression and amplification of the MDM2, CDK4, and HMGI-C genes in atypical lipomatous tumours”. J Pathol. 190 (5): 531–6. doi:10.1002/(SICI)1096-9896(200004)190:5<531::AID-PATH579>3.0.CO;2-W. PMID 10727978.
↑ ^18.0 ^18.1 ^18.2 ^18.3 ^18.4 Dei Tos AP (2000). “Liposarcoma: new entities and evolving concepts”. Ann Diagn Pathol. 4 (4): 252–66. doi:10.1053/adpa.2000.8133. PMID 10982304.
↑ Kraus MD, Guillou L, Fletcher CD (1997). “Well-differentiated inflammatory liposarcoma: an uncommon and easily overlooked variant of a common sarcoma”. Am J Surg Pathol. 21 (5): 518–27. PMID 9158675.
↑ Argani P, Facchetti F, Inghirami G, Rosai J (1997). “Lymphocyte-rich well-differentiated liposarcoma: report of nine cases”. Am J Surg Pathol. 21 (8): 884–95. PMID 9255251.
↑ Dei Tos AP, Mentzel T, Newman PL, Fletcher CD (1994). “Spindle cell liposarcoma, a hitherto unrecognized variant of liposarcoma. Analysis of six cases”. Am J Surg Pathol. 18 (9): 913–21. PMID 8067512.
↑ Hendrickson WA, Ward KB (1975). “Atomic models for the polypeptide backbones of myohemerythrin and hemerythrin”. Biochem Biophys Res Commun. 66 (4): 1349–56. PMID 5.
↑ Evans HL (1979). “Liposarcoma: a study of 55 cases with a reassessment of its classification”. Am J Surg Pathol. 3 (6): 507–23. PMID 534388.
↑ Dahlin DC, Unni KK, Matsuno T (1977). “Malignant (fibrous) histiocytoma of bone–fact or fancy?”. Cancer. 39 (4): 1508–16. PMID 192432.
↑ Ghadimi, Markus P.; Al-Zaid, Tariq; Madewell, John; Peng, Tingsheng; Colombo, Chiara; Hoffman, Aviad; Creighton, Chad J.; Zhang, Yiqun; Zhang, Anna; Lazar, Alexander J.; Pollock, Raphael E.; Lev, Dina (2011). “Diagnosis, Management, and Outcome of Patients with Dedifferentiated Liposarcoma Systemic Metastasis”. Annals of Surgical Oncology. 18 (13): 3762–3770. doi:10.1245/s10434-011-1794-0. ISSN 1068-9265.
↑ G. Lahat, D. A. Anaya, X. Wang, D. Tuvin, D. Lev & R. E. Pollock (2008). “Resectable well-differentiated versus dedifferentiated liposarcomas: two different diseases possibly requiring different treatment approaches”. Annals of surgical oncology. 15 (6): 1585–1593. doi:10.1245/s10434-007-9805-x. PMID 18398663. Unknown parameter |month= ignored (help)
↑ H. L. Evans, K. K. Khurana, B. L. Kemp & A. G. Ayala (1994). “Heterologous elements in the dedifferentiated component of dedifferentiated liposarcoma”. The American journal of surgical pathology. 18 (11): 1150–1157. PMID 7943536. Unknown parameter |month= ignored (help)
↑ W. H. Henricks, Y. C. Chu, J. R. Goldblum & S. W. Weiss (1997). “Dedifferentiated liposarcoma: a clinicopathological analysis of 155 cases with a proposal for an expanded definition of dedifferentiation”. The American journal of surgical pathology. 21 (3): 271–281. PMID 9060596. Unknown parameter |month= ignored (help)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]Sabawoon Mirwais, M.B.B.S, M.D.[3]

Causes

Overview

There are no established causes for liposarcoma.

Causes

There are no established causes for liposarcoma.

References

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Differentiating Liposarcoma from other Diseases

Overview

Liposarcoma must be differentiated from other diseases that cause a painless, growing mass such as spindle cell lipoma, neurofibroma, dermatofibrosarcoma protuberans, and malignant peripheral nerve sheath tumor.

Differential diagnosis

Differential diagnosis of liposarcoma includes nonadipocytic lesions such as:^[1]


Disease	Description

Spindle cell lipoma	Composed of bland, sometimes palisading, CD34-positive spindle cells, ad- mixed with eosinophilic refractile collagen bundles
Neurofibroma	Characterized by a less cellular S-100– positive spindle cell proliferation with wavy nuclei
Dermatofibrosarcoma protuberans	Cytologically bland, monomorphic CD34-positive spindle cell proliferation organized in a distinctive storiform growth pattern and characterized by tendency to infiltrate the surrounding fat in a peculiar ‘‘honeycomb’’ pattern
Malignant peripheral nerve sheath tumor	Generally highly cellular tumors composed of tapering or wavy spindle cells featuring perivascular accentuation and focal S-100– positive immunoreactivity in approximately 50% of cases^[1]

Disease	Clinical feature			Laboratory findings	Imaging findings
Disease	Fever	Weight loss	Abdominal pain	Laboratory findings	Imaging findings
Retroperitoneal hematoma	_	_	✔	Anemia	MRI is the best radiologic tool to differentiate between retroperitoneal masses.
Retroperitoneal abscess	✔	_	✔	Leukocytosis, positive inflammatory markers
Retroperitoneal tumors (.e.g. liposarcoma)	✔	✔	✔	positive tumor marker
Chronic pancreatitis	_	✔	✔	DM type II, amylase and lipase levels may be slightly elevated

