Anatomic Pathology / RB1 Status in SFT

Solitary Fibrous Tumor

Is There a Molecular Relationship With Cellular Angiofibroma,
Spindle Cell Lipoma, and Mammary-Type Myofibroblastoma?
Karen J. Fritchie, MD,1 Paula Carver, MS,2 Yang Sun,3 Galina Batiouchko, MD,3
Steven D. Billings, MD,2,3 Brian P. Rubin, MD, PhD,2,3 Raymond R. Tubbs, DO,2,3
and John R. Goldblum, MD2,3

DOI: 10.1309/AJCPQEG6YNN6CNAL

Upon completion of this activity you will be able to:

describe the clinicopathologic features of solitary fibrous tumor.
compare and contrast the clinicopathologic features of cellular
angiofibroma, mammary-type myofibroblastoma, and spindle cell
lipoma.
discuss the genetic link among cellular angiofibroma, mammary-type
myofibroblastoma, and spindle cell lipoma.

Abstract
Solitary fibrous tumor (SFT) is a mesenchymal
tumor characterized by ovoid cells, branching
blood vessels, stromal hyalinization, and CD34
immunoreactivity. Studies have shown loss of 13q
in a group of morphologically similar entities,
including cellular angiofibroma, mammary-type
myofibroblastoma, and spindle cell lipoma. The
histologic and immunophenotypic overlap between
SFT and the latter group of tumors suggests that these
tumors may be genetically linked.
We tested a group of 40 SFTs to assess for loss
of RB1 (13q14) by fluorescence in situ hybridization
(FISH). All 38 SFTs with evaluable signals failed
to show loss of RB1 (13q14) by FISH. All cases of
cellular angiofibroma (1/1), spindle cell lipoma (6/6),
and mammary-type myofibroblastoma (4/4), which
were used as a control group, showed monoallelic or
biallelic loss of RB1.
The absence of RB1 loss in SFTs suggests that they
are not related to cellular angiofibroma, mammarytype myofibroblastoma, or spindle cell lipoma.

The ASCP is accredited by the Accreditation Council for Continuing

Medical Education to provide continuing medical education for physicians.
The ASCP designates this journal-based CME activity for a maximum of 1
AMA PRA Category 1 Credit per article. Physicians should claim only the
credit commensurate with the extent of their participation in the activity.
This activity qualifies as an American Board of Pathology Maintenance of
Certification Part II Self-Assessment Module.
The authors of this article and the planning committee members and staff
have no relevant financial relationships with commercial interests to disclose.
Questions appear on p 1010. Exam is located at www.ascp.org/ajcpcme.

The entity now known as solitary fibrous tumor (SFT)

was first described by Stout and Murray1 in 1942 as a soft
tissue tumor characterized by cells surrounding thick-walled,
branching staghorn blood vessels. The lesional cells were
thought to be derived from pericytes, and the term hemangiopericytoma was introduced. Although SFT was first recognized as a distinct pleural-based entity in 1931, it has subsequently been described in a variety of extrapleural sites.2 As
the morphologic overlap between SFT and hemangiopericytoma was acknowledged, there was a shift toward favoring the
term solitary fibrous tumor to encompass these histologically
similar entities.3 Although the line of differentiation of SFT
remains uncertain, there is some evidence to support fibroblastic/myofibroblastic origin.4,5 Regardless, it is accepted
that the neoplastic cells are not derived from pericytes, and the
term hemangiopericytoma is best thought of as a descriptive
term rather than a diagnostic entity.
Recent work has shown that cellular angiofibroma harbors a monoallelic deletion of RB1, suggesting a genetic
link between cellular angiofibroma, spindle cell lipoma,
and mammary-type myofibroblastoma.6 While this group of
tumors varies in clinical manifestations, all tumors share similar morphologic features and are characterized by bland ovoid
to spindle-shaped cells with wispy collagen, variably sized
thick-walled blood vessels, and immunoreactivity to CD34,
similar to what is seen in classic SFT. Given the morphologic
overlap of these entities, we tested a group of 40 SFTs and
malignant SFTs to assess for loss of RB1 by fluorescence in
situ hybridization (FISH).

