Lipoma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2] Shanshan Cen, M.D. [3]

Synonyms and keywords:Adipose tumor

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Sahar Memar Montazerin, M.D.[2]

Overview

A lipoma is a common, benign tumor composed of fatty tissue. In 1914, Dr. Gery and colleagues first described Hibernoma, tumor of brown fat tissue. Lipoma may be classified into different subtypes depending on the classification system. They may be classified according to the anatomical location, the related tissues or other characteristics. Lipoma is formed from mature adipocytes and is histologically indistinguishable from fat tissue. Recent studies have observed cytogenetic abnormalities in 50-60% of lipomas, suggesting its role in the lipoma pathogenesis. Rearrangements of chromosome 12 are the most commonly cytogenetic abnormality. In a cross-sectional appearance, the lipoma is pale yellow to orange color and has a uniform greasy surface with a lobular pattern. The subcutaneous lipoma is usually encapsulated and has a distinct lobulated pattern. There is no established cause for lipoma. However, trauma and some genetic abnormalities have been associated with its development. Lipoma must be differentiated from liposarcoma, normal adipose tissue, adrenal myelolipoma, angiomyolipoma, and other lipomatous tumors. Lipoma incidence is 100 per 100,000 individuals worldwide annually. Lipomas tend to affect middle age individuals. It affects men at a greater extent than women. Common risk factors in the development of lipoma are trauma and genetic factors. Lipoma affects trunk, shoulder, upper arm, and neck at a greater extent. These tumors are completely benign and recurrence is one of their complications. Lipoma can be diagnosed clinically. However, a combination of clinical features and imaging studies are usually used for their diagnosis. Biopsy may be indicated in case of rapidly enlarging mass or unusual findings such as firm consistency. The most common symptom of lipoma is an asymptomatic slowly growing mass with a soft consistency. However, the deep lipoma may be symptomatic depending on their site and size. Symptoms include pain, restriction of movement in large lipoma, feeling of fullness or discomfort, and palpitation and dyspnea in mediastinal lipomas. Physical examination of patients with a lipoma is usually remarkable for a mobile, painless mass with a soft consistency. This mass often occurs in the neck, shoulders, back, arms and thighs. Sometimes, lipoma may cause limitation in the range of motions of the extremities depending on their size and locations. Neuromuscular examination of patients with lipoma may be remarkable for positive Tinel’s sign and Phalen’s sign. Lasègue’s sign may be positive in case of lumbosacral lipoma. On CT, the lipoma is seen as a well-delineated mass with absorption density characteristic of fatty tissue. Findings on an MRI suggestive of lipoma include a well-defined lesion with intensity similar to that of subcutaneous fat. Ultrasound may be helpful in the diagnosis of lipoma. Findings on an ultrasound suggestive of lipoma include Hypoechoic, minimally heterogeneous lesion. Treatment options of lipoma include simple excision, liposuction, and deoxycholate injection.

Historical Perspective

In 1914, Dr. Gery and colleagues first described Hibernoma, tumor of brown fat tissue.

Classification

Lipoma may be classified into different subtypes depending on the classification system. They may be classified according to the anatomical location, the related tissues or other characteristics.

Pathophysiology

Lipoma is formed from mature adipocytes and is histologically indistinguishable from fat tissue. Recent studies have observed cytogenetic abnormalities in 50-60% of lipomas, suggesting its role in the lipoma pathogenesis. Rearrangements of chromosome 12 are the most commonly cytogenetic abnormality. In a cross-sectional appearance, the lipoma is pale yellow to orange and has a uniform greasy surface with a lobular pattern. The subcutaneous lipoma is usually encapsulated and has a distinct lobulated pattern.

Causes

There is no established cause for lipoma. However, trauma and some genetic abnormalities have been associated with its development.

Differentiating Lipoma other Diseases

Lipoma must be differentiated from liposarcoma, normal adipose tissue, adrenal myelolipoma, angiomyolipoma, and other lipomatous tumors.