Differentiating Liposarcoma from Other Diseases
Disease entity	Etiology (Genetic or others)	Histopathological findings	Immunohistochemical staining	Risk factors	Common site of involvement	Clinical manifestations	Other associated features
Liposarcoma^[2]^[3]^[4]^[5]^[6]^[7]^[8]^[9]^[10]^[11]	Atypical lipomatous tumor/well differentiated liposarcoma and dedifferentiated liposarcoma are associated with: Presence of a large/giant marker chromosome and/or ring chromosomes at 12q13-15 region Amplification of this chromosome region rich in protooncogenes, including CHOP, CDK4, MDM2, HMGI-C, GLI, SAS, OS1, HMGA2 andOS9 Myxoid liposarcoma is associated with: t(12:16)(q13;p11) – CHOP(DDIT3) / FUSor t(12;22)(q13;q22) – CHOP(DDIT3) / EWS Pleomorphic liposarcoma is associated with: Complex karyotypicaberrations	Well-differentiated liposarcoma: Sclerosing liposarcoma (distinctive stromal cells distributed across the tissue, associated with lipoblasts filled with multiple vacuoles, and collageno us background of fibrillary appearance) Adipocytic liposarcoma (adipocytes with different cell sizes, hyperchromasia, and nuclear atypia. Fibrous sept acontaining hyperchromatic stromal cel ls surrounding adipocytes) Inflammatory liposarcoma (heavy chronic inflammatoryinfiltrate composed of different lympho-plasmacytic aggregates) Spindle cell liposarcoma(proliferation of neural-like spindle cells organized in a fibrous structurecontaining lipoblasts) De-differentiated liposarcoma: Myxoid liposarcoma ( non-homogenous appearance with cystic and soli d components) Round cell liposarcoma (small, round, or spindle cells with sparse eosinophilic and granular cytoplasmand large nuclei,scattered lipoblasts and areas of necrosis) Pleomorphic liposarcoma (pleomorphic cells with enlarged round to bizarre nuclei)	Atypical lipomatous tumor/well differentiated liposarcoma is positive for: MDM2 CDK4 p16 S100 (stains adipocytes and lipoblasts)	Chemical carcinogens Phenoxyacetic herbicides Chlorophenols Dioxin contaminations Arsenic Thorium dioxide (Thorotrast) Radiation (dose of 50 GY) Immunodeficiency(regional acquired immunodeficiency) Genetic susceptibility Li-Fraumeni syndrome Neurofibromatosis(NF1; von Recklinghausen disease) Gardner syndrome (Familial adenomatous polyposis) Retinoblastoma Werner syndrome Nevoid basal cell carcinoma (Gorlin syndrome) Viral infections	Retroperitoneum Esophagus Bowel Mediastinum	Retroperitoneal liposarcoma maybe asymptomatic or causes: Weight loss Abdominal pain Oliguria renal failure (due to ureters or kidneys‘ compression) Palpable abdominal mass Abdominal tenderness Abdominal distention Esophageal liposarcoma may cause: Dysphagia Vomiting Cough Gastrointestinal bleeding Hoarseness Bowel liposarcoma may cause: Gastrointestinal bleeding Mediastinal liposarcoma may cause: Dyspnea Cough Chest pain Weight loss	_
Neurofibroma^[12]^[13]^[14]^[15]^[16]^[17]^[18]^[15]^[19]^[20]^[21]^[22]	Can be sporadic or as a part of Neurofibromatosis 1 and 2 NF1 gene located at chromosomal region 17q11.2, codes forneurofibromin Functional part of neurofibromin GAP (or GTPase-activating protein) accelerates the conversion of the active GTP-bound RAS to its inactive GDP-bound form Loss of RAS controlleads to increased activity of other signaling pathwaysincluding RAF, ERK1/2, PI3K, PAK, MAPK, SCF/c-kit and mTOR-S6 kinase	Uniphasic, low to moderate cellularity No peripheral perineural capsule Random pattern, only rare palisading No well formed verocy bodies Hypocellular with abundant mucinous/myxoid matrix without hypercellular areas Frequent mast cells Contains neural fibroblasts and fibrillary or shredded carrot collagen Random proliferation of Schwann cells and scattered admixed axons No nevoid cells No epithelial component Diffuse growth pattern Scant cytoplasm Wavy spindle cells with buckled nuclei Pseudomeissnerian bodies representing specific differentiation may be present Lacks storiform pattern Neurofibroma with degenerative atypia (“ancient change“) has following microscopic features: Localized cells with large pleomorphic nuclei, cytoplasmic nuclear inclusions, smudgy chromatin, and inconspicuous nuclei Absent or very low mitotic activity Low to moderate cellularity	Positive for: S100 (weaker) SOX10 Neurofilament (and Bielshowsky) GFAP CD34 (stronger) Factor XIIIa Calretinin (focal) MBP (myelin–basic protein) Negative for: EMA (except in plexiform neurofibromas)	Neurofibromatosis 1 Neurofibromatosis 2(multiple neurofibromas, meningiomas of the brainor spinal cord, and ependymomas of the spinal cord)	Can occur anywhere Diffuse neurofibromas commonly involve scalp	Soft masses/bumps on or under skin (internal or superficial) Transient itching (mast cells release histamine) Transient pain Numbness and tingling in the affected area Severe bleeding (sign of tumor growth) Physical disfiguration Cognitive disability Stinging Neurological deficits Changes in movement (clumsiness in hands, trouble walking) Bowel incontinence Scoliosis (an abnormal curvature of the spine, if the tumor creates muscular imbalance or erodes bones of the spine) Following symptoms may occur with genitourinary tract involvement (rarely): Urinary tract infection (most common clinical manifestation) Urinary retention Urinary frequency Urgency Hematuria Pelvic mass Hydronephrosis Urinary incontinence (decreased bladder capacity or compliance) Appears as a focal mass or diffuse bladder wall thickening in case of a plexiform neurofibroma	Nerve often not identified, incorporates nerve, axons often present in lesion Seldom cystic Frequently multiple Widespread soft tissue infiltration Tends to displace adnexa <2cm in diameter Lacks distinct lobulation Lacks fat Affects individuals between 20-40 years of age Men and women are equally affected Plexiform neurofibroma are thought to be congenital and occur earlier in life
Schwannoma^[23]^[24]^[25]^[26]^[27]	Loss of function of the tumor suppressor gene merlin (schwannomin) Direct genetic change involving the NF2 gene on chromosome 22 Can occur spontaneously Mutations and biallelic inactivation of SMARCB1 (spinal schwannomas)	Encapsulated Aggregates of spindled cells with indistinct cytoplasm and elongated nuclei with blunt pointed ends Ancient changes may show nuclear pleomorphism and occasionally nuclear inclusions as well Infrequent extracellular collagen Biphasic: majority entirely, and compactly hypercellular Antoni A & myxoid hypocellular Antoni B areas (may be absent in small tumors) Nuclear palisading evident around fibrillary process (Verocay bodies) in cellular areas Large, irregularly spaced vessels prominent in Antoni B areas Narrow, elongated and wavy cells with tapered ends, interspersed with collagen fibers Tumor cells with ill defined cytoplasm, dense chromatin Often displays degenerative nuclear atypia (ancient change) Rare mitotic figures Blood vessels may show gaping tortuous lumina having thickened hyalinized walls; may have thrombi Dilated vessels surrounded/invested by hemorrhage Foamy macrophages Lymphoid aggregates Amianthoid fibers or collagenous spherules: large nodular masses of collagen with radiating edges No axons except where nerve is attached Malignant transformation may have malignant epithelioid cells and rarely shows divergent differentiation as angiosarcoma-like areas	Positive for: S-100 SOX10 CD56 Podoplanin CD34 (weak) Neurofilament (and Bielshowsky) Factor XIIIa (focal) Calretinin GFAP EMA (capsule) highlights the perineural fibroblasts Laminin Type IV collagen Vimentin CD68 Negative for: Cytokeratin Desmin SMA	NF-2 associated Schwannomatosis Carney complex	Upper limbs Head and neck area (oral cavity, orbit and salivary glands) Deeply seated tumors are mainly in: Posterior mediastinum Retroperitoneum Posterior spinal roots Bone Gastrointestinal tract Pancreas Liver Thyroid Adrenal glands Lymph nodes Penis (rarely) Vulva (rarely)	Symptoms of schwannoma depend on the location of the tumor: Intracranial schwannoma: Acoustic neuroma (most common): Sensorineural hearing loss Vertigo Tinnitus Facial weakness Facial numbness and tingling Headaches Dizziness Difficulty swallowing and hoarseness Taste changes Confusion Trigeminal schwannoma: Trigeminal nerve dysfunction Facial nerve schwannoma: Facial nerve dysfunction Jugular foramen schwannoma: Hearing loss Tinnitus Dysphagia Ataxia Hoarseness Hypoglossal schwannomas: Hypoglossal nerve dysfunction Spinal schwannoma: Back pain Urinary incontinence Urinary retention Clumsiness Weakness Paresthesias Intercostal nerve schwannoma: Usually asymptomatic Intramuscular schwannoma: Painless mass	Nerve often identifiable Eccentric to nerve, axons generally absent within lesion Occasionally cystic Can cause other neoplasms including: Meningioma Mesothelioma Glioma multiforme Breast cancer Colorectal cancer Kidney (clear cell type) carcinoma Hepatocellular carcinoma Prostatic cancer Dermal cancer Affects individuals between 20-50 years of age Men and women are equally affected
Palisaded encapsulated neuroma (PEN) /solitary circumscribed neuroma^[28]	Spontaneous development RET proto-oncogene genetic mutations (inherited PEN)	Solitary dermal or subcutaneous tumor Encapsulated by perineurium Club-like extension in the subcutaneous tissue Moderately cellular lesion with proliferation of schwann cells and axons Nuclear palisading may be present Rare mast cells Silver stains show the axons traversing the Schwann cells	Positive for: EMA S100 (schwann cells) Neurofilament (axons) Collagen type IV EMA (perineurium) Neuron-specific Enolase CD57 (Leu-7) Myelin basic proteins Negative for: GFAP	Positive family history of tumor occurrence Multiple mucosal neuroma syndrome Multiple endocrine neoplasia syndrome (MEN 2B)	90% lesions affect the face involving: Eyelid Nose Oral mucosa Remaining 10% can occur anywhere in body involving: Shoulder Arm Hand Foot Glans of penis	Small, solitary, raised, dome-shaped, firm, flesh-colored painless nodule on skin Cosmetic issues due to facial involvement Scar after surgery	Benign tumor of the nerve fibers Affects middle aged people (40-60 years) No known familial association Affects females more frequently than males
