07/05/20 22.

02

emedicine.medscape.com

Dermatofibroma
Updated: Jun 04, 2018
Author: Joseph C Pierson, MD; Chief Editor: Dirk M Elston, MD

Overview

Background
Dermatofibroma (superficial benign fibrous histiocytoma) is a common cutaneous nodule of unknown etiology that
occurs more often in women. Dermatofibroma frequently develops on the extremities (mostly the lower legs) and is
usually asymptomatic, although pruritus and tenderness can be present. It is actually the most common painful skin
tumor.[1] A number of well-described, histologic subtypes of dermatofibroma have been reported. Removal of the
tumor is usually not typically required unless diagnostic uncertainty exists or particularly troubling symptoms are
present.

This article discusses primarily cutaneous (superficial) dermatofibroma. Subcutaneous (deep) benign fibrous
histiocytomas are also well documented and may have a more aggressive clinical course, as can tumors displaying
cellular, aneurysmal (hemosiderotic), and atypical histologic variants of dermatofibroma.

In addition, benign fibrous histiocytomas are reported in bone, orbital, airway, gastrointestinal, splenic, genitourinary,
and intracranial locations.

Pathophysiology
The precise mechanism for the development of dermatofibroma is unknown. Rather than a reactive tissue change,
evidence that dermatofibroma may be a neoplastic process is demonstrated by its clonal proliferative growth.[2]
Clonality, by itself, is not necessarily synonymous with a neoplastic process; it has been demonstrated in inflammatory
conditions, including atopic dermatitis, lichen sclerosis, and psoriasis. Dermatofibroma tumorigenesis may be due to
distorted protein kinase C activity.[3]

Results from immunohistochemical testing with antibodies to factor XIIIa, which label dermal dendritic cells, are
frequently positive in dermatofibroma, while antibodies to MAC 387, which label monocyte-derived macrophages
(histiocytes), show less consistent results. One study evaluated the expression in dermatofibroma of HSP47, a
recently used marker for skin fibroblasts; CD68, a marker for histiocytes; and factor XIIIa. Most of the spindle-shaped
cells in all 28 cases of dermatofibroma, irrespective of histologic variant, stained positively with HSP47, indicating that
skin fibroblasts are a major constituent of dermatofibroma. Factor XIIIa–positive dendritic cells also are present, but the
presence of CD68-positive histiocytes was inconsistent, especially between histologic variants.[4] CD14+ monocytes
have been proposed as the cell of origin of dermatofibromas.[5]

The cell surface proteoglycan, syndecan-1,[6] and fibroblast growth factor receptor 2, involved in epithelial-
mesenchymal cross-talk,[7] may play a role in the growth of dermatofibromas. Transforming growth factor-beta (TGF-
beta) signaling might be a trigger of the fibrosis seen in dermatofibromas.[8] TGF-beta, along with other fibrinogenic
factors, may be produced by mast cells, which have been reported to occur in abnormally high numbers in
dermatofibromas.[9]

https://emedicine.medscape.com/article/1056742-print Page 1 of 17
 07/05/20 22.02

Gene fusions have been described in dermatofibroma tumorigenesis.[10, 11] ALK gene rearrangement and
overexpression has been demonstrated in the epithelioid and atypical dermatofibroma variants.[12, 13]

Etiology
Historically attributed to be a reactive process to some traumatic insult to the skin (eg, arthropod bite, skin tattooing,
tuberculin skin testing, prior folliculitis),[14, 15, 16, 17] the cause of dermatofibroma is unknown. Clonal analysis
suggest it may represent a true neoplasm.[2]

Altered immunity likely plays a role in many cases of multiple eruptive dermatofibromas associated with various
underlying conditions and medications (see History).

A study of eruptive dermatofibromas in a kindred suggests that a genetic component may exist.[18]

Epidemiology
Frequency
Dermatofibromas are relatively common.

Race
Frequency of dermatofibroma appears to be similar in all races.

Sex

Females are affected by dermatofibroma more commonly than males, with a male-to-female ratio of 1:2, or higher.[19,
20]

Age

Dermatofibroma can occur in patients of any age. In one series, 80% of biopsy specimens were from patients aged 20-
49 years,[19] and in another the mean age of the patients was 42.18±13.72 years.[20]

Prognosis
Typical superficial dermatofibromas are considered benign lesions, and the prognosis for patients with this condition is
excellent. However, discomfort from pain or itching may be significant.

Deep, cellular, aneurysmal (hemosiderotic), and atypical variants, which are notoriously more locally recurrent (≤20%
of cases), can rarely metastasize.[21, 22, 23] (The deep subset of dermatofibroma that arises in the subcutaneous or
deep soft tissue may undergo further classification.[22] ) Such variants, or any indeterminant dermatofibroma, might be
regarded as potentially malignant lesions.[24] In these exceptional cases, pulmonary and nodal metastases were most
commonly seen, some patients developed multiple satellite nodules, and deaths have occurred.[25] The primary
tumors tended to be large and cellular, but aggressive behavior is not entirely predictable, although early or frequent
recurrences of the tumor should raise concern.[25] Array-based comparative genomic hybridization (CGH) may prove
useful in identifying these higher-risk variants.[26, 27, 22]

https://emedicine.medscape.com/article/1056742-print Page 2 of 17
 07/05/20 22.02

The epithelioid variant has also been reported to metastasize, although demonstration of ALK gene rearrangement
may indicate it is a biologically distinct tumor.[12]

In a study of common dermatofibromas with an increased mitotic rate but no other worrisome features, none recurred
or metastasized.[28]

Spontaneous regression has been reported,[29] and this may yield postinflammatory hypopigmentation, although this
appears to be quite rare.

Patient Education
For patient education resources, see the Procedures Center, as well as Mole Removal.

Presentation

History
Dermatofibromas typically arise slowly and most often occur as a solitary nodule on an extremity, particularly the lower
leg, but any cutaneous site is possible. Dermatofibromas are usually asymptomatic, but itching and pain often are
noted. They are the most common of all painful skin tumors.[1] Women who shave their legs may be bothered by the
razor traumatizing the lesion in that region, causing pain, bleeding, erosive changes, and ulceration. Although cases of
unusually rapid growth exist, most dermatofibromas remain static for decades or persist indefinitely. Patients may
describe a hard mole or unusual scar and are often concerned about the possibility of skin cancer.

Several lesions may be present, but rarely are numerous (ie, ≥15) tumors found. This multiple eruptive variant occurs
in less than 1% of patients, approximately 60% of whom have an underlying systemic condition, such as HIV infection
or systemic lupus erythematosus.[30, 31, 32] However, dermatomyositis,[33] Graves disease,[34] Hashimoto
thyroiditis,[35] myasthenia gravis,[35] Down syndrome,[36] leukemia,[37] myelodysplastic syndrome,[38] cutaneous T-
cell lymphoma,[39] multiple myeloma,[39] atopic dermatitis,[40] Crohn disease,[41] and ulcerative colitis[42] have all
been reported in association with the phenomenon. In addition, antiretroviral agents,[43] the biologic agent efalizumab,
[44] antitumor necrosis factor-alpha agents,[45] and the tyrosine kinase inhibitor imatinib[46] have been linked to their
appearance.