Epidemiology and Demographics

Lipoma incidence is 100 per 100,000 individuals worldwide annually. Lipoma tend to affect middle age individuals, especially those of 40 to 60 years of age. It affects men at a greater extent than women.

Risk Factors

Common risk factors in the development of lipoma are trauma and genetic factors.

Screening

There is insufficent evidence to recommend routine screening for lipoma.

Natural History, Complications and Prognosis

Lipoma tends to affect individuals of 40 to 60 years of age. It affects trunk, shoulder, upper arm, and neck at a greater extent. They are completely benign and recurrence is one of their complications.

Diagnosis

Lipoma can be diagnosed clinically. However, a combination of clinical features and imaging studies are usually used for the diagnosis of lipoma. Biopsy may be indicated in case of rapidly enlarging mass or unusual findings such as firm consistency.

History and Symptoms

The most common symptom of lipoma is an asymptomatic slowly growing mass with a soft consistency. However, the deep lipoma may be symptomatic depending on their site and size. Symptoms include pain, restriction of movement in large lipoma, feeling of fullness or discomfort, and palpitation and dyspnea in mediastinal lipomas.

Physical Examination

Physical examination of patients with a lipoma is usually remarkable for a mobile, painless mass with a soft consistency. This mass often occur in the neck, shoulders, back, arms and thighs. Sometimes, lipoma may cause limitation in the range of motions of the extremities depending on their size and locations. Neuromuscular examination of patients with lipoma may be remarkable for positive Tinel’s sign and Phalen’s sign. Lasègue’s sign may be positive in case of lumbosacral lipoma.

Laboratory Findings

There are no diagnostic laboratory findings associated with lipoma.

Electrocardiogram

There is no electrocardiogram finding associated with lipoma.

X Ray

There are no x-ray findings associated with lipoma. however, it may have findings suggestive of the presence of a mass.

CT

On CT, the lipoma is seen as a well-delineated mass with absorption density characteristic of fatty tissue.

MRI

MRI may be helpful in the diagnosis of lipoma. Findings on an MRI suggestive of lipoma include a well-defined lesion with intensity similar to that of subcutaneous fat.

Echocardiography or Ultrasound

Ultrasound may be helpful in the diagnosis of lipoma. Findings on an ultrasound suggestive of lipoma include Hypo-echoic, minimally heterogeneous lesion.

Other Imaging Findings

There are no other imaging findings associated with lipoma.

Other Diagnostic Studies

Other diagnostic studies for lipoma include biopsy, which demonstrates mature fat cells with no malignant feature.

Treatment

Surgery

Surgery of lipoma includes simple excision, liposuction, and deoxycholate injection.

Primary Prevention

There are no established measures for the primary prevention of lipoma.

Secondary Prevention

There are no established measures for the secondary prevention of lipoma. Template:WikiDoc Sources

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]

Overview

In 1914, Dr. Gery and colleagues first described Hibernoma, tumor of brown fat tissue.

Historical Perspective

In 1914, Gery and colleagues first described Hibernoma.^[1]
In 1960, Howard and Helwig first described angiomyolipoma.^[2]
In 1975, Enzinger and Harvey first describe spindle cell lipoma.^[3]
In 1986, Dr. Chan and his colleagues reported the first case of chondroid lipoma.^[4]

References

↑ Bancroft, Laura W.; Kransdorf, Mark J.; Peterson, Jeffrey J.; O’Connor, Mary I. (2006). “Benign fatty tumors: classification, clinical course, imaging appearance, and treatment”. Skeletal Radiology. 35 (10): 719–733. doi:10.1007/s00256-006-0189-y. ISSN 0364-2348.
↑ Howard, W. R. (1960). “Angiolipoma”. Archives of Dermatology. 82 (6): 924. doi:10.1001/archderm.1960.01580060078011. ISSN 0003-987X.
↑ Enzinger, Franz M.; Harvey, Dean A. (1975). “Spindle cell lipoma”. Cancer. 36 (5): 1852–1859. doi:10.1002/1097-0142(197511)36:5<1852::AID-CNCR2820360542>3.0.CO;2-U. ISSN 0008-543X.
↑ Chan, John K.C.; Lee, K.C.; Saw, Daisy (1986). “Extraskeletal chondroma with lipoblast-like cells”. Human Pathology. 17 (12): 1285–1287. doi:10.1016/S0046-8177(86)80574-3. ISSN 0046-8177.