Traumatic neuroma^[29]^[30]^[31]^[32]	Tangle of neural fibers and connective tissue that develops following a peripheral nerve injury Interruption in continuity of nerve causing wallerian degeneration (loss of axons in proximal stump and retraction of axons in distal segment), followed by exuberant regeneration of nerve and formation of mass of Schwann cells, axons and fibrous cells	Numerous well formed small nerve twigs Limited soft tissue infiltration Contains axons in haphazardly arranged nerves within mature collagenous scar with entrapped smooth muscle	Positive for: S100	History of trauma to a nerve (especially during a surgery) Cone biopsy (rare complication) 55% of hysterectomy patients have microneuromas, associated with childbirth	Most common oral locations are: Tongue Near mental foramen of mouth Rarely involves: Head Neck	Firm, oval, whitish, slowly growing, palpable nodule on skin (no discoloration of skin on the top of nodule) </=2cm in size Traumatic neuropathic pain with the presence of a typical trigger point in the area of a neuroma (especially with the pressure application) causing the patient to feel burning, stabbing, raw, gnawing or sickening sensations Paresthesia over the injured area Dysesthesia (painful hypersensitivity to normal light tactile stimuli) Functional impairment Psychological distress (severely decreasing the quality of life)	Also known as: Amputation neuroma Pseudoneuroma
Neurotized melanocytic nevus^[33]^[34]^[35]^[36]	Melan-A (Mart-1) gene Defect in embryologic development causing fast proliferation rate of melanocytes (during first twelve weeks of pregnancy)	Neurotized Nevus is a type of mole in which melanocytes are in the dermis with accompanying fibrosis Biphasic consisting of malignant melanoma and mature appearing neural component Superficial classic nevoid melanocytes (i.e. melanocytes appear like spindle cells resembling a nerve; and hence, called a neurotized nevus) Congenital and nested growth patterns More abundant cytoplasm Tends to surround adnexa Scattered nests of type A or B nevus cells, surrounded by basement membrane, present in the papillary dermis of lesions (otherwise indistinguishable from neurofibromas)	Positive for: S-100 MelanA (MART-1) Negative for: Factor XIIIa Leu-7 GFAP MBP	Sun exposure (ultraviolet light) Hormonal changes during: Pregnancy Diabetes Fair-skinned individuals (Caucasians of America and Europe) Positive family history of mole	Can occur anywhere in body, mostly involving following areas: Head Neck	Slowly growing, benign, oval or round, well-circumscribed macule, papule or nodule Color varies from skin color to light brown to black Cosmetic concerns	_
Cutaneous myxoma (Superficial angiomyxoma)^[37]^[38]^[39]^[40]	Sporadic Associated with: Carney’s syndrome (autosomal dominant condition associated with abnormalities in chromosomes 2p and 17q, especially mutation in the PRKAR1α gene on the chromosome 17q22–q24 locus) NAME syndrome LAMB syndrome	Predominantly involves dermis and subcutis Multilobulated, poorly circumscribed Alcian blue positive, and hyaluronidase sensitive myxoid stroma/acellular mucin pools forming cleft-like spaces Scattered bland stellate to spindled cells with multiple oval nuclei Rarely, pleomorphism, and mitotic figures seen Occasional intranuclear pseudoinclusions Many thin-walled small blood vessels Frequent neutrophils Entrapped epithelial component in 20-30% of cases: Keratinous cyst Thin strands of squamous epithelium Basaloid buds	Positive for: CD34 Smooth muscle actin (90%) Muscle specific actin (67%) Factor XIIIa (60%) Vimentin S-100 (rarely, 40%) Factor VIIIa (variable) Negative for: Cytokeratin Desmin GFAP ER PR	Associated with Carney’s complex/syndrome which includes following: Myxomas: Cutaneous External ear Heart Breast myxoid fibroadenoma Cutaneous melanocytic lesions: Lentigines Blue nevus Endocrine hyperplasia and neoplasia: Pituitary Thyroid Adrenal cortex Testis large cell calcifying Sertoli cell tumor Psammomatous melanotic schwannoma May be associated with NAME or LAMB syndrome	Trunk Limbs Head/face (eyelids and external ear canal in Carney’s syndrome) Neck Perineal Nipples Buttocks	Solitary or multiple flesh-colored nodules 1-5cm in diameter	Sometimes, may be the earliest manifestation of Carney complex Affects men more frequently than women Involves mostly middle-aged population
Nerve sheath myxoma^[41]^[42]^[43]^[44]^[45]^[46]	Unknown etiology	Tumors involve the dermis and/or subcutis Distinct multinodular/multilobular masses Markedly hypocellular with abundant myxoid stroma Peripheral fibrous border made up of collagen IV Schwann cells may show the following different features: Cytoplasmic–nuclear invaginations Small epithelioid Schwann cells in corded, nested, and/or syncytial-like aggregates Schwann cells with a ring-like appearance Scattered spindled and stellate-shaped Schwann cells	Positive for: S-100 Glial fibrillary acidic protein Neuron specific enolase CD57 Epithelial membrane antigen CD34	_	Can occur anywhere in body: Most commonly involves extremities especially: Fingers Knees Rarely involves: Scalp/head Trunk	Painless skin mass or nodule Occasionally painful to touch Skin over the nodule is pink, soft, and usually intact (no ulceration) 0.5-2 cm in size Cosmetic issue (when present in head and neck region)	First described by Harkin and Reed in 1969 Peak incidence in the fourth decade of life Strong predilection for the extremities Also known as: Classical Nerve Sheath Myxoma Cutaneous Lobular Neuro Myxoma Myxomatous Perineuroma
Malignant peripheral nerve sheath tumor (MPNST)/malignant schwannoma^[47]^[48]^[49]^[50]^[51]^[52]	50% arise denovo 50% associated with neurofibromatosis (loss of heterozygosity of p53 on 17p chromosome)	Generalized atypia Increased mitotic activity Diffuse hypercellularity Infiltrative growth Pleomorphic nuclei Areas of geographic necrosis may show divergent differentiation, with tumor palisading at edges, resembling glioblastoma multiforme Monomorphic serpentine cells, large gaping vascular spaces, perivascular plump tumor cells May have bizarre cells 15% have metaplastic cartilage, bone, and muscle May have glandular differentiation, if so, presume malignant May have melanin in tumor cells, particularly if arise from spinal nerve roots (overlaps with primary melanoma of nerves) Some have no discernable Schwannian features at any level Electron microscopy shows: Cell membrane infoldings with lamellar configuration, discontinuous basal lamina, conspicuous intercellular junctions, and occasional dense–core granules	Positive for: CD99/O13 (86%) S-100 (patchy in 62% cases) CD57 (55%) Collagen IV p53 Leu7/CD57 (in neurofibroma-like areas) Protein gene product 9.5 (more sensitive than S100 but not specific) In case of glandular differentiation (malignant), positive for: Keratin EMA CEA Chromogranin Negative for: CD19	Associated with: NF1 May be associated with: Radiations Ganglioneuroma (rarely)	Bulky deep-seated tumor usually arising from major nerves in: Neck Forearm Lower leg Buttock	Painless swelling in extremities (arms or legs, aka peripheral edema) Difficulty moving the extremity with tumor (limping) Localized soreness in tumor area Neurological symptoms Pain or discomfort: numbness, burning, or tingling (pins and needles) Dizziness Loss of balance	Most common frequent soft tissue sarcoma in the pediatrics population
Dermatofibrosarcoma protuberans (DFSP)	t(17,22)(q21;q13) (collagen type 1 alpha 1(COL1A1) gene and platelet derived growth factor (PDGF) beta chain gene), resulting fusion protein is processed into mature platelet-derived growth factor which is a potent growth factor Supernumerary ring chromosomes derived from t(17;22)	Usually forms a mass Non circumscribed, highly cellular, tight storiform pattern (cells radiating in spokes at right angles around a central point that often contains a vessel) deeply infiltrating into subcutaneous tissue and entraping fat cells leading to characteristic honeycomb pattern Areas of fascicular growth (some tumors) Distinct storiform pattern may be absent in early plaque stage Monomorphic, thin and spindly cells with scant eosinophilic cytoplasm and hyperchromatic nuclei (resembling neurofibroma) Numerous mitotic figures (not atypical ones) Non-polarizable and thin collagen Only mild pleomorphism and focal atypia May coexist with giant cell fibroblastoma Usually no significant pleomorphism, no / rare histiocytes, no histiocyte-like cells, no foam cells, no giant cells or other inflammatory cells Variants: Atrophic (depressed lesion), collagenous (with central thick collagen bundles), granular cell, myxoid, palisading, pigmented, and sclerosing	Positive for: CD34 (strong in 95%) Vimentin Actin (focal) ApoD Bcl2 NKI-C3 CD99 Negative for: S-100 Factor XIIIa (usually) Keratin EMA S100 HMB45 Desmin CD117	_	Head Deep soft tissue of (posterior) neck Trunk Arms Legs Doesn’t involve hands and feet	Begins as a minor firm area of skin 1 to 5 cm in diameter Resembles a bruise, birthmark, or pimple Can become a raised nodule after growth May cause redness, open up or bleed	Also called intermediate (borderline) fibrous histiocytoma More common in blacks in US Involves adults of 20 – 40 years of age