American Society for Clinical Pathology

Am J Clin Pathol 2012;137:963-970

963

DOI: 10.1309/AJCPQEG6YNN6CNAL

963
963

CME/SAM

Key Words: Solitary fibrous tumor; RB1; Fluorescence in situ hybridization; FISH

Fritchie et al / RB1 Status in SFT

Materials and Methods

Case Selection
A total of 33 cases of SFT and 7 cases of malignant
SFT with available formalin-fixed, paraffin-embedded tissue were selected from the Cleveland Clinic (Cleveland,
OH) Anatomic Pathology database from January 1, 2000, to
April 1, 2011. Cases classified as SFTs consisted of CD34+,
ovoid-spindle-shaped cells admixed with variable amounts
of hyalinized stroma and branching, staghorn-type blood
vessels. While criteria for malignancy vary throughout the
literature, we considered a tumor to be malignant if greater
than 4 mitotic figures per 10 high-power fields (HPFs) were
identified or the tumor exhibited significant nuclear pleomorphism, necrosis, or areas of increased cellularity.3,4,7,8
In addition, 1 case of cellular angiofibroma, 6 cases of
spindle cell lipoma, and 4 cases of mammary-type myofibroblastoma with formalin-fixed, paraffin-embedded tissue
were selected from the Cleveland Clinic Anatomic Pathology database. This group of tumors was characterized by
bland, variably CD34+ cells. Spindle cell lipomas typically
contained a lipomatous component and thick bundles of
eosinophilic collagen and were located in the upper back,
shoulder, and neck region. The diagnosis of cellular angiofibroma was considered if the tumor was located in the
inguinal or vulvovaginal region and was highly vascular.
Mammary-type myofibroblastomas arose at mammary and
extramammary locations and expressed varying amounts of
myogenic markers.
Tissue Microarrays
Two tissue microarrays (TMAs) containing the 40 SFTs
and malignant SFTs were designed. A third TMA containing the cases of cellular angiofibroma, spindle cell lipoma,
and mammary-type myofibroblastoma was also created. For
each case, the area with the most representative histologic
features was selected from the tissue block. The cylindrical tissue samples (2 mm) were cored from the previously
described areas in the blocks and extruded into the recipient
array blocks using a manual tissue microarrayer (TMArrayer,
Pathology Devices, Westminster, MD).
FISH Analysis
FISH studies for the detection of RB1 were carried out
on interphase nuclei present on formalin-fixed, paraffinembedded tissue sections as reported previously.9 A directly
labeled SpectrumOrange DNA LSI (13q14; Rb locus; Vysis,
Downers Grove, IL) probe was used for the assessment
of chromosome 13 loss, while a directly labeled SpectrumGreen chromosome 8 enumeration DNA probe (CEP8;
Vysis) was used as the control because an alphacentromeric
chromosome 13 enumeration probe was not available. Only
964
964

Am J Clin Pathol 2012;137:963-970

DOI: 10.1309/AJCPQEG6YNN6CNAL

nuclei with at least 2 CEP8 signals were counted. A qualitative review was performed, with RB1 loss based on the loss
of RB1 in at least 20% of the cells.