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Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]

Overview

Lipoma may be classified into different subtypes depending on the classification system. They may be classified according to the anatomical location, the related tissues or other characteristics.

Classification

Lipomas can be classified according to their anatomical locations into:^[1]

Another suggested classification is according to the related structure:

Muscles-related lipoma
Nerve-related lipoma
Bone-related lipoma
Synovial-related lipoma

World health organization (WHO) classification system classified lipomatous tumors into the following sub types:^[2]

Lipoma
Lipomatosis
Lipomatosis of nerve
Lipoblastoma/lipoblastomatosis
Angiolipoma
Myolipoma of soft tissue
Chondroid lipoma
Spindle-cell lipoma/pleomorphic lipoma
Hibernoma

Weiss and Goldblum classified Lipomatous tumors into the following subtypes. This classification system has shown more clinical utility.^[3]

Lipoma which may be classified as superficial or deep, single or multiple
Variants of lipoma including:
- Angiolipoma
- Myolipoma
- Chondroid lipoma
- Lipoblastoma
- Lpindle-cell/pleomorphic lipoma
Lipomatous tumors including:
- Intramuscular lipoma
- Intermuscular lipoma
- Lipomatosis of nerve
- Lipoma of the tendon sheath and joint
Infiltrating lipomas including
- Diffuse lipomatosis
- Symmetric lipomatosis
- Adiposis dolorosa
Hibernoma

References

↑ Al-Qattan, M. M.; Al-Lazzam, A. M.; Al Thunayan, A.; Al Namlah, A.; Mahmoud, S.; Hashem, F.; Tulbah, A. (2012). “CLASSIFICATION OF BENIGN FATTY TUMOURS OF THE UPPER LIMB”. Hand Surgery. 10 (01): 43–59. doi:10.1142/S0218810405002541. ISSN 0218-8104.
↑ Bancroft, Laura W.; Kransdorf, Mark J.; Peterson, Jeffrey J.; O’Connor, Mary I. (2006). “Benign fatty tumors: classification, clinical course, imaging appearance, and treatment”. Skeletal Radiology. 35 (10): 719–733. doi:10.1007/s00256-006-0189-y. ISSN 0364-2348.
↑ Goldblum, John (2014). Enzinger and Weiss’s soft tissue tumors. Philadelphia, PA: Saunders/Elsevier. ISBN 9781455737635.

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Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]

Overview

Lipoma is formed from mature adipocyte cells and is histologically indistinguishable from fat tissue. Recent studies have observed cytogenetic abnormalities in 50-60% of lipomas, suggesting its role in the lipoma pathogenesis. Rearrangements of chromosome 12 are the most commonly cytogenetic abnormality. In a cross-sectional appearance, the lipoma is pale yellow to orange and has a uniform greasy surface with a lobular pattern. The subcutaneous lipoma is usually encapsulated and has a distinct lobulated pattern.

Pathophysiology

Lipoma is formed from mature adipocytes and is histologically indistinguishable from fat tissue.
Recent studies have observed cytogenet ic abnormalities in 50-60% of lipomas, suggesting its role in the lipoma pathogenesis.^[1]^[2]
Rearrangements of chromosome 12 is the most commonly cytogenetic abnormality.
The DDIT3 gene, located on the long arm of chromosome 12, has been suggested to play a role in adipocytic differentiation.^[3]
This gene encodes a protein family, known to be enhancer binding protein.
Members of this protein family are highly expressed in fat and are engaged in the growth arrest of fat cells.