Spindle cell lipoma	16q abnormalities (usually)	Delicate encapsulation Floret cell formation No degenerative atypia Mixture of mature adipocytes and mildly pleomorphic bland spindle cells (pale eosinophilic cytoplasm with uniform wavy nuclei similar to neurofibroma) in mucinous / myxoid or fibrous background with thick collagen bundles Spindle cells arranged in short fascicles with occasional nuclear palisading Hemangiopericytic or angiomatous vascular pattern may be seen Minimal or no fat Variable mast cells and lymphocytes No storiform pattern, no lipoblasts, no/rare mitotic activity	Positive for: CD34 (strongly, spindle cells) Androgen receptors in men and usually women (spindle cells) S-100(stains only adipocytes) Spindle cells are negative for: S100 Desmin	_	Neck Posterior upper back Shoulder	Multiple well-circumscribed painless nodules involving several body parts	_
Ganglioneuroma^[53]^[54]	Genes involved in the pathogenesis of ganglioneuroma include: MYCN oncogene Chromosome 1p36 Activating RET protooncogene mutation (adrenal ganglioneuromas)	Derived from the primordial neural crest cells (undifferentiated cells of the sympathetic nervous system) Admixture of ganglion cells, schwann cells, and fibrous tissue Doesn’t contain neuroblasts, intermediate cells, or mitotic figures Characterized by spindle-shaped cells with cell borders in a fibrillar matrix containing ganglion cells with large round nuclei, prominent nucleoli, and abundant eosinophilic cytoplasm No significant atypia, necrosis or mitotic activity is present Well differentiated neuronal tumors that do not contain immature elements Ganglion cells are mature to mildly dysmorphic: Mature: compact, eosinophilic cytoplasm with distinct cell borders, single eccentric nucleus, prominent nucleolus Dysmorphic: single or multiple pyknotic nuclei Vary in distribution and number, may be quite sparse May contain finely granular, gold to brown pigment (lipofuscin or neuromelanin) Schwann cells: Ensheath neuritic processes Arranged in small intersecting fascicles, separated by loose myxoid stroma Two histologic subtypes: Mature = every ganglion cell is mature Maturing = minor component of scattered collections of differentiating neuroblasts or maturing ganglion cells (unlike intermixed subtype of ganglioneuroblastoma, these immature foci do not form distinct microscopic nests) Background may include lobules of mature adipose tissue (especially at periphery of lesion), mast cells, chronic inflammation, dense collagenized stroma Mild variation in cellularity may be present Masculinizing ganglioneuroma is an admixture of ganglioneuroma and Leydig cells with crystalloids of Reinke or strands/clusters of cells resembling adrenal cortical cells Electron microscopy: Mixture of neural bundles and normal appearing ganglion cells with eccentric nuclei and large numbers of cytoplasmic organelles	Positive for: Schwann cells/stroma: S100 Synaptophysin Neurofilament (NF) protein Ganglion cells: S100 Synaptophysin Chromogranin A NF protein Glial fibrillary acidic protein (GFAP) PGP 9.5 Type IV collagen Vasoactive intestinal peptide (VIP) Negative for: EMA Cytokeratin HMB45 WT1 CD99 CD45 Desmin Myogenic markers (myogenin, MyoD1)	Ganglioneuromas may be associated with: Multiple endocrine neoplasia type IIb (mucosal ganglioneuromas) Turner syndrome Neurofibromatosis type 1	Located along distribution of sympathetic nervous system: Posterior paraspinal mediastinum (most common) Adrenal gland (~20-30% of cases) Paraspinal retroperitoneum (especially presacral space) Cervical and parapharyngeal area in neck Urinary bladder Prostate Bone Pancreas Skin Orbit Paratesticular area Appendix Gastrointestinal tract	Symptoms of ganglioneuroma vary depending on the location of tumor, and include the following: Mediastinum: Dyspnea Chest pain Trachea compression Retroperitoneum: Abdominal pain Bloating Spinal cord: Paresis Pain and numbness/loss of sensation in limbs Patients with ganglioneuroma may also have paraneoplastic syndrome, which may manifest with: Diarrhea Diaphoresis Hirsutism Enlarged clitoris (in females) High blood pressure Sweating	Ganglioneuromas are included in the neuroblastic tumors group, which includes: Ganglioneuroma (benign) Ganglioneuroblastoma (intermediate) Neuroblastoma (aggressive)
Leiomyoma^[55]^[56]^[57]^[58]^[59]^[60]^[61]^[62]^[56]^[59]^[63]	Loss of normal chromosome 1q (hereditary leiomyomatosis) Renal cell cancer(HLRCC) gene mutation	Prominent cellular atypia Nuclear atypia, including nuclear pleomorphism, hyperchromatism, irregularity in nucle ar membranes, high nuclear size, and prominent nucleoli Cigar-shaped nuclei Abundant mitoses, mitotic index higher than 10 or more per 10 high-power fields Areas of coagulative necrosis (tumor cell necrosis) Palisading and extensive degenerative changes in the form of hyalinization, calcification, and myxoid changes Elongated cells with eosinophilic or occasional fibrillar cytoplasm with distinct cell membranes	Positive for: HHF35 (90%) Alpha-smooth muscle actin (90%) Vimentin Desmin (75%) H-caldesmon PTAH (stains myofibrils) Keratin (30%) ER (usually in uterine and female retroperitoneal tumors) S100 (occasionally weak staining) EMA (may be focal) CD34 Negative for: CD117	Immundeficiency (HIV) Digoxin exposure Human herpes virus type-8 (HHV-8) Epstein barr virus Long term tamoxifen use History of pelvic radiations Hereditary breast carcinoma with BRCA1 mutation Hereditary nonpolyposis colorectal carcinoma with MSH2 mutation Li-Fraumeni syndrome Malignant melanoma Retinoblastoma	Uterus Abdomen Esophagus Rectum Skin / subcutis Retroperitoneum Extremities Large vessels (inferior vena cava, saphenous vein, femoral vein, pulmonary artery, femoral artery) Superficial or deep soft tissues Bone Breast Colon Epididymis Mediastinum Lungs	Asymptomatic (uterine leiomyosarcomamay be associated with: Irregular vaginal bleeding(intermenstrual or postmenopausal) New lump or a massprotruding into vaginaor growing mass in abdomen or pelvis Abdominal pain Abdominal distension Pelvic pain Urinary symptoms Esophageal leiomyosarcoma may cause: Dysphagia Hematemesis rectal leiomyosarcomamay cause: Black, tarry stools Rectal bleeding	_
Inflammatory myofibroblastic tumor(IMT)^[55]^[56]^[57]^[58]^[59]^[60]^[61]^[62]^[56]^[59]^[63]	Unknown underlying etiology, may be due to inflammatory reaction to: Infection Underlying low grade malignancy Mutations such as: ALK (anaplastic lymphoma kinase)gene mutations in the tyrosine kinase locus at band 2p23	Spindle to stellate-shaped cells Spindle cellsarranged in short fascicles with a focal storiform (whorled or cartwheel-like) architecture Spindle cells show features of fibroblastsand myofibroblasts Variably dense, chronic, mixed polymorphic infiltrateof mononuclear inflammatory cells (plasma cells and lymphocytes, histiocytes, neutrophils, and occasional eosinophils) Histiocytes have multinucleated forms with finely vacuolated cytoplasmic lipiddroplets Plasma cells with cytoplasmic Russell bodies (globular cytoplasmic inclusions of immunoglobulin) and polyclonal pattern of light chain expression Absent hyperchromasia and atypical mitoses	Positive for: IG+ (plasma cells) IL-1 IL-6 Smooth muscle actin Desmin Calponin Activin-like kinase 1 Negative for: Beta-catenin	Multiorgan disease in association with chronicpersistent Eikenella corrodens infection Epstein Barr virus infection Human herpes virus-8(HHV-8) infection(Kaposi’s sarcoma, multicentric Castleman’s disease)	Lungs Gastrointestinal system Pelvic region Bladder Uterus Retroperitoneum Skin Bone (femur, temporal bone, jaw bone) CNS Soft tissues Larynx Heart (right ventricleis most commonly involved) Pancreas (rarely)	Asymptomatic (70%) Painless asymptomatic mass/lump/swelling Pulmonary IMT presents as: Chest pain Cough Dyspnea Hemoptysis (recurrent) Fever Fatigue Weight loss Appetite loss Bone IMT presents with: Mild bone pain Easy fractures Headache Dizziness Numbness at tumorsite Bone marrowinvolvement in some cases Heart IMT presents with: Chest pain Difficulty breathing Palpitations Fainting Obstruction of blood flow in the heart (large tumors) Bladder IMT presents with: Painless hematuria Chronic pelvic pain Difficulty in urinating Presence of burning sensation CNS IMT presents with: Presence of solitary or multiple tumors at various locations in the brain Recurrent headaches Headache Nausea and vomiting Blurred vision Double vision Drooping of the eyelid Dizziness Back pain (if spineinvolved) Seizures	Also known as: Pseudo-inflammatory tumors Inflammatory pseudotumor Plasma cell granuloma Inflammatory pseudotumor Fibrous histiocytoma Fibroxanthoma Xanthogranuloma Inflammatorypseudosarcoma Atypical fibromyxoid tumor Atypical myfibroblastic tumor
Fibroepithelial polyp/Acrochordon^[64]^[65]^[66]^[67]^[68]^[69]^[70]^[71]^[72]^[73]^[74]^[75]^[76]^[77]^[78]^[79]^[80]^[81]^[82]^[83]	Associated with: HPV 6 (low risk) HPV 11	Fibrovascular cores covered by squamous epithelium Larger lesions may have a flattened epidermis Smaller lesions can have epidermal hyperplasia or seborrheic keratosis-like changes Central core composed of loose collagen with increased blood vessels In larger lesion, may have a central core of adipose tissue Pagetoid dyskeratosis is sometimes present as an incidental finding May have ischemic necrosis due to torsion	Positive for: Desmin Vimentin ER PR Negative for: Actin	Associated with: Diabetes (elevated blood sugar and insulin) Abnormal lipid profile Other components of metabolic syndrome Birt-Hogg-Dube syndrome Acromegaly Polycystic ovary syndrome May increase in number during pregnancy	Occurs usually in intertriginous areas (i.e. axilla, groin) Face Neck Eyelids Vulva Tonsils Ureter Bowel Urinary bladder Bronchi	Soft papilloma, flesh colored to dark brown, sessile to pedunculated A few millimeters to multiple centimeters in size Larger lesions often attach to skin by slender stalks	Benign skin lesions in adults, excised for cosmetic reasons Also known as: Skin tag Soft fibroma Cutaneous papilloma Cutaneous tag Fibroma pendulum Fibroma molluscum