Both congenital[47] and acquired[48] cases of multiple clustered dermatofibromas have been reported.

Physical Examination
Typically, the clinical appearance of dermatofibroma is a solitary, 0.5- to 1-cm nodule. A sizable minority of patients
may have several lesions, but rarely (< 1% of cases) are more than 15 lesions present. (See History) The overlying
skin can range from flesh to gray, yellow, orange, pink, red, purple, blue, brown, or black, or a combination of hues
(see the image below). On palpation, the hard nodule may feel like a small pebble fixed to the skin surface and is
freely movable over the subcutis. Tenderness may be elicited with manipulation of the lesion.

https://emedicine.medscape.com/article/1056742-print Page 3 of 17
 07/05/20 22.02

Erythematous, slightly hyperpigmented nodule on the leg. Courtesy of David Barnette, MD.

The characteristic tethering of the overlying epidermis to the underlying lesion with lateral compression (pinching),
called the dimple sign, may be a useful clinical sign for diagnosis.[49] However, presence of the dimple sign does not
always assure the lesion is dermatofibroma,[50] and dermatoscopy may be useful in supporting the clinical impression.
[51]

The extremities are the most common sites of involvement, particularly the legs.[19, 20] Although any cutaneous site
can be seen, palm, sole, digital, oral, and genital involvement is relatively rare. Giant (>5 cm in diameter),[52] atrophic,
[53] polypoid,[54] and dermatofibroma with spreading satellitosis[55] variants have been reported. The largest reported
tumor was 17 x 9 x 4 cm.[56]

Multiple clustered dermatofibromas[48] are rare and can mimic dermatofibrosarcoma protuberans. This phenomenon
has been reported in a segmental distribution.[57]

A halo of dermatitis (Meyerson phenomenon) surrounding a dermatofibroma occurred in one patient.[58]

DDx

Diagnostic Considerations
Also consider the following:

Cutaneous chondroma
Desmoplastic trichoepithelioma
Foreign body granuloma
Granular cell tumor
Nodular fasciitis
Nodular scabies
Sclerosing sweat duct carcinoma
Neurothekeoma
Omphalomesenteric duct cyst
Neurofibroma
Dermatomyofibroma
Epithelioid sarcoma

https://emedicine.medscape.com/article/1056742-print Page 4 of 17
 07/05/20 22.02

Differential Diagnoses
Acrochordon

Anal polyp

Angiomatoid fibrous histiocytoma

Atypical Fibroxanthoma

Atypical Mole (Clark Nevus or Dysplastic Nevus)

Basal Cell Carcinoma

Blue Nevi

Cutaneous Manifestations of HIV

Cutaneous Melanoma

Cutaneous Squamous Cell Carcinoma

Cutaneous T-Cell Lymphoma

Cylindroma

Dermatofibrosarcoma Protuberans

Dermatologic Manifestations of Juvenile Xanthogranuloma

Cutaneous Lipomas

Dermatologic Manifestations of Merkel Cell Carcinoma

Dermatologic Manifestations of Metastatic Carcinomas

Dermatologic Manifestations of Neurilemmoma (Schwannoma)

Epithelioid sarcoma

Erythema Elevatum Diutinum

Infantile Digital Fibromatosis

Keloid and Hypertrophic Scar

Keratoacanthoma

Leiomyoma

Mastocytosis

Melanocytic Nevi

Multicentric Reticulohistiocytosis

Multinucleate Cell Angiohistiocytoma

Pilomatrixoma

Plaquelike myofibroblastic tumor

Prurigo Nodularis

Spiradenoma

https://emedicine.medscape.com/article/1056742-print Page 5 of 17
 07/05/20 22.02

Spitz Nevus

Supernumerary Nipple

Targetoid Hemosiderotic Hemangioma

Workup

Workup

Imaging Studies
A study of localized lesions of the skin imaged via variable-frequency ultrasound included the image of a hypoechoic
solid nodule created by a dermatofibroma.[59] Dermatofibromas have been analyzed by high-definition optical
coherent tomography.[60]

Dermatofibroma can mimic a malignant lesion on fluorodeoxyglucose positron-emission tomography (FDG-PET)

scans.[61]

Procedures
For those trained in dermoscopy, this may be a useful adjunctive diagnostic technique for dermatofibromas. The most
common pattern seen is a peripheral pigment network with a central white area.[62] Dermoscopy of a xanthomatous
dermatofibroma shows a homogeneous pattern with shades of yellow and a peripheral pigment network.[63] A green
color may indicate the hemosiderotic variant.[64] If a suggestive melanocytic or atypical pattern is noted with
dermoscopy, a diagnostic biopsy is warranted.[65]

Confocal laser scanning microscopy findings have been described.[66]

If any diagnostic uncertainty exists, excisional biopsy into the subcutaneous fat is advised.

Histologic Findings
The overlying epidermis is usually acanthotic. Pseudoepitheliomatous hyperplasia and a basaloid proliferation may be
noted. The hyperplasia may be caused by the action of fibroblasts on epidermal keratinocytes.[67] Increased pigment
may be seen, which may be iron or melanin. Most lesions display a grenz zone of normal papillary dermis overlying the
tumor.

The bulk of the tumor is within the mid dermis where no capsule is present and the periphery of the lesion blends with
the surrounding tissue. Whorling fascicles of a spindle cell proliferation with excessive collagen deposition are
characteristic. At the periphery, the spindle cells characteristically wrap around normal collagen bundles (see the
images below). Occasionally, melanocytes have been reported to be interspersed amongst the spindle cells.[68]

https://emedicine.medscape.com/article/1056742-print Page 6 of 17
 07/05/20 22.02

Acanthotic epithelium with basilar hyperpigmentation (dirty feet) over a dermal spindle cell proliferation (X10). Courtesy
of David Barnette, MD.

Collagen trapping by the dermal fibrohistiocytic infiltrate (X40). Courtesy of David Barnette, MD.