Genetics

Genetic abnormalities associated with lipoma pathogenesis include:^[4]
- Translocations in 12q13-15
- Interstitial deletions of 13q
- Rearrangements in 6p21-23

Gross pathology

Gross pathology of lipoma may differ depending on anatomical location.^[5]
Subcutaneous lipoma appear as a a soft, well-circumscribed rounded mass with different size ranging from millimeters to 5 cm or more.
Lipomas larger than 10 cm are not common.
In cross-sectional appearance, the lipoma is pale yellow to orange and has a uniform greasy surface with a lobular pattern.
Lipoma is usually encapsulated.
Focal hemorrhage or fat necrosis may also occur, but it is much less common than in liposarcomas.
Intramuscular lipomas are usually larger than subcutaneous lipomas and may be encapsulated or diffuse.^[6]
Grayish streaks of fibrous tissue may also be seen in fibrolipoma which has a firmer texture compared to ordinary lipoma.

Microscopic pathology

Microscopically, lipomas are formed from mature fat cells.^[8]
There is no nuclear hyperchromasia.
Subcutaneous lipoma is usually encapsulated and have a distinct lobulated pattern.
Cystic like changes may also be seen in lipoma due to impaired blood supply.
Infection or trauma may cause fat necrosis or local liquefaction of fat, which may appear with phagocytic cells and formation of lipid cysts.
A possible benign finding in lipoma is the collection of histiocytes and the vacuolization of the nucleus.^[9]
Intramuscular lipoma may be well-demarcated from the adjacent muscular tissue or have a diffuse pattern with alternating adipocytes and skeletal muscle cells.

Histologic view of spindle cell lipoma^[10]

Histologic view of subcutaneous lipoma^[11]

Immunohistochemistry

Lipomas may have following immunohistochemical markers:^[12]

Gallery

Histopathologic slide of renal angiomyolipoma. Nephrectomy specimen. H & E stain.^[13]
Histopathologic slide of renal angiomyolipoma. Nephrectomy specimen. H & E stain.^[13]
Histopathologic slide of renal angiomyolipoma. Nephrectomy specimen. H & E stain.^[13]
Histopathologic image of renal angiomyolipoma. Nephrectomy specimen. HMB-45 immunostain.^[13]

References

↑ Sreekantaiah C, Leong SP, Karakousis CP, McGee DL, Rappaport WD, Villar HV, Neal D, Fleming S, Wankel A, Herrington PN (January 1991). “Cytogenetic profile of 109 lipomas”. Cancer Res. 51 (1): 422–33. PMID 1988102.
↑ Weiss SW (1996). “Lipomatous tumors”. Monogr Pathol. 38: 207–39. PMID 8744279.
↑ Adelmant G, Gilbert JD, Freytag SO (June 1998). “Human translocation liposarcoma-CCAAT/enhancer binding protein (C/EBP) homologous protein (TLS-CHOP) oncoprotein prevents adipocyte differentiation by directly interfering with C/EBPbeta function”. J. Biol. Chem. 273 (25): 15574–81. doi:10.1074/jbc.273.25.15574. PMID 9624148.
↑ Willén, Helena; Åkerman, Måns; Dal Cin, Paola; De Wever, Ivo; Fletcher, Christopher D.M; Mandahl, Nils; Mertens, Fredrik; Mitelman, Felix; Rosai, Juan; Rydholm, Anders; Sciot, Raf; Tallini, Giovanni; Van Den Berghe, Herman; Vanni, Roberta (1998). “Comparison of Chromosomal Patterns with Clinical Features in 165 Lipomas: A Report of the CHAMP Study Group”. Cancer Genetics and Cytogenetics. 102 (1): 46–49. doi:10.1016/S0165-4608(97)00292-6. ISSN 0165-4608.
↑ Miettinen, Markku (2010). Modern soft tissue pathology : tumors and non-neoplastic conditions. Cambridge New York: Cambridge University Press. ISBN 9780521874090.
↑ Miettinen, Markku (2010). Modern soft tissue pathology : tumors and non-neoplastic conditions. Cambridge New York: Cambridge University Press. ISBN 9780521874090.
↑ Image courtesy of Sebastian E Valbuena, Greg A O’Toole and Eric Roulot, wikimedia commons
↑ Simango, Stephen; Ramdial, Pratistadevi K.; Madaree, Anil (2000). “Subpectoral post-traumatic lipoma”. British Journal of Plastic Surgery. 53 (7): 627–629. doi:10.1054/bjps.2000.3396. ISSN 0007-1226.
↑ Miettinen, Markku (2010). Modern soft tissue pathology : tumors and non-neoplastic conditions. Cambridge New York: Cambridge University Press. ISBN 9780521874090.
↑ wikimedia commons
↑ Pathological and histological images courtesy of Ed Uthman at flickr, wikimedia commons
↑ Fletcher, Christopher (2002). Pathology and genetics of tumours of soft tissue and bone. Lyon: IARC Press. ISBN 9283224132.
↑ ^13.0 ^13.1 ^13.2 ^13.3 http://librepathology.org/wiki/index.php/Angiomyolipoma