References

↑ ^1.0 ^1.1 Dei Tos AP (2000). “Liposarcoma: new entities and evolving concepts”. Ann Diagn Pathol. 4 (4): 252–66. doi:10.1053/adpa.2000.8133. PMID 10982304.
↑ Khin Thway, Rashpal Flora, Chirag Shah, David Olmos & Cyril Fisher (2012). “Diagnostic utility of p16, CDK4, and MDM2 as an immunohistochemical panel in distinguishing well-differentiated and dedifferentiated liposarcomas from other adipocytic tumors”. The American journal of surgical pathology. 36 (3): 462–469. doi:10.1097/PAS.0b013e3182417330. PMID 22301498. Unknown parameter |month= ignored (help)
↑ J. Rosai, M. Akerman, P. Dal Cin, I. DeWever, C. D. Fletcher, N. Mandahl, F. Mertens, F. Mitelman, A. Rydholm, R. Sciot, G. Tallini, H. Van den Berghe, W. Van de Ven, R. Vanni & H. Willen (1996). “Combined morphologic and karyotypic study of 59 atypical lipomatous tumors. Evaluation of their relationship and differential diagnosis with other adipose tissue tumors (a report of the CHAMP Study Group)”. The American journal of surgical pathology. 20 (10): 1182–1189. PMID 8827023. Unknown parameter |month= ignored (help)
↑ Dal Cin, Paola; Kools, Patrick; Sciot, Raf; De Wever, Ivo; Van Damme, Boudewijn; Van de Ven, Wim; Van Den Berghe, Herman (1993). “Cytogenetic and fluorescence in situ hybridization investigation of ring chromosomes characterizing a specific pathologic subgroup of adipose tissue tumors”. Cancer Genetics and Cytogenetics. 68 (2): 85–90. doi:10.1016/0165-4608(93)90001-3. ISSN 0165-4608.
↑ Dei Tos, Angelo P.; Doglioni, Claudio; Piccinin, Sara; Sciot, Raf; Furlanetto, Alberto; Boiocchi, Mauro; Dal Cin, Paola; Maestro, Roberta; Fletcher, Christopher D. M.; Tallini, Giovanni (2000). “Coordinated expression and amplification of theMDM2,CDK4, andHMGI-C genes in atypical lipomatous tumours”. The Journal of Pathology. 190 (5): 531–536. doi:10.1002/(SICI)1096-9896(200004)190:5<531::AID-PATH579>3.0.CO;2-W. ISSN 0022-3417.
↑ Dei Tos, A (2000). “Liposarcoma: New entities and evolving concepts”. Annals of Diagnostic Pathology. 4 (4): 252–266. doi:10.1053/adpa.2000.8133. ISSN 1092-9134.
↑ M. D. Kraus, L. Guillou & C. D. Fletcher (1997). “Well-differentiated inflammatory liposarcoma: an uncommon and easily overlooked variant of a common sarcoma”. The American journal of surgical pathology. 21 (5): 518–527. PMID 9158675. Unknown parameter |month= ignored (help)
↑ P. Argani, F. Facchetti, G. Inghirami & J. Rosai (1997). “Lymphocyte-rich well-differentiated liposarcoma: report of nine cases”. The American journal of surgical pathology. 21 (8): 884–895. PMID 9255251. Unknown parameter |month= ignored (help)
↑ H. L. Evans (1979). “Liposarcoma: a study of 55 cases with a reassessment of its classification”. The American journal of surgical pathology. 3 (6): 507–523. PMID 534388. Unknown parameter |month= ignored (help)
↑ A. P. Dei Tos, T. Mentzel, P. L. Newman & C. D. Fletcher (1994). “Spindle cell liposarcoma, a hitherto unrecognized variant of liposarcoma. Analysis of six cases”. The American journal of surgical pathology. 18 (9): 913–921. PMID 8067512. Unknown parameter |month= ignored (help)
↑ D. C. Dahlin, K. K. Unni & T. Matsuno (1977). “Malignant (fibrous) histiocytoma of bone–fact or fancy?”. Cancer. 39 (4): 1508–1516. PMID 192432. Unknown parameter |month= ignored (help)
↑ Rodriguez, Fausto J.; Folpe, Andrew L.; Giannini, Caterina; Perry, Arie (2012). “Pathology of peripheral nerve sheath tumors: diagnostic overview and update on selected diagnostic problems”. Acta Neuropathologica. 123 (3): 295–319. doi:10.1007/s00401-012-0954-z. ISSN 0001-6322.
↑ Choi, Kwangmin; Komurov, Kakajan; Fletcher, Jonathan S.; Jousma, Edwin; Cancelas, Jose A.; Wu, Jianqiang; Ratner, Nancy (2017). “An inflammatory gene signature distinguishes neurofibroma Schwann cells and macrophages from cells in the normal peripheral nervous system”. Scientific Reports. 7 (1). doi:10.1038/srep43315. ISSN 2045-2322.
↑ Liao, Chung-Ping; Booker, Reid C.; Brosseau, Jean-Philippe; Chen, Zhiguo; Mo, Juan; Tchegnon, Edem; Wang, Yong; Clapp, D. Wade; Le, Lu Q. (2018). “Contributions of inflammation and tumor microenvironment to neurofibroma tumorigenesis”. Journal of Clinical Investigation. 128 (7): 2848–2861. doi:10.1172/JCI99424. ISSN 0021-9738.
↑ ^15.0 ^15.1 Staser, K.; Yang, F.-C.; Clapp, D. W. (2010). “Mast cells and the neurofibroma microenvironment”. Blood. 116 (2): 157–164. doi:10.1182/blood-2009-09-242875. ISSN 0006-4971.
↑ Muir, David; Neubauer, Debbie; Lim, Ingrid T.; Yachnis, Anthony T.; Wallace, Margaret R. (2001). “Tumorigenic Properties of Neurofibromin-Deficient Neurofibroma Schwann Cells”. The American Journal of Pathology. 158 (2): 501–513. doi:10.1016/S0002-9440(10)63992-2. ISSN 0002-9440.
↑ Wilkinson, Lana M.; Manson, David; Smith, Charles R. (2004). “Best Cases from the AFIP”. RadioGraphics. 24 (suppl_1): S237–S242. doi:10.1148/rg.24si035170. ISSN 0271-5333.
↑ Bernthal, Nicholas; Jones, Kevin; Monument, Michael; Liu, Ting; Viskochil, David; Randall, R. (2013). “Lost in Translation: Ambiguity in Nerve Sheath Tumor Nomenclature and Its Resultant Treatment Effect”. Cancers. 5 (4): 519–528. doi:10.3390/cancers5020519. ISSN 2072-6694.
↑ Mautner, V. F.; Friedrich, R. E.; von Deimling, A.; Hagel, C.; Korf, B.; Knöfel, M. T.; Wenzel, R.; Fünsterer, C. (2003). “Malignant peripheral nerve sheath tumours in neurofibromatosis type 1: MRI supports the diagnosis of malignant plexiform neurofibroma”. Neuroradiology. 45 (9): 618–625. doi:10.1007/s00234-003-0964-6. ISSN 0028-3940.
↑ Shen, M H; Harper, P S; Upadhyaya, M (1996). “Molecular genetics of neurofibromatosis type 1 (NF1)”. Journal of Medical Genetics. 33 (1): 2–17. doi:10.1136/jmg.33.1.2. ISSN 1468-6244.
↑ Rubin, Joshua B.; Gutmann, David H. (2005). “Neurofibromatosis type 1 — a model for nervous system tumour formation?”. Nature Reviews Cancer. 5 (7): 557–564. doi:10.1038/nrc1653. ISSN 1474-175X.
↑ Gray, Mark H. (1990). “Immunohistochemical Demonstration of Factor XIIIa Expression in Neurofibromas”. Archives of Dermatology. 126 (4): 472. doi:10.1001/archderm.1990.01670280056009. ISSN 0003-987X.
↑ Schwannoma. Dr Tim Luijkx and Dr Sara Wein et al. http://radiopaedia.org/articles/schwannoma
↑ Vestibular Schwannoma. Wikipedia(2015) https://en.wikipedia.org/wiki/Vestibular_schwannoma Accessed on October 2 2015
↑ Giordano J, Rogers LV (1989). “Peripherally administered serotonin 5-HT3 receptor antagonists reduce inflammatory pain in rats”. European Journal of Pharmacology. 170 (1–2): 83–6. PMID 2612565. |access-date= requires |url= (help)
↑ Kolvenbach H, Lauven PM, Schneider B, Kunath U (1989). “Repetitive intercostal nerve block via catheter for postoperative pain relief after thoracotomy”. The Thoracic and Cardiovascular Surgeon. 37 (5): 273–6. doi:10.1055/s-2007-1020331. PMID 2588243. Retrieved 2015-11-20.
↑ Opaleva-Stegantseva VA, Ivanov AG, Gavrilina IA, Khar’kov EI, Ratovskaia VI (1986). “[Incidence of sudden death cases in acute coronary insufficiency and acute myocardial infarction at the pre-hospital stage in Krasnoyarsk]”. Kardiologiia (in Russian). 26 (5): 23–6. PMID 3735913. |access-date= requires |url= (help)
↑ Misago N, Inoue T, Narisawa Y (2007). “Unusual benign myxoid nerve sheath lesion: myxoid palisaded encapsulated neuroma (PEN) or nerve sheath myxoma with PEN/PEN-like features?”. Am J Dermatopathol. 29 (2): 160–4. doi:10.1097/01.dad.0000256688.91974.09. PMID 17414438.
↑ Lee EJ, Calcaterra TC, Zuckerbraun L (1998). “Traumatic neuromas of the head and neck”. Ear Nose Throat J. 77 (8): 670–4, 676. PMID 9745184.
↑ Hanna SA, Catapano J, Borschel GH (2016). “Painful pediatric traumatic neuroma: surgical management and clinical outcomes”. Childs Nerv Syst. 32 (7): 1191–4. doi:10.1007/s00381-016-3109-z. PMID 27179535.
↑ Foltán R, Klíma K, Spacková J, Sedý J (2008). “Mechanism of traumatic neuroma development”. Med Hypotheses. 71 (4): 572–6. doi:10.1016/j.mehy.2008.05.010. PMID 18599222.
↑ Yao C, Zhou X, Zhao B, Sun C, Poonit K, Yan H (2017). “Treatments of traumatic neuropathic pain: a systematic review”. Oncotarget. 8 (34): 57670–57679. doi:10.18632/oncotarget.16917. PMC 5593675. PMID 28915703.
↑ Gray MH, Smoller BR, McNutt NS, Hsu A (1990). “Neurofibromas and neurotized melanocytic nevi are immunohistochemically distinct neoplasms”. Am J Dermatopathol. 12 (3): 234–41. PMID 1693815.
↑ Chen Y, Klonowski PW, Lind AC, Lu D (2012). “Differentiating neurotized melanocytic nevi from neurofibromas using Melan-A (MART-1) immunohistochemical stain”. Arch Pathol Lab Med. 136 (7): 810–5. doi:10.5858/arpa.2011-0335-OA. PMID 22742554.
↑ Singh N, Chandrashekar L, Kar R, Sylvia MT, Thappa DM (2015). “Neurotized congenital melanocytic nevus resembling a pigmented neurofibroma”. Indian J Dermatol. 60 (1): 46–50. doi:10.4103/0019-5154.147789. PMC 4318062. PMID 25657396.
↑ Gray MH, Smoller BR, McNutt NS, Hsu A (1990). “Immunohistochemical demonstration of factor XIIIa expression in neurofibromas. A practical means of differentiating these tumors from neurotized melanocytic nevi and schwannomas”. Arch Dermatol. 126 (4): 472–6. PMID 1690969.
↑ https://www.sciencedirect.com/topics/medicine-and-dentistry/cutaneous-myxoma
↑ Alaiti, Samer; Nelson, Fern P.; Ryoo, Jei W. (2000). “Solitary cutaneous myxoma”. Journal of the American Academy of Dermatology. 43 (2): 377–379. doi:10.1067/mjd.2000.101878. ISSN 0190-9622.