The subcutis typically is preserved, but if involved (especially when a storiform [cartwheel] pattern is observed), be
alert to the possibility of the lesion being a dermatofibrosarcoma protuberans (DFSP).[69]

Antibodies toward factor XIIIa and CD34 are useful in distinguishing the two tumors, with the former suggesting
dermatofibroma and the latter suggesting DFSP.[70] However, occasional CD34 positivity occurs in the cellular variant
of dermatofibroma.[71, 72] Dermatofibromas retain elastic fibers, while these are fragmented or displaced in DFSP.
This can be assessed with fluorescence microscopy of hematoxylin and eosin (H&E) sections or with an elastic stain.
[73]

Stromelysin-3 (ST-3) expression of dermatofibroma by immunohistochemical staining may also be useful in

differentiation from DFSP.[74]

Transforming growth factor-beta type I and type II receptor expression patterns may also help distinguish between
dermatofibroma and DFSP.[8] Thrombospondin-1 (TSP-1) mediates TGF-beta I activation, and its elevated expression
in DFSP may aid in the differential diagnosis.[75]

https://emedicine.medscape.com/article/1056742-print Page 7 of 17
 07/05/20 22.02

Immunostaining with insulinlike growth factor–binding protein 7 (IGFBP7) is positive more frequently in dermatofibroma
and aids in the differentiation from DFSP.[76]

Nestin, expressed in only 13% of dermatofibroma, but 94% of DFSP, could be a useful marker to distinguish between
these two tumors.[77]

Collagen triple helix repeat containing-1 (Cthrc1) staining is positive much more frequently in DFSP and is another
potential discriminating test.[78]

D2-40 immunostain appears to be a sensitive marker for dermatofibromas, including the cellular variant, can aid in
differentiation from DFSP.[79]

Cathepsin K expression[80] and immunohistochemical analysis of chemokine receptor CXCR4[81] are other possible
tools in delineating the two tumors.

Indeterminate tumors that share histologic and immunohistochemical features of dermatofibroma and DFSP have
been described[82] ; however, those studied do not harbor the COL1A1-PDGFB chimeric transcripts of DFSP.[83]

Expression of FGFR3/FOXN1 and FGF2/FGFR4 in dermatofibroma pathogenesis may also help differentiate from
DFSP.[84]

CD99 has been used alone or in combination with factor XIIIa and CD34 to differentiate dermatofibroma from DFSP.
[85, 86, 87]

Leukocyte-specific protein 1 (LSP1) may aid in differentiation of dermatofibroma from DFSP.[5]

5-Hydroxymethylcytosine (5-hmC) may be a useful marker to distinguish dermatofibroma from DFSP.[88]

Fluorescence in situ hybridization (FISH) analysis may be helpful in differentiating dermatofibroma from DFSP.[89]

B-cell lymphoma 2 (Bcl-2) expression may help distinguish subcutaneous dermatofibroma from DFSP.[90]

One clinicopathologic classification scheme[91] describes the following four categories of dermatofibroma:

Those with architectural peculiarities, such as deep penetrating, atrophic, giant, aneurysmal (angiomatoid),
hemangiopericytomalike, palisading, or ossifying variants

Cellular/stromal dermatofibromas, such as clear cell, granular cell, myofibroblastic, sclerotic, monster cell,
atypical (pseudosarcomatous), hemosiderotic, cholesterotic (lipidized), and myxoid variants: While the
cholesterotic variant has been described in association with metabolic syndrome,[92] it is more likely that
cholesterol results from breakdown of cell membranes within the lesion rather than as a result of circulating
lipids.

Dermatofibromas with architectural and cellular/stromal changes in homogeneous arrangement, including

epithelioid cell, cellular benign, smooth muscle proliferative, basal cell carcinoma–like, pseudolymphomatous,
Multinucleate Cell Angiohistiocytoma (perhaps not a subtype of dermatofibroma), cellular neurothekeoma,
plexiform fibrohistiocytic tumor, plexiform xanthoma, and plexiform xanthomatous tumor subtypes

A complex, composite, or combined dermatofibroma[93] category with 2 or more architectural and

cellular/stromal patterns in a single lesion

Of the variants listed above, keep in mind that the uncommon sclerotic fibromalike dermatofibroma should be
differentiated from sclerotic fibroma. One study[94] showed 7 of 7 of the former lesions to be negative for CD34 and
CD99, while 3 of 3 solitary fibromas were positive for CD34 and CD99. For comparison, 14 of 14 "common-type"
dermatofibromas in this study were negative for CD34, while 4 demonstrated positivity with CD99.

A histologic review of 192 dermatofibromas found 80% common type, 5.7% aneurysmal, 5.7% hemosiderotic, 2.6%
epithelioid, 2.1% cellular, 2.1% lipidized, 1% atrophic, and 0.5% clear cell.[95]

Immunoperoxidase staining is consistently positive for both CD10 and actin in dermatofibromas.[96] CD10 was
positive in 11 of 11 dermatofibromas and only positive in 1 of 7 epithelioid dermatofibromas, so it was postulated that
epithelioid dermatofibroma may be a distinct entity.[97]

Lichenoid dermatofibroma,[98] ulcerated dermatofibroma,[98] erosive dermatofibroma,[98] dermatofibroma with diffuse

https://emedicine.medscape.com/article/1056742-print Page 8 of 17
 07/05/20 22.02

eosinophilic infiltrate,[99] dermatofibroma accompanied by perforating dermatosis,[100] and one showing perforating
dermatosis with floret-type multinucleated giant cells have been described.[101] Dermatofibromas with overlying
sebaceous hyperplasia,[102] with intracytoplasmic eosinophilic globules,[103] signet-ring cells,[104] amyloid light chain
deposition,[105] and incidental acantholysis[106] have also been reported. A case of an apocrine gland cyst with a
hemosiderotic dermatofibroma was termed an apocrine hemosiderotic dermatofibroma.[107] Cutaneous
adenodermatofibroma (entrapped apocrine structures without hemosiderotic changes), keloidal, collapsing
angiokeloidal, and dermatofibromas with dystrophic calcification variants have been reported.[108, 109, 110, 111] Blue
nevus associated with dermatofibroma has been reported, as has coexisting leukemia cutis.[112, 113]

One case of mycosis fungoides showed histologic features of dermatofibroma.[114]

Induction of hyperplasia in nearby structures by dermatofibroma is frequently described. In a study of over 10,000
dermatofibromas, associated induction (where follicular germinative and sebaceous glandular induction were seen in
6% of cases), cellular alterations, and stromal alterations are outlined with their attributes.[96] Dermatofibromas of the
shoulder have a high incidence of sebaceous induction with seborrheic keratosis‒like hyperplasia.[115]

A case series[116] reported the uncommon occurrence of dermatofibroma and melanocytic lesions in the same biopsy
specimen. Four of 14 specimens showed the 2 processes to seemingly merge imperceptibly. The lesions included
junctional, dermal, and compound nevi, as well as a single case of melanoma in situ. Knowledge of this relationship
can help prevent rendering the wrong diagnosis and is facilitated by the use of immunohistochemistry, with the
melanocytic lesions showing S-100 and Mart-1 positivity with FXIIIa negativity and the dermatofibroma showing S-100
and Mart-1 negativity and FXIIIa positivity. Another tool is Sox10 immunoreactivity, which is positive in melanocytic
lesions, but not fibrohistiocytic proliferations.[117] A case report[118] documenting an invasive melanoma occurring in
association with a dermatofibroma underscores the role of these immunohistochemical stains.

INI-1, present in 100% of dermatofibromas, but decreased or absent in the vast majority of epithelioid sarcomas in one
study, can help distinguish between the 2 lesions.[119]

Treatment

Approach Considerations
No treatment is usually necessary for dermatofibromas. Simple reassurance that the lesion is benign may be indicated,
unless one of the aggressive subtypes is suspected or diagnosed.