Results
We identified 33 cases of SFT and 7 cases of malignant
SFT. Of the patients represented, 21 were men and 19 were
women. The ages of patients ranged from 31 to 78 years
(mean, 56.4 years). The tumors occurred in a variety of
thoracic and extrathoracic locations. Histologic examination
revealed variably cellular neoplasms composed of spindled
to ovoid-shaped cells. In 25 of the 40 tumors, a prominent
hemangiopericytoma-like vascular pattern could be identified at least focally Image 1A, while the blood vessels were
less conspicuous in the remaining tumors. Stromal hyalinization and thick bands of eosinophilic collagen were present in 29 of the lesions Image 1B. Four tumors displayed
lipomatous differentiation Image 1C.
A subset of the SFTs in this study showed features that
have been associated with aggressive behavior, including
increased mitotic activity, increased cellularity, cytologic
atypia, and necrosis Image 2.3,4,7,10 Specifically, 5 of the
tumors exhibited a focal increase in cellularity, and 4 tumors
were diffusely hypercellular. Of the tumors, 6 showed mild
cytologic atypia, 7 showed moderate cytologic atypia, and
4 showed severe nuclear atypia. In 7 tumors, there was
necrosis ranging from 5% to 75% of the tumor (mean, 26%).
The mitotic rate of the tumors ranged from 0 to 20 mitotic
figures/10 HPFs (mean, 2.7 mitotic figures/10 HPFs). Based
on these histologic features, 7 tumors were classified as
malignant SFTs.
Immunohistochemical staining for CD34 was performed in 29 of the 40 cases. In 28 of 29 cases, CD34 was
diffusely positive in the neoplastic cells Image 1D. In the
remaining case, CD34 staining was focal. A variety of other
immunohistochemical stains were performed in a proportion
of the cases, including cytokeratins, smooth muscle actin,
desmin, S-100, HMB45, Melan A, CD31, and bcl-2. In the
2 cases in which it was applied, bcl-2 was positive; all the
other markers were negative.
Follow-up was available for 38 of 40 patients, ranging
from 0.5 to 132 months (average, 35.7 months). One patient
had lymph node metastasis at diagnosis. In the remainder of
patients, 26 had 12 or more months of follow-up. No recurrences or distant metastases were reported.
FISH analysis in 31 cases of SFT and 7 cases of
malignant SFT failed to show loss of RB1 Image 3A. Two
cases of SFT had too few FISH signals and could not be
evaluated. The case of cellular angiofibroma showed biallelic loss of RB1. Of the 6 cases of spindle cell lipoma, 5
American Society for Clinical Pathology

Anatomic Pathology / Original Article

Image 1 Morphologic and immunophenotypic features of solitary fibrous tumor. A, Ovoid to spindle-shaped cells surround
ectatic branching staghorn blood vessels. Variable amounts of stromal hyalinization (B) and adipocytic differentiation (C) are
present. D, The lesional cells are strongly positive for CD34 (A-D, 100).

showed monoallelic loss of RB1 Image 3B, and the sixth

case showed biallelic loss. Of the 4 cases of mammary-type
myofibroblastoma, 3 showed monoallelic loss of RB1, and
the fourth case showed biallelic loss. The clinicopathologic
features of tumors are summarized in Table 1.The results
of the FISH studies are summarized in Table 2.

Discussion
Spindle cell lipoma was first described by Enzinger
and Harvey11 in 1975 as a lipomatous tumor with a marked
predilection for the shoulder and posterior neck region of

middle-aged to elderly men. Although pleomorphic lipoma

was initially thought to represent a separate entity, it is now
accepted that both of these tumors are part of a spectrum
of neoplasms characterized by similar clinical, morphologic, and genetic features.12,13 Morphologically, spindle
cell/pleomorphic lipoma typically contains 3 components:
mature adipose tissue; spindle cells arranged in short, parallel bundles; and ropy birefringent collagen Image 4A. The
proportions of these components may vary, and some tumors
may have little or no fat.3,14 These tumors show strong staining for CD34.15,16
Myofibroblastoma was first described by Wargotz et
17
al in 1987 as a distinct stromal tumor of the breast, even

American Society for Clinical Pathology

Am J Clin Pathol 2012;137:963-970

965

DOI: 10.1309/AJCPQEG6YNN6CNAL

965
965

Fritchie et al / RB1 Status in SFT

Image 2 Some cases of solitary fibrous tumor showed histologic features of malignancy, including increased cellularity (A,
H&E, 40), increased mitotic activity (B, H&E, 200), cytologic atypia (C, H&E, 400), and necrosis (D, H&E, 100).
A

Image 3 A, Fluorescence in situ hybridization (FISH) analysis of a solitary fibrous tumor from the lung of a 58-year-old woman.
Loss of RB1 was not observed. B, FISH analysis of a spindle cell lipoma from the scapula of a 38-year-old man showing
monoallelic RB1 loss.
966
966