↑ Carney, J. Aidan (1986). “Cutaneous Myxomas”. Archives of Dermatology. 122 (7): 790. doi:10.1001/archderm.1986.01660190068018. ISSN 0003-987X.
↑ Iida, Ken; Egi, Takeshi; Shigi, Masato; Sogabe, Yusuke; Ohashi, Hirotsugu (2019). “Cutaneous Myxoma of Multiple Lesions”. Plastic and Reconstructive Surgery – Global Open. 7 (2): e2040. doi:10.1097/GOX.0000000000002040. ISSN 2169-7574.
↑ Fetsch JF, Laskin WB, Miettinen M (2005). “Nerve sheath myxoma: a clinicopathologic and immunohistochemical analysis of 57 morphologically distinctive, S-100 protein- and GFAP-positive, myxoid peripheral nerve sheath tumors with a predilection for the extremities and a high local recurrence rate”. Am J Surg Pathol. 29 (12): 1615–24. PMID 16327434.
↑ Yadav SK, Singh S, Sarin N, Naeem R, Pruthi SK (2019). “Nerve Sheath Myxoma of Scalp: A Rare Site of Presentation”. Int J Trichology. 11 (1): 34–37. doi:10.4103/ijt.ijt_45_18. PMC 6385516. PMID 30820132.
↑ Bhat A, Narasimha A, C V, Vk S (2015). “Nerve sheath myxoma: report of a rare case”. J Clin Diagn Res. 9 (4): ED07–9. doi:10.7860/JCDR/2015/10911.5810. PMC 4437072. PMID 26023558.
↑ Avninder S, Ramesh V, Vermani S (2007). “Benign nerve sheath myxoma (myxoid neurothekeoma) in the leg”. Dermatol Online J. 13 (2): 14. PMID 17498433.
↑ Kim BW, Won CH, Chang SE, Lee MW (2014). “A case of nerve sheath myxoma on finger”. Indian J Dermatol. 59 (1): 99–101. doi:10.4103/0019-5154.123526. PMC 3884944. PMID 24470676.
↑ Pulitzer DR, Reed RJ (1985). “Nerve-sheath myxoma (perineurial myxoma)”. Am J Dermatopathol. 7 (5): 409–21. PMID 4091218.
↑ Valeyrie-Allanore, L.; Ismaili, N.; Bastuji-Garin, S.; Zeller, J.; Wechsler, J.; Revuz, J.; Wolkenstein, P. (2005). “Symptoms associated with malignancy of peripheral nerve sheath tumours: a retrospective study of 69 patients with neurofibromatosis 1”. British Journal of Dermatology. 153 (1): 79–82. doi:10.1111/j.1365-2133.2005.06558.x. ISSN 0007-0963.
↑ Evans DG, Baser ME, McGaughran J, Sharif S, Howard E, Moran A (2002). “Malignant peripheral nerve sheath tumours in neurofibromatosis 1”. J Med Genet. 39 (5): 311–4. PMC 1735122. PMID 12011145.
↑ Panigrahi S, Mishra SS, Das S, Dhir MK (2013). “Primary malignant peripheral nerve sheath tumor at unusual location”. J Neurosci Rural Pract. 4 (Suppl 1): S83–6. doi:10.4103/0976-3147.116480. PMC 3808069. PMID 24174807.
↑ Ferrari A, Bisogno G, Carli M (2007). “Management of childhood malignant peripheral nerve sheath tumor”. Paediatr Drugs. 9 (4): 239–48. doi:10.2165/00148581-200709040-00005. PMID 17705563.
↑ Neville H, Corpron C, Blakely ML, Andrassy R (2003). “Pediatric neurofibrosarcoma”. J Pediatr Surg. 38 (3): 343–6, discussion 343-6. doi:10.1053/jpsu.2003.50105. PMID 12632346.
↑ Zehou, Ouidad; Fabre, Elizabeth; Zelek, Laurent; Sbidian, Emilie; Ortonne, Nicolas; Banu, Eugeniu; Wolkenstein, Pierre; Valeyrie-Allanore, Laurence (2013). “Chemotherapy for the treatment of malignant peripheral nerve sheath tumors in neurofibromatosis 1: a 10-year institutional review”. Orphanet Journal of Rare Diseases. 8 (1): 127. doi:10.1186/1750-1172-8-127. ISSN 1750-1172.
↑ Vasiliadis, K.; Papavasiliou, C.; Fachiridis, D.; Pervana, S.; Michaelides, M.; Kiranou, M.; Makridis, C. (2012). “Retroperitoneal extra-adrenal ganglioneuroma involving the infrahepatic inferior vena cava, celiac axis and superior mesenteric artery: A case report”. International Journal of Surgery Case Reports. 3 (11): 541–543. doi:10.1016/j.ijscr.2012.07.008. ISSN 2210-2612.
↑ https://radiopaedia.org/articles/ganglioneuroma
↑ ^55.0 ^55.1 Coffin CM, Watterson J, Priest JR, Dehner LP (1995). “Extrapulmonary inflammatory myofibroblastic tumor (inflammatory pseudotumor). A clinicopathologic and immunohistochemical study of 84 cases”. Am J Surg Pathol. 19 (8): 859–72. PMID 7611533.
↑ ^56.0 ^56.1 ^56.2 ^56.3 Wenig BM, Devaney K, Bisceglia M (1995). “Inflammatory myofibroblastic tumor of the larynx. A clinicopathologic study of eight cases simulating a malignant spindle cell neoplasm”. Cancer. 76 (11): 2217–29. PMID 8635024.
↑ ^57.0 ^57.1 Ramachandra S, Hollowood K, Bisceglia M, Fletcher CD (1995). “Inflammatory pseudotumour of soft tissues: a clinicopathological and immunohistochemical analysis of 18 cases”. Histopathology. 27 (4): 313–23. PMID 8847061.
↑ ^58.0 ^58.1 Häusler M, Schaade L, Ramaekers VT, Doenges M, Heimann G, Sellhaus B (2003). “Inflammatory pseudotumors of the central nervous system: report of 3 cases and a literature review”. Hum Pathol. 34 (3): 253–62. doi:10.1053/hupa.2003.35. PMID 12673560.
↑ ^59.0 ^59.1 ^59.2 ^59.3 Rabban JT, Zaloudek CJ, Shekitka KM, Tavassoli FA (2005). “Inflammatory myofibroblastic tumor of the uterus: a clinicopathologic study of 6 cases emphasizing distinction from aggressive mesenchymal tumors”. Am J Surg Pathol. 29 (10): 1348–55. PMID 16160478.
↑ ^60.0 ^60.1 Kovach SJ, Fischer AC, Katzman PJ, Salloum RM, Ettinghausen SE, Madeb R; et al. (2006). “Inflammatory myofibroblastic tumors”. J Surg Oncol. 94 (5): 385–91. doi:10.1002/jso.20516. PMID 16967468.
↑ ^61.0 ^61.1 Coffin CM, Dehner LP, Meis-Kindblom JM (1998). “Inflammatory myofibroblastic tumor, inflammatory fibrosarcoma, and related lesions: an historical review with differential diagnostic considerations”. Semin Diagn Pathol. 15 (2): 102–10. PMID 9606802.
↑ ^62.0 ^62.1 Berardi RS, Lee SS, Chen HP, Stines GJ (1983). “Inflammatory pseudotumors of the lung”. Surg Gynecol Obstet. 156 (1): 89–96. PMID 6336632.
↑ ^63.0 ^63.1 Coffin CM, Hornick JL, Fletcher CD (2007). “Inflammatory myofibroblastic tumor: comparison of clinicopathologic, histologic, and immunohistochemical features including ALK expression in atypical and aggressive cases”. Am J Surg Pathol. 31 (4): 509–20. doi:10.1097/01.pas.0000213393.57322.c7. PMID 17414097.
↑ Cukic O, Jovanovic MB (2019). “Large Fibroepithelial Polyp of the Palatine Tonsil”. Ear Nose Throat J: 145561319841203. doi:10.1177/0145561319841203. PMID 30997841.
↑ Vatansever M, Dinç E, Dursun Ö, Oktay ÖÖ, Arpaci R (2019). “Atypical presentation of fibroepithelial polyp: a report of two cases”. Arq Bras Oftalmol. doi:10.5935/0004-2749.20190050. PMID 30916216.
↑ Rexhepi M, Trajkovska E, Besimi F, Rufati N (2018). “Giant Fibroepithelial Polyp of Vulva: A Case Report and Review of Literature”. Pril (Makedon Akad Nauk Umet Odd Med Nauki). 39 (2–3): 127–130. doi:10.2478/prilozi-2018-0051. PMID 30864355.
↑ Jabbour J, Chappell JR, Busby M, McCubbery NW, Brown DF, Park SJK; et al. (2019). “Glottic Obstruction from Fibroepithelial Polyp”. Am J Case Rep. 20: 219–223. doi:10.12659/AJCR.914907. PMC 6388646. PMID 30778021.
↑ Hong P, Cai Y, Li Z, Fan S, Yang K, Hao H; et al. (2019). “Modified Laparoscopic Partial Ureterectomy for Adult Ureteral Fibroepithelial Polyp: Technique and Initial Experience”. Urol Int. 102 (1): 13–19. doi:10.1159/000494804. PMID 30448831.
↑ Uçar M, Baş E, Akkoç A, Topçuoğlu M (2018). “Fibroepithelial Polyp of the Ureter: A Rare Cause of Hydronephrosis”. J Endourol Case Rep. 4 (1): 166–168. doi:10.1089/cren.2018.0031. PMC 6225073. PMID 30426076.
↑ Chaker K, Rhouma SB, Daly KM, Zehani A, Bibi M, Chehida MAB; et al. (2019). “Benign fibroepithelial polyp of the ureter: A case report”. Urol Case Rep. 22: 52–53. doi:10.1016/j.eucr.2018.10.019. PMC 6226574. PMID 30425926.
↑ Hajji F, Moufid K, Ghoundale O, Touiti D (2019). “A rare case of successful endoscopic management of a fibroepithelial polyp with intussusception of the ureter and periodic prolapse into bladder”. Ann R Coll Surg Engl. 101 (2): e66–e70. doi:10.1308/rcsann.2018.0198. PMC 6351868. PMID 30421620.
↑ Lee H, Sade I, Gilani S, Zhong M, Lombardo G (2018). “A Giant Fibroepithelial Polyp of the Small Bowel Associated with High-Grade Obstruction”. Am Surg. 84 (7): e210–e211. PMID 30401014.
↑ Chaker K (2019). “Benign fibroepithelial polyp of the ureter: A case report”. Urol Case Rep. 22: 15–16. doi:10.1016/j.eucr.2018.09.021. PMC 6180234. PMID 30319938.
↑ Lozano-Peña AK, Lamadrid-Zertuche AC, Ocampo-Candiani J (2019). “Giant fibroepithelial polyp of the vulva”. Australas J Dermatol. 60 (1): 70–71. doi:10.1111/ajd.12886. PMID 30009441.
↑ Eckstein M, Agaimy A, Woenckhaus J, Winter A, Bittmann I, Janzen J; et al. (2019). “DICER1 mutation-positive giant botryoid fibroepithelial polyp of the urinary bladder mimicking embryonal rhabdomyosarcoma”. Hum Pathol. 84: 1–7. doi:10.1016/j.humpath.2018.05.015. PMID 29883781.
↑ Akdere H, Çevik G (2018). “Rare Fibroepithelial Polyp Extending Along the Ureter: A Case Report”. Balkan Med J. 35 (3): 275–277. doi:10.4274/balkanmedj.2017.1537. PMC 5981127. PMID 29843497.
↑ Ballard DH, Rove KO, Coplen DE, Chen TY, Hulett Bowling RL (2018). “Fibroepithelial polyp causing urethral obstruction: Diagnosis by cystourethrogram”. Clin Imaging. 51: 164–167. doi:10.1016/j.clinimag.2018.05.009. PMC 6404776. PMID 29800931.
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↑ Gupta R, Smita S, Sinha R, Sinha N, Sinha L (2018). “Giant fibroepithelial polyp of the thigh and retroperitoneal fibromatosis in a young woman: a rare case”. Skeletal Radiol. 47 (9): 1299–1304. doi:10.1007/s00256-018-2904-x. PMID 29487969.
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Epidemiology and Demographics