Intralesional steroid injections have been attempted with variable results.

Surgical Care
For cosmetically unacceptable lesions, those that are particularly symptomatic, if there is any diagnostic uncertainty, or
when one of the aggressive subtypes is suspected, complete excision, including the subcutaneous fat, is the ideal
procedure. Obtaining a 3-mm margin has been shown to completely remove typical dermatofibromas.[120] One of the
aggressive histologic subtypes, aneurysmal dermatofibroma, has been successfully treated via Mohs micrographic
surgery.[121]

An inverted pyramidal biopsy technique may allow for an aesthetically pleasing result, while still providing adequate
tissue for histologic findings.[122]

Superficially shaving the lesion or cryosurgery can be attempted for cosmesis or to decrease the symptoms; however,
recurrences are more likely.

Carbon dioxide and pulsed-dye laser treatments have been used in the treatment of dermatofibromas.[123, 124]

https://emedicine.medscape.com/article/1056742-print Page 9 of 17
 07/05/20 22.02

Long-Term Monitoring
If the dermatofibroma is not removed and significant change occurs in the color, size, border, or symptoms, the patient
should seek follow-up evaluation.

If complete removal has been previously attempted, patients with lesions that recur should seek follow-up evaluation.
An aggressive subtype or another diagnosis should be ruled out.

If multiple eruptive lesions develop, screening for a family history of such and for underlying associated diseases and
medications is warranted (See History).

Questions & Answers

Overview

What is a dermatofibroma?

What is the pathophysiology of dermatofibroma?

What causes dermatofibroma?

How common are dermatofibromas?

What is the racial distribution of dermatofibroma?

Are dermatofibromas more common in males or females?

What are the age-related demographics of dermatofibroma?

What is the prognosis of dermatofibroma?

What patient education resources are available on dermatofibroma?

Presentation

What is the clinical history of dermatofibroma?

What are the physical exam findings in dermatofibroma?

DDX

Which conditions should be considered in the diagnosis of dermatofibroma?

What are the differential diagnoses for Dermatofibroma?

Workup

Which imaging studies are indicated in the workup of dermatofibroma?

Which clinical procedures are indicated in the workup of dermatofibroma?

What are the histologic characteristics of a dermatofibroma?

What are the histologic findings in dermatofibroma?

How are dermatofibromas classified?

https://emedicine.medscape.com/article/1056742-print Page 10 of 17
 07/05/20 22.02

What are the histologic characteristics of dermatofibromas?

Treatment

How are dermatofibromas treated?

When is surgical care indicated in the treatment of a dermatofibroma?

When is follow-up evaluation indicated in dermatofibroma?

Contributor Information and Disclosures

Author

Joseph C Pierson, MD Dermatology Residency Program Director, University of Vermont College of Medicine

Joseph C Pierson, MD is a member of the following medical societies: Association of Professors of Dermatology, New
England Dermatological Society, American Academy of Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

Christine C Tam, MD Managing Member, Certified Dermatologists

Christine C Tam, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Former Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of
Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and
White Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Dermatology, American Society for MOHS Surgery, Association of Military Dermatologists, Phi Beta Kappa

Disclosure: Nothing to disclose.

Edward F Chan, MD Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of
Medicine

Edward F Chan, MD is a member of the following medical societies: American Academy of Dermatology, American
Society of Dermatopathology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical
University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Diane

https://emedicine.medscape.com/article/1056742-print Page 11 of 17
 07/05/20 22.02

Pierson, DO, to the development and writing of this article.

References

1. Naversen DN, Trask DM, Watson FH, Burket JM. Painful tumors of the skin: "LEND AN EGG". J Am Acad Dermatol. 1993
Feb. 28(2 Pt 2):298-300. [Medline].

2. Chen TC, Kuo T, Chan HL. Dermatofibroma is a clonal proliferative disease. J Cutan Pathol. 2000 Jan. 27(1):36-9. [Medline].

3. Plaszczyca A, Nilsson J, Magnusson L, Brosjö O, Larsson O, Vult von Steyern F, et al. Fusions involving protein kinase C
and membrane-associated proteins in benign fibrous histiocytoma. Int J Biochem Cell Biol. 2014 Apr 8. [Medline].

4. Kuroda K, Tajima S. Proliferation of HSP47-positive skin fibroblasts in dermatofibroma. J Cutan Pathol. 2008 Jan. 35(1):21-6.
[Medline].

5. Jin SY, Choi JS, Choi YL, Choi YL, Kim do H, Lee SH. Identification of leukocyte-specific protein 1-positive cells: a clue to the
cell of origin and a marker for the diagnosis of dermatofibroma. Ann Dermatol. 2015 Apr. 27 (2):157-62. [Medline].

6. Sellheyer K, Smoller BR. Dermatofibroma: upregulation of syndecan-1 expression in mesenchymal tissue. Am J

Dermatopathol. 2003 Oct. 25(5):392-8. [Medline].

7. Skroza N, Rotolo S, Ceccarelli S, et al. Modulation of the expression of the FGFR2-IIIb and FGFR2-IIIc molecules in
dermatofibroma. J Dermatol Sci. 2008 Jul. 51(1):53-7. [Medline].

8. Kubo M, Ihn H, Yamane K, Tamaki K. The expression levels and the differential expression of transforming growth factor-
beta receptors in dermatofibroma and dermatofibrosarcoma protuberans. Br J Dermatol. 2006 May. 154(5):919-25.
[Medline].

9. Yamamoto T. Dermatofibroma: a possible model of local fibrosis with epithelial/mesenchymal cell interaction. J Eur Acad
Dermatol Venereol. 2009 Apr. 23(4):371-5. [Medline].

10. Walther C, Hofvander J, Nilsson J, Magnusson L, Domanski HA, Gisselsson D, et al. Gene fusion detection in formalin-fixed
paraffin-embedded benign fibrous histiocytomas using fluorescence in situ hybridization and RNA sequencing. Lab Invest.
2015 Sep. 95 (9):1071-6. [Medline].

11. Panagopoulos I, Gorunova L, Bjerkehagen B, Lobmaier I, Heim S. LAMTOR1-PRKCD and NUMA1-SFMBT1 fusion genes
identified by RNA sequencing in aneurysmal benign fibrous histiocytoma with t(3;11)(p21;q13). Cancer Genet. 2015 Nov. 208
(11):545-51. [Medline].

12. Doyle LA, Mariño-Enriquez A, Fletcher CD, Hornick JL. ALK rearrangement and overexpression in epithelioid fibrous
histiocytoma. Mod Pathol. 2015 Jul. 28 (7):904-12. [Medline].

13. Szablewski V, Laurent-Roussel S, Rethers L, Rommel A, Van Eeckhout P, Camboni A, et al. Atypical fibrous histiocytoma of
the skin with CD30 and p80/ALK1 positivity and ALK gene rearrangement. J Cutan Pathol. 2014 Sep. 41 (9):715-9.
[Medline].