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Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]

Overview

There is no established cause for lipoma. However, trauma and some genetic abnormalities have been associated with its development.

Causes

There is no established cause for lipoma. However, trauma and some genetic abnormalities have been associated with its development.^[1]^[2]
For more information on lipoma causes click here.

References

↑ Aust MC, Spies M, Kall S, Jokuszies A, Gohritz A, Vogt P (2007). “Posttraumatic lipoma: fact or fiction?”. Skinmed. 6 (6): 266–70. PMID 17975353.
↑ Miettinen, Markku (2010). Modern soft tissue pathology : tumors and non-neoplastic conditions. Cambridge New York: Cambridge University Press. ISBN 9780521874090.

Template:WikiDoc Sources

Differentiating Lipoma from other Diseases

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

Overview

Lipoma must be differentiated from liposarcoma, normal adipose tissue, adrenal myelolipoma, angiomyolipoma, and other lipomatous tumors.

Differentiating Lipoma from other Diseases

Lipoma must be differentiated from liposarcoma, normal adipose tissue, adrenal myelolipoma, angiomyolipoma, and other lipomatous tumors.

Lipoma should be differentiated from other lipomatous tumors. Table below compares and describes the characteristics of different lipomatous tumors:


Lipomatous tumor	Age of onset	Gender preponderance	Location	Clinical features	Pathologic features	Other features	Histologic view
Angiolipoma^[1]^[2]	Second and third decades of life	Female < male	More commonly seen in forearm May also affect trunk and upper arm	Subcutaneous nodule Tender to palpation Less than 2 cm	Encapsulated, yellow nodules with a reddish tinge A combination of fatty tissue and vascular channels Fibrin thrombi is present in vascular channels (characteristic finding)	Benign	^[3]
Myolipoma^[4]	Fifth and sixth decades of life	Female > male	More commonly seen in retroperitoneum, abdomen, pelvis, inguinal region, or abdominal wall May also affect extremities	Subcutaneous mass which may also engage superficial muscular fascia Size differs depending on the location	Partially encapsulated mass with partially yellow-white cut surface A combination of mature adipocytes and sheets of well-differentiated smooth muscle cells No nuclear atypia Sieve-like appearance at low magnification (due to interspersed location of smooth muscle component)	Benign Usually large and located in the deep soft tissues	^[5]
Myelolipoma^[6]^[7]	Fifth decade of life	Female = male	More commonly seen in adrenal glands Other possible locations include: Thoracic Retroperitoneum Presacral region	Usually asymptomatic May cause abdominal pain, nausea, and constipation (depending on the location and size) Uncommonly, may cause retroperitoneal hemorrhage 3 to 7 cm	A combination of bone marrow elements and adipose tissue in varying proportions May show myxoid changes	Well-circumscribed radiolucent mass in radiologic imaging May have hromonal activity	^[8]
Spindle Cell/Pleomorphic Lipoma^[9]	Fifth to seventh decades of life	Female < male	More commonly seen in posterior neck, shoulder, and back It is also reported in oral cavity	Subcutaneous nodule with firm consistency Slowly growing and painless Mostly between 3 to 5 cm	Similar to ordinary lipoma A combination of mature fat cells and spindle cell or pleomorphic elements Lipomatous component may vary in amount	Immunohistochemically positive for CD34 Benign	^[10]