Overview

Liposarcoma is the second most common type of all soft tissue sarcomas in adults. The incidence of liposarcoma was estimated to be 0.25 cases per 100,000 individuals. Men are slightly more affected with liposarcoma than women. It is most frequent in middle-aged and older adults. The incidence of liposarcoma was estimated to be 0.25 cases per 100,000 individuals. Liposarcoma affects people of all ethnic groups but slightly more in the people from black ethnic background.

Epidemiology and Demographics

Incidence

The incidence of liposarcoma was estimated to be 0.25 cases per 100,000 individuals.^[1]

Age

Liposarcoma most frequently occurs in the middle-aged and older adults (age 40 and above).
Tumors of adult life have a median age of 55 – 60 years.

*Courtesy: SEER Cancer Statistics Review 1975-2011*^[2]

Gender

Men are slightly more affected with liposarcoma than women.

*Courtesy: SEER Cancer Statistics Review 1975-2011*

Race

Liposarcoma affects people of all ethnic groups but slightly more in the people from black ethnic background.

References

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Risk Factors

Overview

Liposarcoma is the second most common type of all soft tissue sarcomas in adults. The incidence of liposarcoma was estimated to be 0.25 cases per 100,000 individuals. Men are slightly more affected with liposarcoma than women. It is most frequent in middle-aged and older adults. The incidence of liposarcoma was estimated to be 0.25 cases per 100,000 individuals. Liposarcoma affects people of all ethnic groups but slightly more in the people from black ethnic background.

Epidemiology and Demographics

Incidence

The incidence of liposarcoma was estimated to be 0.25 cases per 100,000 individuals.^[1]

Age

Liposarcoma most frequently occurs in the middle-aged and older adults (age 40 and above).
Tumors of adult life have a median age of 55 – 60 years.

Gender

Men are slightly more affected with liposarcoma than women.

Race

Liposarcoma affects people of all ethnic groups but slightly more in the people from black ethnic background.

References

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]

Natural History, Complications and Prognosis

Overview

The natural history of liposarcoma depends on the histopathological sub-type and location of the tumor. If left untreated, liposarcomas may remain silent for a long time, especially if they are located in the retroperitoneum. Liposarcoma may metastasize to other organs. Lung is the most common location for metastatic disease. Retroperitoneal liposarcomas may affect adjacent organs and structures, that can lead to kidney disease or vascular compression. The prognosis of liposarcoma will depend on the histopathological sub-type. Atypical lipomatous neoplasm/well-differentiated liposarcoma has a low metastasis risk, but may recur locally. The prognosis for this sub-type is better than for other sub-types of liposarcoma. The 5-year disease free survival rate for liposarcoma located in the extremities is 74%.

Natural History, Complications, and Prognosis

Natural History

The natural history of liposarcoma depends on the histopathological sub-type and location of the tumor.
If left untreated, liposarcomas may remain silent for a long time, especially if they are located in the retroperitoneum.^[1]
The most common presentation of a liposarcoma located in the extremities is a painless growing mass without additional symptoms.

Complications

Liposarcoma may metastasize to other organs.
Lung is the most common location for metastatic disease.
A myxoid liposarcoma metastasizes more commonly to extrapulmonary locations, such as retroperitoneum, pericardium, chest wall, pleura, and pelvic soft tissue.^[1]
Retroperitoneal liposarcomas may affect adjacent organs and structures, that can lead to kidney disease or vascular compression.^[2]
A case of pancreatitis has been reported due to a dedifferentiated retroperitoneal liposarcoma.^[3]
Other complications can include:

Intestinal obstruction, ischemia, and/or perforation^[4]
Hydronephrosis^[5]
Ureteric fistula
Aortic rupture

Prognosis

The prognosis of liposarcoma will depend on the histopathological sub-type.
Atypical lipomatous neoplasm/well-differentiated liposarcoma has a low metastasis risk, but may recur locally. The prognosis for this sub-type is better than for other sub-types of liposarcoma.^[1]
The pleomorphic liposarcoma has a high metastasis potential and a high recurrence rate. The 5-year disease free survival rate for pleomorphic liposarcoma is 40%.^[6]
The 5-year disease free survival rate for liposarcoma located in the extremities is 74%.^[7]

References

↑ ^1.0 ^1.1 ^1.2 Peterson, Jeffrey J.; Kransdorf, Mark J.; Bancroft, Laura W.; O’Connor, Mary I. (2003). “Malignant fatty tumors: classification, clinical course, imaging appearance and treatment”. Skeletal Radiology. 32 (9): 493–503. doi:10.1007/s00256-003-0647-8. ISSN 0364-2348.
↑ Amit Gupta, Omar Pacha, Rony Skaria, Tam Huynh, Luan Truong & Abdul Abdellatif (2012). “Retroperitoneal sarcoma presenting as acute renal failure, secondary to bilateral renal artery invasion”. Clinical nephrology. 78 (2): 164–168. PMID 22790462. Unknown parameter |month= ignored (help)
↑ Yusuke Arakawa, Kazuo Yoshioka, Hitomi Kamo, Koichiro Kawano, Takeshi Yamaguchi, Yuko Sumise, Natsu Okitsu, Shizuo Ikeyama, Kojiro Morimoto, Yoshihiro Nakai & Seiki Tashiro (2013). “Huge retroperitoneal dedifferentiated liposarcoma presented as acute pancreatitis: report of a case”. The journal of medical investigation : JMI. 60 (1–2): 164–168. PMID 23614927.
↑ Kazim Duman, Mustafa Girgin & Gokhan Artas (2016). “A case report: Giant intra-abdominal liposarcoma presenting acute renal failure”. Annals of medicine and surgery (2012). 12: 90–93. doi:10.1016/j.amsu.2016.09.005. PMID 27942382. Unknown parameter |month= ignored (help)
↑ Kazim Duman, Mustafa Girgin & Gokhan Artas (2016). “A case report: Giant intra-abdominal liposarcoma presenting acute renal failure”. Annals of medicine and surgery (2012). 12: 90–93. doi:10.1016/j.amsu.2016.09.005. PMID 27942382. Unknown parameter |month= ignored (help)
↑ A. M. Oliveira & A. G. Nascimento (2001). “Pleomorphic liposarcoma”. Seminars in diagnostic pathology. 18 (4): 274–285. PMID 11757868. Unknown parameter |month= ignored (help)
↑ D. B. Pearlstone, P. W. Pisters, R. J. Bold, B. W. Feig, K. K. Hunt, A. W. Yasko, S. Patel, A. Pollack, R. S. Benjamin & R. E. Pollock (1999). “Patterns of recurrence in extremity liposarcoma: implications for staging and follow-up”. Cancer. 85 (1): 85–92. PMID 9921978. Unknown parameter |month= ignored (help)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [2]

Diagnosis

Treatment

Medical Therapy | Surgery | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Related Chapters

Lipoma

Resources

it:Liposarcoma

Template:WikiDoc Sources

[NCCN-1] 1.0 ^1.1 “NCCN Guidelines for Patients – Soft Tissue Sarcoma”.