14. Evans J, Clarke T, Mattacks CA, Pond CM. Dermatofibromas and arthropod bites: is there any evidence to link the two?.
Lancet. 1989 Jul 1. 2(8653):36-7. [Medline].

15. Lobato-Berezo A, Churruca-Grijelmo M, Martínez-Pérez M, Imbernón-Moya A, Vargas-Laguna ME, Fernández-Cogolludo E,

et al. Dermatofibroma Arising within a Black Tattoo. Case Rep Dermatol Med. 2014. 2014:745304. [Medline].

16. Watanabe K, Fukuda H, Niiyama S, Oharasaki T, Mukai H. Multiple dermatofibromas subsequent to folliculitis. Eur J
Dermatol. 2013 Nov-Dec. 23 (6):890-1. [Medline].

17. Nomura E, Yamamoto T. Photoletter to the editor: Fibrous histiocytoma developing at the site of tuberculin skin test. J
Dermatol Case Rep. 2012 Dec 31. 6 (4):130-1. [Medline].

18. Samlaska C, Bennion S. Eruptive dermatofibromas in a kindred. Cutis. 2002 Mar. 69(3):187-8, 190. [Medline].

19. Han TY, Chang HS, Lee JH, Lee WM, Son SJ. A clinical and histopathological study of 122 cases of dermatofibroma (benign
fibrous histiocytoma). Ann Dermatol. 2011 May. 23(2):185-92. [Medline].

20. Şenel E, Yuyucu Karabulut Y, Doğruer Şenel S. Clinical, histopathological, dermatoscopic and digital microscopic features of
dermatofibroma: a retrospective analysis of 200 lesions. J Eur Acad Dermatol Venereol. 2015 Oct. 29 (10):1958-66.
[Medline].

https://emedicine.medscape.com/article/1056742-print Page 12 of 17
 07/05/20 22.02

21. Kaddu S, McMenamin ME, Fletcher CD. Atypical fibrous histiocytoma of the skin: clinicopathologic analysis of 59 cases with
evidence of infrequent metastasis. Am J Surg Pathol. 2002 Jan. 26(1):35-46. [Medline].

22. Gleason BC, Fletcher CD. Deep "benign" fibrous histiocytoma: clinicopathologic analysis of 69 cases of a rare tumor
indicating occasional metastatic potential. Am J Surg Pathol. 2008 Mar. 32(3):354-62. [Medline].

23. Szumera-Cieckiewicz A, Ptaszynski K. Benign fibrous histiocytoma of the skin metastasizing to the inguinal lymph node. Pol
J Pathol. 2011 Sep. 62(3):183-6. [Medline].

24. Kimyai-Asadi A, Goldberg LH, Greenberg C, et al. Cellular, atypical, and indeterminate dermatofibromas: benign or
malignant?. Dermatol Surg. 2008 Sep. 34(9):1264-71; discussion 1271-2. [Medline].

25. Doyle LA, Fletcher CD. Metastasizing "benign" cutaneous fibrous histiocytoma: a clinicopathologic analysis of 16 cases. Am
J Surg Pathol. 2013 Apr. 37 (4):484-95. [Medline].

26. Charli-Joseph Y, Saggini A, Doyle LA, Fletcher CD, Weier J, Mirza S, et al. DNA copy number changes in tumors within the
spectrum of cellular, atypical, and metastasizing fibrous histiocytoma. J Am Acad Dermatol. 2014 Apr 19. [Medline].

27. Mentzel T, Wiesner T, Cerroni L, Hantschke M, Kutzner H, Rütten A, et al. Malignant dermatofibroma: clinicopathological,
immunohistochemical, and molecular analysis of seven cases. Mod Pathol. 2013 Feb. 26 (2):256-67. [Medline].

28. Fernandez-Flores A, Manjon JA. Mitosis in dermatofibroma: a worrisome histopathologic sign that does not necessarily equal
recurrence. J Cutan Pathol. 2008 Sep. 35(9):839-42. [Medline].

29. Niemi KM. The benign fibrohistiocytic tumours of the skin. Acta Derm Venereol Suppl (Stockh). 1970. 50(63):Suppl 63:1-66.
[Medline].

30. Massone C, Parodi A, Virno G, Rebora A. Multiple eruptive dermatofibromas in patients with systemic lupus erythematosus
treated with prednisone. Int J Dermatol. 2002 May. 41(5):279-81. [Medline].

31. García-Millán C, Aldanondo I, Fernández-Lorente M, Carrillo R, Jaén P. [Multiple eruptive dermatofibromas in 2 patients
infected with the human immunodeficiency virus]. Actas Dermosifiliogr. 2007 Dec. 98(10):702-6. [Medline].

32. Marque M, Pallure V, Huet P, Bessis D, Guillot B. [Multiple familial "eruptive" dermatofibromas]. Ann Dermatol Venereol.
2013 Jun-Jul. 140 (6-7):452-4. [Medline].

33. Huang PY, Chu CY, Hsiao CH. Multiple eruptive dermatofibromas in a patient with dermatomyositis taking prednisolone and
methotrexate. J Am Acad Dermatol. 2007 Nov. 57(5 Suppl):S81-4. [Medline].

34. Lopez N, Fernandez A, Bosch RJ, Herrera E. Multiple eruptive dermatofibromas in a patient with Graves-Basedow disease.
J Eur Acad Dermatol Venereol. 2008 Mar. 22(3):402-3. [Medline].

35. Kimura Y, Kaneko T, Akasaka E, Nakajima K, Aizu T, Nakano H, et al. Multiple eruptive dermatofibromas associated with
Hashimoto's thyroiditis and myasthenia gravis. Eur J Dermatol. 2010 Jul-Aug. 20(4):538-9. [Medline].

36. Monteagudo B, Suarez-Amor O, Cabanillas M, et al. [Down syndrome: another cause of immunosuppression associated with
multiple eruptive dermatofibromas?]. Dermatol Online J. 2009 Sep 15. 15(9):15. [Medline].

37. Alexandrescu DT, Wiernik PH. Multiple eruptive dermatofibromas occurring in a patient with chronic myelogenous leukemia.
Arch Dermatol. 2005 Mar. 141(3):397-8. [Medline].

38. Bhattacharjee P, Umar SA, Fatteh SM. Multiple eruptive dermatofibromas occurring in a patient with myelodysplastic
syndrome. Acta Derm Venereol. 2005. 85(3):270-1. [Medline].

39. Zaccaria E, Rebora A, Rongioletti F. Multiple eruptive dermatofibromas and immunosuppression: report of two cases and
review of the literature. Int J Dermatol. 2008 Jul. 47(7):723-7. [Medline].

40. Yazici AC, Baz K, Ikizoglu G, Koca A, Kokturk A, Apa DD. Familial eruptive dermatofibromas in atopic dermatitis. J Eur Acad
Dermatol Venereol. 2006 Jan. 20(1):90-2. [Medline].

41. Beyazit Y, Caner S, Kurt M, Kekilli M, Aydog G, Ibis M. Dermatofibroma in a patient with Crohn's disease: a novel clinical
manifestation. J Crohns Colitis. 2010 Oct. 4(4):490-1. [Medline].