Am J Clin Pathol 2012;137:963-970

DOI: 10.1309/AJCPQEG6YNN6CNAL

American Society for Clinical Pathology

Anatomic Pathology / Original Article

Table 1
Clinicopathologic Features of Tumors Analyzed
Diagnosis/Case No./
Sex/Age (y)
SFT
1/M/49
2/F/45
3/M/30
4/M/67
5/F/47
6/F/45
7/F/56
8/M/61
9/F/36
10/F/54
11/M/76
12/M/57
13/F/31
14/F/34
15/M/45
16/F/71
17/M/45
18/M/61
19/F/53
20/F/63
21/F/55
22/M/64
23/F/38
24/M/69
25/F/66
26/M/63
27/F/56
28/F/54
29/F/52
30/M/58
31/M/61
32/M/75
33/M/73
Malignant SFT
34/F/66
35/M/77
36/M/78
37/M/54
38/M/54
39/M/61
40/F/54
Cellular angiofibroma
41/M/64
Myofibroblastoma
42/F/53
43/F/53
44/M/59
45/F/57
Spindle cell lipoma
46/M/70
47/M/57
48/M/61
49/M/87
50/M/38
51/M/70

Site

Size
(cm)

CD34
Immunoreactivity

FISH
Results

Outcome (Follow-up, mo)

Pancreas
Omentum
Thigh
Pelvis
Lip
Hip
Chest
Lung/pleura
Lung
Parotid
Retroperitoneum
Lung
Lung
Pleura
Lung
Lung
Thigh
Pleura
Pleura
Pleura
Kidney
Lung
Chest wall
Parotid
Pleura
Pleura
Lung
Mediastinum
Lung
Colon
Perineum
Parotid
Rib

3.4
3
6.8
4
1.2
15
8
3.5
4.4
1.5
8.3
8
5
20
6
8
9
4
9
7
2.1
1.3
6.2
5.3
5.5
3
4
9
3.2
8.5
8
2
4.2

Positive
ND
Positive
Positive
Positive
ND
Positive
Positive
Positive
Positive
ND
Positive
Positive
Positive
ND
Positive
Positive
ND
ND
ND
Positive
Positive
Positive
Positive
ND
Positive
Positive
Positive
Positive
ND
Positive
Positive
Positive

NE
NL
NL
NL
NE
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL
NL

NER (132)
NA
NER (78)
NER (104)
NER (97)
NER (12)
NER (0.5)
NER (81)
NER (64)
NER (0.5)
NER (26)
NER (64)
NER (36)
NER (51)
NER (19)
NER (17)
NER (17)
NER (41)
NER (41)
NER (64)
NER (39)
NER (36)
NER (37)
NER (30)
NER (33)
NER (6)
NER (22)
NA
NER (1.5)
NER (0.5)
NER (9)
NER (4)
NER (3)

Orbit
Pleura
Pleura/chest mass
Pelvis
Chest
Pelvis
Mediastinum/pleura

3.1
17
26
13
11.5
24
19

Positive
ND
ND
Focally positive
Positive
Positive
Positive

NL
NL
NL
NL
NL
NL
NL

NER (47)
NER (119)
NER (0.5)
Lymph node metastasis at diagnosis (2)
NER (20)
NER (1)
NER (1.5)

Inguinal region

11

Positive

BL

NED (27)

Breast
Ischiorectal fossa
Breast
Vulva

1
4.8
NK
5

ND
Negative
Positive
Focally positive

ML
BL
ML
ML

NED (108)
NED (89)
NED (27)
NED (40)

Posterior part of neck

Back
Scapular region
Back of neck
Scapular region
Upper part of back

4
2.2
12
4
1.5
3.1

ND
ND
ND
Positive
ND
ND

ML
BL
ML
ML
ML
ML

NED (39)
NED (34)
NED (27)
NED (16)
NED (10)
NED (12)

BL, biallelic loss of RB1; FISH, fluorescence in situ hybridization; ML, monoallelic loss of RB1; NA, not available; ND, not done; NE, too few FISH signals for evaluation;
NED, no evidence of disease; NER, no evidence of recurrence; NK, not known; NL, no loss of RB1; SFT, solitary fibrous tumor.

though similar lesions had been reported earlier as spindle

cell tumor of the breast.18,19 More recently, these tumors
have been noted at extramammary sites as well, and the
term mammary-type myofibroblastoma is often used when
referring to this group of tumors.20 While earlier studies

reported a male predominance, this tumor may also occur

in female patients.3,17,20 Gross examination of mammarytype myofibroblastoma shows a nodular, well circumscribed
mass, while microscopic examination typically reveals
uniform, slender spindle cells with morphologic features of