Chondroid Lipoma^[11]	Third or fourth decade of life	Female > male	More commonly seen in limbs and limb girdles May also involve trunk, and the head and neck region, particularly the oral cavity	Slowly growing painless mass Sizes ranges from 1 to 11 cm	Encapsulated tumor with a yellow, white, or pink-tan cut surface A combination of mature adipocytes in association with nests of vacuolated cells in a myxochondroid or hyalinized fibrous background	Heterogeneous soft tissue mass in radiologic imaging Benign	^[12]
Hibernoma^[13]	Third decade of life	Female = male	Most commonly seen in thigh May also affect shoulder, back, neck, chest, arm, and abdominal cavity/retroperitoneum	Slowly growing, painless, subcutaneous mass Affects intramuscular in 10% of the cases Size varies between 5 to 15 cm	Well-defined, soft, and mobile mass A combination of vacuolated granular eosinophilic cells with abundant mithochondria and high vascular content	Immunohistochemically positive for S-100 Benign	^[14]
Intramuscular and Intermuscular Lipomas^[15]	Fourth to seventh decades of life	Female < male	Most commonly seen in large muscles of the extremities, especially in thigh, shoulder, and upper arm	Painless, slowly growing mass Visible during muscle contraction	Infiltrative adipose thissue within the muscle Absence of nuclear atypia	May be very small or more than 20 cm	^[16]
Thymolipoma^[17]	Median age of onset is 33	Female = male	Anterior mediastinum	Asymptomatic Symptoms may present if the mass compress the surrounding thoracic structures. Possible symptoms include: Cough Dyspnea Hemoptysis Chest pain Hoarseness	A combination of mature fat cells with interspersed thymic epithelial cells	Anterior mediastinal mass Benign	^[18]
Lipomas of Tendon Sheaths and Joints^[19]	Second and third decades of life	Female = male Lipoma of joints affects men more frequently than women	Most commonly seen in wrist and hand May also affect ankle and foot Bilateral and symmetric location in 50% of the cases	May cause severe pain, trigger finger, or even symptoms of carpal tunnel syndrome	May have 2 different shape: A single adipose tissue extending along the tendon sheet A lipomatous lesion composed mostly from hypertrophic synovial villi	Radiologic imaging may show a lesion of less density than the surrounding tissue	_
Lumbosacral Lipoma^[20]^[21]	First decade of life	Female > male	It occurs in the lumbosacral region and overlies the spine	Initially, asymptomatic Later signs and symptoms of progressive myelopathy or radiculopathy in the lower legs, bladder, or bowel	Uncapsulated mass that consists of lobulated adipose tissue Vascular proliferation and smooth muscle tissue may be present	Almost always associated with spina bifida or a similar laminar defect (lipomyeloschisis)	_
Neural Fibrolipoma (Lipofibromatous Hamartoma of Nerves)^[22]	First three decades of life	Female > male (in the presence of macrodactyly)	Most commonly affect median nerve and its branches May also affect ulnar, radial, peroneal, and cranial nerves	May cause neuropathy, pain, paresthesia, and decreased sensation Carpal tunnel syndrome may also occur	A sausage-shaped mass with soft texture that has diffusely infiltrated a large nerve and its branches Fibrofatty tissue surronding and infiltrating the nerve trunk	Overgrowth of bone and macrodactyly may be seen in one third of the cases	_