42. Hiraiwa T, Hanami Y, Yamamoto T. Hidradenitis suppurativa and multiple dermatofibromas in a patient with ulcerative colitis.
J Dermatol. 2013 Dec. 40 (12):1071-2. [Medline].

43. Bachmeyer C, Cordier F, Blum L, Cazier A, Vérola O, Aractingi S. Multiple eruptive dermatofibromas after highly active
antiretroviral therapy. Br J Dermatol. 2000 Dec. 143(6):1336-7. [Medline].

https://emedicine.medscape.com/article/1056742-print Page 13 of 17
 07/05/20 22.02

44. Santos-Juanes J, Coto-Segura P, Mallo S, Galache C, Soto J. Multiple eruptive dermatofibromas in a patient receiving
efalizumab. Dermatology. 2008. 216(4):363. [Medline].

45. Caldarola G, Bisceglia M, Pellicano R. Multiple eruptive plaque-like dermatofibromas during anti-TNFa treatment. Int J
Dermatol. 2013 May. 52(5):638-41. [Medline].

46. Llamas-Velasco M, Fraga J, Solano-López GE, Steegmann JL, García Diez A, Requena L. Multiple eruptive
dermatofibromas related to imatinib treatment. J Eur Acad Dermatol Venereol. 2014 Jul. 28 (7):979-81. [Medline].

47. Finch J, Berke A, McCusker M, Chang MW. Congenital Multiple Clustered Dermatofibroma in a 12-Year-Old Girl. Pediatr
Dermatol. 2011 Dec 30. [Medline].

48. Gershtenson PC, Krunic AL, Chen HM. Multiple clustered dermatofibroma: case report and review of the literature. J Cutan
Pathol. 2010 Sep. 37(9):e42-5. [Medline].

49. Fitzpatrick TB, Gilchrest BA. Dimple sign to differentiate benign from malignant pigmented cutaneous lesions. N Engl J Med.
1977 Jun 30. 296(26):1518. [Medline].

50. Lookingbill DP. A malignant dimple. N Engl J Med. 1977 Oct 13. 297(15):841-2. [Medline].

51. Meffert JJ, Peake MF, Wilde JL. Dimpling' is not unique to dermatofibromas. Dermatology. 1997. 195(4):384-6. [Medline].

52. Requena L, Farina MC, Fuente C, et al. Giant dermatofibroma. A little-known clinical variant of dermatofibroma. J Am Acad
Dermatol. 1994 May. 30(5 Pt 1):714-8. [Medline].

53. Ohnishi T, Sasaki M, Nakai K, Watanabe S. Atrophic dermatofibroma. J Eur Acad Dermatol Venereol. 2004 Sep. 18(5):580-
3. [Medline].

54. Kai H, Fujita H, Yamamoto M, Asahina A. Letter: Polypoid dermatofibroma with a slim pedicle: A case report. Dermatol
Online J. 2012 Mar 15. 18(3):16. [Medline].

55. Curco N, Jucgla A, Bordas X, Moreno A. Dermatofibroma with spreading satellitosis. J Am Acad Dermatol. 1992 Dec. 27(6
Pt 1):1017-9. [Medline].

56. Kalsi H, Rahman A, Harbol T, Sidhu J. Giant Hemosiderotic Dermatofibroma: The Largest Giant Dermatofibroma Reported to
Date. Am J Dermatopathol. 2015 Oct. 37 (10):778-82. [Medline].

57. Bhabha FK, Magee J, Ng SY, Grills CE, Su J, Orchard D. Multiple clustered dermatofibroma presenting in a segmental
distribution. Australas J Dermatol. 2016 Feb. 57 (1):e20-2. [Medline].

58. Schofield C, Weedon D, Kumar S. Dermatofibroma and halo dermatitis. Australas J Dermatol. 2012 May. 53(2):145-7.
[Medline].

59. Wortsman X, Wortsman J. Clinical usefulness of variable-frequency ultrasound in localized lesions of the skin. J Am Acad
Dermatol. 2010 Feb. 62(2):247-56. [Medline].

60. Picard A, Long-Mira E, Chuah SY, Passeron T, Lacour JP, Bahadoran P. Interest of high-definition optical coherent
tomography (HD-OCT) for non-invasive imaging of dermatofibroma: a pilot study. J Eur Acad Dermatol Venereol. 2016 Mar.
30 (3):485-7. [Medline].

61. Demir MK, Ozdemir H, Genchallaç H, Altaner S, Kartal O. Dermatofibroma mimicking malignancy on integrated F-18
fluorodeoxyglucose PET-CT. Diagn Interv Radiol. 2009 Mar. 15(1):61-3. [Medline].

62. Zaballos P, Puig S, Llambrich A, Malvehy J. Dermoscopy of dermatofibromas: a prospective morphological study of 412
cases. Arch Dermatol. 2008 Jan. 144(1):75-83. [Medline].

63. Cavicchini S, Tourlaki A, Tanzi C, Alessi E. Dermoscopy of solitary yellow lesions in adults. Arch Dermatol. 2008 Oct.
144(10):1412. [Medline].

64. Roldán-Marín R, Barreiro-Capurro A, García-Herrera A, Puig S, Alarcón-Salazar I, Carrera C, et al. Green colour as a novel
dermoscopic finding in the diagnosis of haemosiderotic dermatofibroma. Australas J Dermatol. 2013 Jul 19. [Medline].

65. Ferrari A, Argenziano G, Buccini P, Cota C, Sperduti I, De Simone P, et al. Typical and atypical dermoscopic presentations of
dermatofibroma. J Eur Acad Dermatol Venereol. 2013 Nov. 27(11):1375-80. [Medline].

66. Pereira Guedes RV, Noronha de Menezes NM, Leite IB, Baptista MA. Benign fibrous histiocytoma: Particular aspects on
confocal laser scanning microscopy. Eur J Dermatol. 2012 Mar-Apr. 22(2):288-9. [Medline].

https://emedicine.medscape.com/article/1056742-print Page 14 of 17
 07/05/20 22.02

67. Kideryova L, Lacina L, Dvorankova B, et al. Phenotypic characterization of human keratinocytes in coculture reveals
differential effects of fibroblasts from benign fibrous histiocytoma (dermatofibroma) as compared to cells from its malignant
form and to normal fibroblasts. J Dermatol Sci. 2009 Jul. 55(1):18-26. [Medline].

68. Nair V, Weinreb I, MacNeil N, Szollosi Z, Chetty R, Ghazarian D. A unique biphasic variant of cutaneous fibrous histiocytoma
with a storiform pattern and intralesional pigmented melanocytes: "storiform melano-fibrous histiocytoma". Eur J Dermatol.
2008 May-Jun. 18(3):332-6. [Medline].

69. Wick MR, Ritter JH, Lind AC, Swanson PE. The pathological distinction between "deep penetrating" dermatofibroma and
dermatofibrosarcoma protuberans. Semin Cutan Med Surg. 1999 Mar. 18(1):91-8. [Medline].