American Society for Clinical Pathology

Am J Clin Pathol 2012;137:963-970

967

DOI: 10.1309/AJCPQEG6YNN6CNAL

967
967

Fritchie et al / RB1 Status in SFT

Table 2
Results of FISH Studies

Diagnosis
SFT
Malignant SFT
Cellular angiofibroma
Spindle cell lipoma
Mammary-type
myofibroblastoma

No. of Cases
With Evaluable
FISH Signal

No. (%) of Cases With

Monoallelic or Biallelic
Loss of RB1

31
7
1
6
4

0 (0)
0 (0)
1 (100)
6 (100)
4 (100)

FISH, fluorescence in situ hybridization; SFT, solitary fibrous tumor.

myofibroblasts admixed with broad bands of hyalinized collagen Image 4B.17 Hyalinized blood vessels can be found in
some tumors but are not usually a prominent feature. Mature
fat may also be found within these lesions.17,20 These tumors
variably express CD34, desmin, and actin.3,17,20
Cellular angiofibroma is a mesenchymal neoplasm that
was initially described by Nucci et al21 in 1997 and usually
involves the vulvovaginal region of middle-aged women or
inguinoscrotal region of adult men.22 These tumors are typically well circumscribed with a multilobulated gross appearance.22 Microscopically, cellular angiofibroma is composed of

Image 4 Representative images of spindle cell lipoma, mammary-type myofibroblastoma, and cellular angiofibroma. A,
Spindle cell lipoma consists of uniform spindle cells, mature adipose tissue, and ropy collagen (H&E, 100). B, Mammary-type
myofibroblastoma exhibits similar morphologic features, including bland spindled cells and fat and thick bands of collagen (H&E,
200). C, Images of cellular angiofibroma also show a similar spindle cell population surrounding thick-walled hyalinized blood
vessels (H&E, 100). D, The lesional cells exhibit variable immunoreactivity for CD34 (100).

968
968

Am J Clin Pathol 2012;137:963-970

DOI: 10.1309/AJCPQEG6YNN6CNAL

American Society for Clinical Pathology

Anatomic Pathology / Original Article

short spindle cells in an edematous or fibrous stroma admixed

with small to medium-sized, thick-walled, and often hyalinized
blood vessels Image 4C.21,22 Short bundles of collagen are
often identified, and a subset of tumors contain mature adipose
tissue as individual adipocytes or larger lobules of fat.22 These
tumors may express CD34 Image 4D with variable amounts
of smooth muscle actin and desmin.3,6,21,22
In 1994, Mandahl and colleagues13 studied a group of
spindle cell and pleomorphic lipomas and showed an association with monosomy 16 or loss of 16q. Most of the tumors
also showed monosomy 13 or partial loss of 13q. Dal Cin
and coworkers23 subsequently showed that aberrations of
chromosome 13 may occur independently from deletion of
16q. The morphologic link between mammary-type myofibroblastoma and spindle cell lipoma was acknowledged
early on by Chan et al18 and Toker et al.19 The genetic
relationship of these 2 entities was confirmed by Pauwels
et al24 in 2000 when they described 2 cases of myofibroblastoma, both of which showed partial monosomy 13q.
Subsequently, Maggiani et al25 showed losses of RB/13q14
and FKHR/13q14 loci within an extramammary-type myofibroblastoma, providing further evidence of the link between
myofibroblastoma and spindle cell lipoma. Cellular angiofibroma also shares morphologic features of spindle cell
lipoma and mammary-type myofibroblastoma, and recent
work has suggested that all 3 entities may be related. In
2007, Hameed and colleagues26 described loss of chromosomes 13 and 16 in a case of cellular angiofibroma. Additional FISH studies of the same case revealed deletion of
13q14 (RB1). Maggiani et al25 described 2 additional cases
of cellular angiofibroma in which FISH studies showed
deletion of the chromosome 13q14 region that spanned RB1
and FOX1A1 loci. In 2011, Flucke and colleagues6 showed
monoallelic deletion of RB1 by FISH in a series of 7 cases
of cellular angiofibroma.
SFT is a mesenchymal neoplasm that shares many morphologic features with spindle cell lipoma, mammary-type
myofibroblastoma, and cellular angiofibroma, including
uniform fusiform to spindled cells, variable stromal hyalinization and mature adipose tissue, a distinct vasculature,
and CD34 immunoreactivity. Given the morphologic and
immunophenotypic overlap, it has been suggested that SFT
may belong to this group of lesions.27,28 Although Miettinen
and colleagues29 found that cytogenetic abnormalities were
more common in SFTs larger than 10 cm, few recurrent
numeric or structural aberrations have been reported.29-49 In
a study of 12 pleural-based SFTs, Krismann and coworkers42 showed that 4 cases showed losses on arm 13q by
comparative genomic hybridization. Other studies have also
described loss in chromosome 13 in rare cases of SFT.29,41,46
In our group of 38 cases of SFT and malignant SFT with
evaluable FISH signals, none (0/38) showed loss of 13q14