In general, there is little differential for a classic lipoma. The main differential is^[23]:

Liposarcoma
Normal adipose tissue

In certain locations then other fatty masses should be considered :

Retroperitoneum

Adrenal myelolipoma
Angiomyolipoma (AML)

Chest

Thymolipoma

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^[24]^[25]^[26]^[27]^[28]^[29]^[30]^[31]^[32]^[33]	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^[34]^[35]^[36]^[37]^[38]^[39]^[40]^[37]^[41]^[42]^[43]^[44]	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^[45]^[46]^[47]^[48]^[49]	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^[50]	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^[51]^[52]^[53]^[54]	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^[55]^[56]^[57]^[58]	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)^[59]^[60]^[61]^[62]	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^[63]^[64]^[65]^[66]^[67]^[68]	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^[69]^[70]^[71]^[72]^[73]^[74]	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^[75]^[76]	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^[77]^[78]^[79]^[80]^[81]^[82]^[83]^[84]^[78]^[81]^[85]	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)^[77]^[78]^[79]^[80]^[81]^[82]^[83]^[84]^[78]^[81]^[85]	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^[86]^[87]^[88]^[89]^[90]^[91]^[92]^[93]^[94]^[95]^[96]^[97]^[98]^[99]^[100]^[101]^[102]^[103]^[104]^[105]	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

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↑ Contributed by Dr. Dharam Ramnani in Webpathology
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↑ Kang, Hyun-Seung; Wang, Kyu-Chang; Kim, Kwang Myung; Kim, Seung Ki; Cho, Byung Kyu (2006). “Prognostic factors affecting urologic outcome after untethering surgery for lumbosacral lipoma”. Child’s Nervous System. 22 (9): 1111–1121. doi:10.1007/s00381-006-0088-5. ISSN 0256-7040.
↑ Jones, Victoria; Wykes, Victoria; Cohen, Nicki; Thompson, Dominic; Jacques, Tom S (2018). “The pathology of lumbosacral lipomas: macroscopic and microscopic disparity have implications for embryogenesis and mode of clinical deterioration”. Histopathology. 72 (7): 1136–1144. doi:10.1111/his.13469. ISSN 0309-0167.
↑ Al-Jabri T, Garg S, Mani GV (September 2010). “Lipofibromatous hamartoma of the median nerve”. J Orthop Surg Res. 5: 71. doi:10.1186/1749-799X-5-71. PMC 2955673. PMID 20920178.
↑ Lipoma.Dr Ahmed Abd Rabou and Dr Frank Gaillard, et al. Radiopaedia.org 2015.http://radiopaedia.org/articles/lipoma
↑ 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.
↑ ^37.0 ^37.1 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.
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↑ 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)
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↑ 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
↑ ^77.0 ^77.1 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.
↑ ^78.0 ^78.1 ^78.2 ^78.3 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.
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↑ ^81.0 ^81.1 ^81.2 ^81.3 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.
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↑ 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.
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↑ 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.
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Epidemiology and Demographics

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

Overview

Lipoma incidence is 100 per 100,000 individuals worldwide annually. Lipoma tend to affect middle age individuals, especially those of 40 to 60 years of age. It affects men at a greater extent than women.

Epidemiology and Demographics

Incidence

Lipoma incidence is 100 per 100,000 individuals worldwide annually.^[1]

Prevalence

There is no available data on the prevalence of lipoma.

Age

Lipoma tend to affect middle age individuals, especially those of 40 to 60 years of age.^[2]

Gender

Lipoma affects men at a greater extent than women.^[1]

Race

Lipoma develops in all races equally.

References

↑ ^1.0 ^1.1 Rydholm A, Berg NO (December 1983). “Size, site and clinical incidence of lipoma. Factors in the differential diagnosis of lipoma and sarcoma”. Acta Orthop Scand. 54 (6): 929–34. doi:10.3109/17453678308992936. PMID 6670522.
↑ Salam GA (March 2002). “Lipoma excision”. Am Fam Physician. 65 (5): 901–4. PMID 11898962.