70. Goldblum JR, Tuthill RJ. CD34 and factor-XIIIa immunoreactivity in dermatofibrosarcoma protuberans and dermatofibroma.
Am J Dermatopathol. 1997 Apr. 19(2):147-53. [Medline].

71. Volpicelli ER, Fletcher CD. Desmin and CD34 positivity in cellular fibrous histiocytoma: an immunohistochemical analysis of
100 cases. J Cutan Pathol. 2012 Aug. 39 (8):747-52. [Medline].

72. John AM, Holahan HH, Singh P, Handler MZ, Lambert WC. When Immunohistochemistry Deceives Us: The Pitfalls of CD34
and Factor XIIIa Stains in Dermatofibroma and Dermatofibrosarcoma Protuberans. Skinmed. 2017. 15 (1):53-55. [Medline].

73. Borucki R, Perry DM, Lopez-Garcia DR, Kazlouskaya V, Elston DM. Fluorescence microscopy for the evaluation of elastic
tissue patterns within fibrous proliferations of the skin on hematoxylin-eosin-stained slides. J Am Acad Dermatol. 2018 Jan 5.
[Medline].

74. Kim HJ, Lee JY, Kim SH, et al. Stromelysin-3 expression in the differential diagnosis of dermatofibroma and
dermatofibrosarcoma protuberans: comparison with factor XIIIa and CD34. Br J Dermatol. 2007 Aug. 157(2):319-24.
[Medline].

75. Maekawa T, Jinnin M, Ihn H. The expression levels of thrombospondin-1 in dermatofibroma and dermatofibrosarcoma
protuberans. Eur J Dermatol. 2011 Jul-Aug. 21(4):534-8. [Medline].

76. Li J, Yu Y, Yang Y, Wang L, Cao J, Liang X, et al. IGFBP7, a novel immunohistochemical marker in differentiating
dermatofibroma from dermatofibrosarcoma protuberans. J Eur Acad Dermatol Venereol. 2012 Mar. 26(3):382-5. [Medline].

77. Mori T, Misago N, Yamamoto O, Toda S, Narisawa Y. Expression of nestin in dermatofibrosarcoma protuberans in
comparison to dermatofibroma. J Dermatol. 2008 Jul. 35(7):419-25. [Medline].

78. Wang L, Xiang YN, Zhang YH, Tu YT, Chen HX. Collagen triple helix repeat containing-1 in the differential diagnosis of
dermatofibrosarcoma protuberans and dermatofibroma. Br J Dermatol. 2011 Jan. 164(1):135-40. [Medline].

79. Bandarchi B, Ma L, Marginean C, Hafezi S, Zubovits J, Rasty G. D2-40, a novel immunohistochemical marker in
differentiating dermatofibroma from dermatofibrosarcoma protuberans. Mod Pathol. 2010 Mar. 23(3):434-8. [Medline].

80. Yan X, Takahara M, Xie L, Tu Y, Furue M. Cathepsin K expression: a useful marker for the differential diagnosis of
dermatofibroma and dermatofibrosarcoma protuberans. Histopathology. 2010 Sep. 57(3):486-8. [Medline].

81. Toyozawa S, Yamamoto Y, Ishida Y, Kondo T, Nakamura Y, Furukawa F. Immunohistochemical analysis of CXCR4
expression in fibrohistiocytic tumors. Acta Histochem Cytochem. 2010 May 1. 43(2):45-50. [Medline]. [Full Text].

82. Horenstein MG, Prieto VG, Nuckols JD, Burchette JL, Shea CR. Indeterminate fibrohistiocytic lesions of the skin: is there a
spectrum between dermatofibroma and dermatofibrosarcoma protuberans?. Am J Surg Pathol. 2000 Jul. 24(7):996-1003.
[Medline].

83. Wang WL, Patel KU, Coleman NM, et al. COL1A1:PDGFB chimeric transcripts are not present in indeterminate
fibrohistiocytic lesions of the skin. Am J Dermatopathol. 2010 Apr. 32(2):149-53. [Medline].

84. Ishigami T, Hida Y, Matsudate Y, Murao K, Kubo Y. The involvement of fibroblast growth factor receptor signaling pathways in
dermatofibroma and dermatofibrosarcoma protuberans. J Med Invest. 2013. 60(1-2):106-13. [Medline].

85. Kazlouskaya V, Malhotra S, Kabigting FD, Lal K, Elston DM. CD99 expression in dermatofibrosarcoma protuberans and
dermatofibroma. Am J Dermatopathol. 2014 May. 36(5):392-6. [Medline].

86. Mentzel T. Cutaneous mesenchymal tumours: an update. Pathology. 2014 Feb. 46(2):149-59. [Medline].

87. West KL, Cardona DM, Su Z, Puri PK. Immunohistochemical markers in fibrohistiocytic lesions: factor XIIIa, CD34, S-100
and p75. Am J Dermatopathol. 2014 May. 36(5):414-9. [Medline].

88. Mikoshiba Y, Ogawa E, Uchiyama R, Uchiyama A, Uhara H, Okuyama R. 5-Hydroxymethylcytosine is a useful marker to

https://emedicine.medscape.com/article/1056742-print Page 15 of 17
 07/05/20 22.02

differentiate between dermatofibrosarcoma protuberans and dermatofibroma. J Eur Acad Dermatol Venereol. 2016 Jan. 30
(1):130-1. [Medline].

89. Karanian M, Pérot G, Coindre JM, Chibon F, Pedeutour F, Neuville A. Fluorescence in situ hybridization analysis is a helpful
test for the diagnosis of dermatofibrosarcoma protuberans. Mod Pathol. 2015 Feb. 28 (2):230-7. [Medline].

90. Kaur H, Kaur J, Gill KS, Mannan R, Arora S. Subcutaneous dermatofibroma: a rare case report with review of literature. J
Clin Diagn Res. 2014 Apr. 8 (4):FD01-2. [Medline].

91. Zelger BG, Zelger B. [Dermatofibroma. A clinico-pathologic classification scheme]. Pathologe. 1998 Nov. 19(6):412-9.
[Medline].

92. Deguchi M, Aiba S. Cholesterotic Fibrous Histiocytoma in a Patient with Metabolic Syndrome. Case Rep Dermatol. 2017
May-Aug. 9 (2):136-140. [Medline].

93. Zelger BG, Sidoroff A, Zelger B. Combined dermatofibroma: co-existence of two or more variant patterns in a single lesion.
Histopathology. 2000 Jun. 36(6):529-39. [Medline].

94. Gonzalez-Vela MC, Val-Bernal JF, Martino M, Gonzalez-Lopez MA, Garcia-Alberdi E, Hermana S. Sclerotic fibroma-like
dermatofibroma: an uncommon distinctive variant of dermatofibroma. Histol Histopathol. 2005 Jul. 20(3):801-6. [Medline].