(RB1) by FISH, whereas all cases of cellular angiofibroma,

spindle cell lipoma, and mammary-type myofibroblastoma
showed monoallelic or biallelic loss, arguing against the
concept that SFT is genetically related to these entities.
We failed to show a genetic link between SFT and
cellular angiofibroma, spindle cell lipoma, and mammarytype myofibroblastoma by assessing a series of SFTs and
malignant SFTs for loss of RB1. Our findings suggest that
although SFTs may share overlapping morphologic and
immunophenotypic characteristics with cellular angiofibroma, mammary-type myofibroblastoma, and spindle cell
lipoma, they are genetically unrelated.
From the Departments of 1Laboratory Medicine and Pathology,
Mayo Clinic, Rochester, MN; and 2Anatomic Pathology and
3Molecular Pathology, Cleveland Clinic, Cleveland, OH.
Address reprint requests to Dr Fritchie: Dept of Anatomic
Pathology, Mayo Clinic, Hilton 11, 200 First Street, SW,
Rochester, MN 55905.

References
1. Stout AP, Murray MR. Hemangiopericytoma: A vascular
tumor featuring Zimmermanns pericytes. Ann Surg.
1942;116:26-33.
2. Klemperer P, Rabin CB. Primary neoplasms of the pleura: a
report of five cases. Arch Pathol. 1931:11.
3. Weiss SW, Goldblum JR, eds. Enzinger and Weisss Soft Tissue
Tumors. St Louis, Mo: Mosby Elsevier; 2008.
4. Fletcher CDM, Unni KK, Mertens F, eds. World Health
Organization Classification of Tumours: Pathology and Genetics
of Tumours of Soft Tissue and Bone. Lyon, France: IARC
Press; 2002.
5. Bainbridge TC, Singh RR, Mentzel T, et al. Solitary fibrous
tumor of urinary bladder: report of two cases. Hum Pathol.
1997;28:1204-1206.
6. Flucke U, van Krieken JH, Mentzel T. Cellular angiofibroma:
analysis of 25 cases emphasizing its relationship to spindle cell
lipoma and mammary-type myofibroblastoma. Mod Pathol.
2011;24:82-89.
7. Gold JS, Antonescu CR, Hajdu C, et al. Clinicopathologic
correlates of solitary fibrous tumors. Cancer. 2002;94:10571068.
8. Vallat-Decouvelaere AV, Dry SM, Fletcher CD. Atypical
and malignant solitary fibrous tumors in extrathoracic
locations: evidence of their comparability to intra-thoracic
tumors. Am J Surg Pathol. 1998;22:1501-1511.
9. Downs-Kelly E, Goldblum JR, Patel RM, et al. The utility of
fluorescence in situ hybridization (FISH) in the diagnosis of
myxoid soft tissue neoplasms. Am J Surg Pathol. 2008;32:8-13.
10. England DM, Hochholzer L, McCarthy MJ. Localized
benign and malignant fibrous tumors of the pleura: a
clinicopathologic review of 223 cases. Am J Surg Pathol.
1989;13:640-658.
11. Enzinger FM, Harvey DA. Spindle cell lipoma. Cancer.
1975;36:1852-1859.
12. Shmookler BM, Enzinger FM. Pleomorphic lipoma: a benign
tumor simulating liposarcoma: a clinicopathologic analysis of
48 cases. Cancer. 1981;47:126-133.