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[1] Kate Lynn J. Bill, Lucia Casadei, Bethany C. Prudner, Hans Iwenofu, Anne M. Strohecker & Raphael E. Pollock (2016). “Liposarcoma: molecular targets and therapeutic implications”. Cellular and molecular life sciences : CMLS. 73 (19): 3711–3718. doi:10.1007/s00018-016-2266-2. PMID 27173057. Unknown parameter |month= ignored (help)

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[4] Emily Z. Keung, Jason L. Hornick, Monica M. Bertagnolli, Elizabeth H. Baldini & Chandrajit P. Raut (2014). “Predictors of outcomes in patients with primary retroperitoneal dedifferentiated liposarcoma undergoing surgery”. Journal of the American College of Surgeons. 218 (2): 206–217. doi:10.1016/j.jamcollsurg.2013.10.009. PMID 24315890. Unknown parameter |month= ignored (help)

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[6] Emily Z. Keung, Jason L. Hornick, Monica M. Bertagnolli, Elizabeth H. Baldini & Chandrajit P. Raut (2014). “Predictors of outcomes in patients with primary retroperitoneal dedifferentiated liposarcoma undergoing surgery”. Journal of the American College of Surgeons. 218 (2): 206–217. doi:10.1016/j.jamcollsurg.2013.10.009. PMID 24315890. Unknown parameter |month= ignored (help)

[7] N. Azumi, J. Curtis, R. L. Kempson & M. R. Hendrickson (1987). “Atypical and malignant neoplasms showing lipomatous differentiation. A study of 111 cases”. The American journal of surgical pathology. 11 (3): 161–183. PMID 3826477. Unknown parameter |month= ignored (help)

[8] Elizabeth Fabre-Guillevin, Jean-Michel Coindre, Nicolas de Saint Aubain Somerhausen, Francoise Bonichon, Eberhard Stoeckle & Nguyen Binh Bui (2006). “Retroperitoneal liposarcomas: follow-up analysis of dedifferentiation after clinicopathologic reexamination of 86 liposarcomas and malignant fibrous histiocytomas”. Cancer. 106 (12): 2725–2733. doi:10.1002/cncr.21933. PMID 16688768. Unknown parameter |month= ignored (help)

[GhadimiAl-Zaid2011-9] Ghadimi, Markus P.; Al-Zaid, Tariq; Madewell, John; Peng, Tingsheng; Colombo, Chiara; Hoffman, Aviad; Creighton, Chad J.; Zhang, Yiqun; Zhang, Anna; Lazar, Alexander J.; Pollock, Raphael E.; Lev, Dina (2011). “Diagnosis, Management, and Outcome of Patients with Dedifferentiated Liposarcoma Systemic Metastasis”. Annals of Surgical Oncology. 18 (13): 3762–3770. doi:10.1245/s10434-011-1794-0. ISSN 1068-9265.

[10] G. Lahat, D. A. Anaya, X. Wang, D. Tuvin, D. Lev & R. E. Pollock (2008). “Resectable well-differentiated versus dedifferentiated liposarcomas: two different diseases possibly requiring different treatment approaches”. Annals of surgical oncology. 15 (6): 1585–1593. doi:10.1245/s10434-007-9805-x. PMID 18398663. Unknown parameter |month= ignored (help)

[11] H. L. Evans, K. K. Khurana, B. L. Kemp & A. G. Ayala (1994). “Heterologous elements in the dedifferentiated component of dedifferentiated liposarcoma”. The American journal of surgical pathology. 18 (11): 1150–1157. PMID 7943536. Unknown parameter |month= ignored (help)

[12] W. H. Henricks, Y. C. Chu, J. R. Goldblum & S. W. Weiss (1997). “Dedifferentiated liposarcoma: a clinicopathological analysis of 155 cases with a proposal for an expanded definition of dedifferentiation”. The American journal of surgical pathology. 21 (3): 271–281. PMID 9060596. Unknown parameter |month= ignored (help)

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[14] G. Lahat, D. A. Anaya, X. Wang, D. Tuvin, D. Lev & R. E. Pollock (2008). “Resectable well-differentiated versus dedifferentiated liposarcomas: two different diseases possibly requiring different treatment approaches”. Annals of surgical oncology. 15 (6): 1585–1593. doi:10.1245/s10434-007-9805-x. PMID 18398663. Unknown parameter |month= ignored (help)

[15] Emily Z. Keung, Jason L. Hornick, Monica M. Bertagnolli, Elizabeth H. Baldini & Chandrajit P. Raut (2014). “Predictors of outcomes in patients with primary retroperitoneal dedifferentiated liposarcoma undergoing surgery”. Journal of the American College of Surgeons. 218 (2): 206–217. doi:10.1016/j.jamcollsurg.2013.10.009. PMID 24315890. Unknown parameter |month= ignored (help)

[16] Khin Thway, Robin L. Jones, Jonathan Noujaim, Shane Zaidi, Aisha B. Miah & Cyril Fisher (2016). “Dedifferentiated Liposarcoma: Updates on Morphology, Genetics, and Therapeutic Strategies”. Advances in anatomic pathology. 23 (1): 30–40. doi:10.1097/PAP.0000000000000101. PMID 26645460. Unknown parameter |month= ignored (help)

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[pmid10982304-18] 18.0 ^18.1 ^18.2 ^18.3 ^18.4 Dei Tos AP (2000). “Liposarcoma: new entities and evolving concepts”. Ann Diagn Pathol. 4 (4): 252–66. doi:10.1053/adpa.2000.8133. PMID 10982304.

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[26] G. Lahat, D. A. Anaya, X. Wang, D. Tuvin, D. Lev & R. E. Pollock (2008). “Resectable well-differentiated versus dedifferentiated liposarcomas: two different diseases possibly requiring different treatment approaches”. Annals of surgical oncology. 15 (6): 1585–1593. doi:10.1245/s10434-007-9805-x. PMID 18398663. Unknown parameter |month= ignored (help)

[27] H. L. Evans, K. K. Khurana, B. L. Kemp & A. G. Ayala (1994). “Heterologous elements in the dedifferentiated component of dedifferentiated liposarcoma”. The American journal of surgical pathology. 18 (11): 1150–1157. PMID 7943536. Unknown parameter |month= ignored (help)

[28] W. H. Henricks, Y. C. Chu, J. R. Goldblum & S. W. Weiss (1997). “Dedifferentiated liposarcoma: a clinicopathological analysis of 155 cases with a proposal for an expanded definition of dedifferentiation”. The American journal of surgical pathology. 21 (3): 271–281. PMID 9060596. Unknown parameter |month= ignored (help)

[pmid10982304-1] 1.0 ^1.1 Dei Tos AP (2000). “Liposarcoma: new entities and evolving concepts”. Ann Diagn Pathol. 4 (4): 252–66. doi:10.1053/adpa.2000.8133. PMID 10982304.

[2] Khin Thway, Rashpal Flora, Chirag Shah, David Olmos & Cyril Fisher (2012). “Diagnostic utility of p16, CDK4, and MDM2 as an immunohistochemical panel in distinguishing well-differentiated and dedifferentiated liposarcomas from other adipocytic tumors”. The American journal of surgical pathology. 36 (3): 462–469. doi:10.1097/PAS.0b013e3182417330. PMID 22301498. Unknown parameter |month= ignored (help)

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[9] H. L. Evans (1979). “Liposarcoma: a study of 55 cases with a reassessment of its classification”. The American journal of surgical pathology. 3 (6): 507–523. PMID 534388. Unknown parameter |month= ignored (help)

[10] A. P. Dei Tos, T. Mentzel, P. L. Newman & C. D. Fletcher (1994). “Spindle cell liposarcoma, a hitherto unrecognized variant of liposarcoma. Analysis of six cases”. The American journal of surgical pathology. 18 (9): 913–921. PMID 8067512. Unknown parameter |month= ignored (help)

[11] D. C. Dahlin, K. K. Unni & T. Matsuno (1977). “Malignant (fibrous) histiocytoma of bone–fact or fancy?”. Cancer. 39 (4): 1508–1516. PMID 192432. Unknown parameter |month= ignored (help)

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[Sarcoma-1] “Sarcoma help”.

[2] “SEER Stat Sheets”.

[Sarcoma-1] “Sarcoma help”.

[2] “SEER Stat Sheets”.

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Health Dictionary

Liposarcoma

Introduction

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differential Diagnosis

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

Staging

History and Symptoms

Physical Examination

Laboratory Findings

Biopsy

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

References

Overview

Historical Perspective

Discovery

Famous Cases

References

Overview

Classification

References

Overview

Pathophysiology

Pathogenesis

Genetics

Well-Differentiated Liposarcoma

Associated Conditions

Gross Pathology

Microscopic Pathology

Well-Differentiated Liposarcoma

Sclerosing Liposarcoma

Adipocytic Liposarcoma

Inflammatory Liposarcoma

Spindle Cell Lipocarcinoma

De-differentiated Liposarcoma

Myxoid Liposarcoma

Round Cell Liposarcoma

Pleiomorphic Liposarcoma

Images

References

Overview

Causes

References

Overview

Differential diagnosis

References

Overview

Epidemiology and Demographics

Incidence

Age

Gender

Race

References

Overview

Epidemiology and Demographics

Incidence

Age

Gender

Race

References

Overview

Natural History, Complications, and Prognosis

Natural History

Complications

Prognosis

References

Diagnosis