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Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]

Overview

Common risk factors in the development of lipoma are trauma and genetic factors.

Risk Factors

Common risk factors in the development of lipoma are:^[1]^[2]^[3]

References

↑ Aust, M.C.; Spies, M.; Kall, S.; Gohritz, A.; Boorboor, P.; Kolokythas, P.; Vogt, P.M. (2007). “Lipomas after blunt soft tissue trauma: are they real? Analysis of 31 cases”. British Journal of Dermatology. 157 (1): 92–99. doi:10.1111/j.1365-2133.2007.07970.x. ISSN 0007-0963.
↑ Charifa A, Badri T. PMID 29493968. Missing or empty |title= (help)
↑ Fletcher, Christopher (2002). Pathology and genetics of tumours of soft tissue and bone. Lyon: IARC Press. ISBN 9283224132.

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Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]

Overview

There is insufficent evidence to recommend routine screening for lipoma.

Screening

There is insufficent evidence to recommend routine screening for lipoma.

References

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]

Overview

Lipoma tends to affect individuals of 40 to 60 years of age. They are completely benign and recurrence is one of their complications.

Natural History

Lipoma usually affects individuals of 40 to 60 years of age.^[1]^[2]^[3]
It usually presents with a slowly growing soft tissue mass, typically less than 10 cm.
Trunk, shoulder, upper arm, and neck are the most commonly affected locations.
They are completely benign, but recurrence is one of the complications.
Malignant transformation is rarely reported.
Recurrence is more common among deeply located lipomas, given the increased difficulty for complete removal.

Complications

The complications of lipoma listed below:^[4]
- Recurrence (<5%)
- Malignant transformation (rarely reported)

Prognosis

Prognosis is excellent. ^[4]
Lipomas are completely benign.

References

↑ Rydholm, Anders; Berg, Nils O. (2009). “Size, Site and Clinical Incidence of Lipoma:Factors in the Differential Diagnosis of Lipoma and Sarcoma”. Acta Orthopaedica Scandinavica. 54 (6): 929–934. doi:10.3109/17453678308992936. ISSN 0001-6470.
↑ Miettinen, Markku (2010). Modern soft tissue pathology : tumors and non-neoplastic conditions. Cambridge New York: Cambridge University Press. ISBN 9780521874090.
↑ Phalen, George S.; Kendrick, James I.; Rodriguez, Juan M. (1971). “Lipomas of the upper extremity”. The American Journal of Surgery. 121 (3): 298–306. doi:10.1016/0002-9610(71)90208-X. ISSN 0002-9610.
↑ ^4.0 ^4.1 Bancroft, Laura W.; Kransdorf, Mark J.; Peterson, Jeffrey J.; O’Connor, Mary I. (2006). “Benign fatty tumors: classification, clinical course, imaging appearance, and treatment”. Skeletal Radiology. 35 (10): 719–733. doi:10.1007/s00256-006-0189-y. ISSN 0364-2348.

Diagnosis

Treatment

Case Studies

Case #1

Resources

Lipoma Excision by Gohar A. Salam, in American Family Physician. March 1, 2002.

Template:WikiDoc Sources

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Lipoma

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Lipoma other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

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X Ray

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Echocardiography or Ultrasound

Other Imaging Findings

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Treatment

Surgery

Primary Prevention

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Overview

Historical Perspective

References

Overview

Classification

References

Overview

Pathophysiology

Genetics

Gross pathology

Microscopic pathology

Immunohistochemistry

Gallery

References

Overview

Causes

References

Overview

Differentiating Lipoma from other Diseases

References

Overview

Epidemiology and Demographics

Incidence

Prevalence

Age

Gender

Race

References

Overview

Risk Factors

References

Overview

Screening

References

Overview

Natural History

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