95. Alves JV, Matos DM, Barreiros HF, Bártolo EA. Variants of dermatofibroma - a histopathological study. An Bras Dermatol.
2014 Jun. 89(3):472-7. [Medline]. [Full Text].

96. McCalmont TH. Everything you wanted to know about dermatofibroma but were afraid to ask. J Cutan Pathol. 2014 Jan.
41(1):5-8. [Medline].

97. de Feraudy S, Mar N, McCalmont TH. Evaluation of CD10 and procollagen 1 expression in atypical fibroxanthoma and
dermatofibroma. Am J Surg Pathol. 2008 Aug. 32(8):1111-22. [Medline].

98. Sanchez Yus E, Soria L, de Eusebio E, Requena L. Lichenoid, erosive and ulcerated dermatofibromas. Three additional
clinico-pathologic variants. J Cutan Pathol. 2000 Mar. 27(3):112-7. [Medline].

99. Aiba S, Terui T, Tagami H. Dermatofibroma with diffuse eosinophilic infiltrate. Am J Dermatopathol. 2000 Jun. 22(3):281-4.
[Medline].

100. Aydin E, Vardareli OS, Bilezikci B, Ozgirgin ON. [Dermatofibroma accompanied by perforating dermatosis in the auricle: a
case report]. Kulak Burun Bogaz Ihtis Derg. 2005. 15(3-4):83-6. [Medline].

101. Kim EJ, Park HS, Yoon HS, Cho S. A case of perforating dermatofibroma with floret-like giant cells. Clin Exp Dermatol. 2015
Apr. 40 (3):305-8. [Medline].

102. Fuciarelli K, Cohen PR. Sebaceous hyperplasia: a clue to the diagnosis of dermatofibroma. J Am Acad Dermatol. 2001 Jan.
44(1):94-5. [Medline].

103. Spaun E, Zelger B. Dermatofibroma with intracytoplasmic eosinophilic globules: an unusual phenomenon. J Cutan Pathol.
2009 Jul. 36(7):796-8. [Medline].

104. Garrido-Ruiz MC, Carrillo R, Enguita AB, Peralto JL. Signet-ring cell dermatofibroma. Am J Dermatopathol. 2009 Feb.
31(1):84-7. [Medline].

105. Quigley BC, Ricciuti J, Morgan MB. Amyloid Light Chain Deposition Associated with Dermatofibroma: Serendipity or
Association?. Am J Dermatopathol. 2010 Jan 23. [Medline].

106. Yamamoto T. Incidental acantholysis of the overlying epidermis of dermatofibroma. J Eur Acad Dermatol Venereol. 2009 Jun.
23(6):735-6. [Medline].

107. Gonzalez S. Regarding the case report of Dr Phillip W. Allen on apocrine gland cyst with hemosiderotic dermatofibroma. Adv
Anat Pathol. 2008 Nov. 15(6):376; author reply 376. [Medline].

108. Santos-Briz A, Llamas-Velasco M, Arango L, Yuste M, Paredes BE, Kutzner H. Cutaneous adenodermatofibroma: report of 2
cases. Am J Dermatopathol. 2013 Aug. 35(6):e103-5. [Medline].

109. Kanitakis J. Keloidal dermatofibroma: report of a rare dermatofibroma variant in a young white woman. Am J Dermatopathol.
2013 May. 35(3):400-1. [Medline].

110. Schnebelen AM, Brown JA, Cheung WL, Hiatt KM, Smoller BR. Collapsing angiokeloidal dermatofibroma. Am J
Dermatopathol. 2012 Oct. 34(7):e103-5. [Medline].

https://emedicine.medscape.com/article/1056742-print Page 16 of 17
 07/05/20 22.02

111. Famenini S, Cassarino DS. Dermatofibroma-associated dystrophic calcification. J Cutan Pathol. 2014 Jan. 41(1):68-70.
[Medline].

112. Baderca F, Mates I, Solovan C. Unusual variant of blue nevus associated with dermatofibromas. Rom J Morphol Embryol.
2013. 54(2):413-7. [Medline].

113. Maughan C, Kolker S, Markus B, Young J. Leukemia cutis coexisting with dermatofibroma as the initial presentation of B-cell
chronic lymphocytic leukemia/small lymphocytic lymphoma. Am J Dermatopathol. 2014 Jan. 36(1):e14-5. [Medline].

114. Morcos SM, Girardi M, Subtil A, Wilson LD, Cowper SE. Mycosis fungoides exhibiting features of a dermatofibroma: a case
report and review of the literature. J Cutan Pathol. 2012 Jan. 39(1):40-6. [Medline].

115. Zeidi M, North JP. Sebaceous induction in dermatofibroma: a common feature of dermatofibromas on the shoulder. J Cutan
Pathol. 2015 Jun. 42 (6):400-5. [Medline].

116. King R, Googe PB, Page RN, Mihm MC Jr. Melanocytic lesions associated with dermatofibromas: a spectrum of lesions
ranging from junctional nevus to malignant melanoma in situ. Mod Pathol. 2005 Aug. 18(8):1043-7. [Medline].

117. Shin J, Vincent JG, Cuda JD, Xu H, Kang S, Kim J, et al. Sox10 is expressed in primary melanocytic neoplasms of various
histologies but not in fibrohistiocytic proliferations and histiocytoses. J Am Acad Dermatol. 2012 Oct. 67(4):717-26. [Medline].

118. Kovach BT, Boyd AS. Melanoma associated with a dermatofibroma. J Cutan Pathol. 2007 May. 34(5):420-2. [Medline].

119. Orrock JM, Abbott JJ, Gibson LE, Folpe AL. INI1 and GLUT-1 expression in epithelioid sarcoma and its cutaneous neoplastic
and nonneoplastic mimics. Am J Dermatopathol. 2009 Apr. 31(2):152-6. [Medline].

120. Kim HJ, Kim IH. A 3-mm margin completely removes dermatofibromas: a study of 151 cases. Dermatol Surg. 2015 Feb. 41
(2):283-6. [Medline].

121. Halim K, Karia PS, Schmults CD. Aneurysmal dermatofibroma successfully treated with Mohs micrographic surgery.
Dermatol Surg. 2015 Jan. 41 (1):168-70. [Medline].

122. Weber PJ, Moody BR, Foster JA. Inverted pyramidal biopsy. Dermatol Surg. 2001 Jul. 27(7):681-4. [Medline].

123. Krupa Shankar DS, Kushalappa AA, Suma KS, Pai SA. Multiple dermatofibromas on face treated with carbon dioxide laser.
Indian J Dermatol Venereol Leprol. 2007 May-Jun. 73(3):194-5. [Medline].

124. Alonso-Castro L, Boixeda P, Segura-Palacios JM, de Daniel-Rodríguez C, Jiménez-Gómez N, Ballester-Martínez A.

Dermatofibromas treated with pulsed dye laser: Clinical and dermoscopic outcomes. J Cosmet Laser Ther. 2012 Apr.
14(2):98-101. [Medline].

https://emedicine.medscape.com/article/1056742-print Page 17 of 17