American Society for Clinical Pathology

Am J Clin Pathol 2012;137:963-970

969

DOI: 10.1309/AJCPQEG6YNN6CNAL

969
969

Fritchie et al / RB1 Status in SFT

13. Mandahl N, Mertens F, Willen H, et al. A new cytogenetic

subgroup in lipomas: loss of chromosome 16 material in
spindle cell and pleomorphic lipomas. J Cancer Res Clin
Oncol. 1994;120:707-711.
14. Billings SD, Folpe AL. Diagnostically challenging spindle cell
lipomas: a report of 34 low-fat and fat-free variants. Am J
Dermatopathol. 2007;29:437-442.
15. Suster S, Fisher C. Immunoreactivity for the human
hematopoietic progenitor cell antigen (CD34) in lipomatous
tumors. Am J Surg Pathol. 1997;21:195-200.
16. Templeton SF, Solomon AR. Spindle cell lipoma is strongly
CD34 positive: an immunohistochemical study. J Cutan
Pathol. 1996;23:546-550.
17. Wargotz ES, Weiss SW, Norris HJ. Myofibroblastoma of the
breast: sixteen cases of a distinctive benign mesenchymal
tumor. Am J Surg Pathol. 1987;11:493-502.
18. Chan K, Ghadially FN, Alagaratnam TT. Benign spindle
cell tumor of the breast: a variant of spindle cell lipoma or
fibroma of breast. Pathology. 1984;16:331-336.
19. Toker C, Tang CK, Whitely JF, et al. Benign spindle cell
breast tumor. Cancer. 1981;48:1615-1622.
20. McMenamin ME, Fletcher CDM. Mammary-type
myofibroblastoma of soft tissue: a tumor closely related to
spindle cell lipoma. Am J Surg Pathol. 2001;25:1022-1029.
21. Nucci MR, Granter SR, Fletcher CD. Cellular angiofibroma:
a benign neoplasm distinct from angiomyofibroblastoma and
spindle cell lipoma. Am J Surg Pathol. 1997;21:636-644.
22. Iwasa Y, Fletcher CD. Cellular angiofibroma:
clinicopathologic and immunohistochemical analysis of 51
cases. Am J Surg Pathol. 2004;28:1426-1435.
23. Dal Cin P, Sciot R, Polito P, et al. Lesions of 13q may occur
independently of deletion of 16q in spindle cell/pleomorphic
lipomas. Histopathology. 1997;31:222-225.
24. Pauwels P, Sciot R, Croiset F, et al. Myofibroblastoma of
the breast: genetic link with spindle cell lipoma. J Pathol.
2000;191:282-285.
25. Maggiani F, Debiec-Rychter M, Verbeeck G, et al.
Extramammary myofibroblastoma is genetically related to
spindle cell lipoma. Virchows Arch. 2006;449:244-247.
26. Hameed M, Clark K, Amer HZ, et al. Cellular angiofibroma
is genetically similar to spindle cell lipoma: a case report.
Cancer Genet Cytogenet. 2007;177:131-134.
27. Damiani S, Miettinen M, Peterse JL, et al. Solitary fibrous
tumour (myofibroblastoma) of the breast. Virchows Arch.
1994;425:89-92.
28. Magro G, Bisceglia M, Michal M, et al. Spindle cell lipomalike tumor, solitary fibrous tumor and myofibroblastoma
of the breast: a clinico-pathological analysis of 13 cases in
favor of a unifying histogenetic concept. Virchows Arch.
2002;440:249-260.
29. Miettinen MM, el-Rifai W, Sarlomo-Rikala M, et al. Tumor
size-related DNA copy number changes occur in solitary
fibrous tumors but not in hemangiopericytomas. Mod Pathol.
1997;10:1194-1200.
30. Amo-Takyi BK, Gunther K, Peters I, et al. Benign solitary
fibrous pleural tumour: evidence of primitive features and
complex genomic imbalances, including loss of 20q. APMIS.
2001;109:601-606.
31. Dal Cin P, Pauwels P, Berghe HVD. Solitary fibrous tumour
of the pleura with t(4;15)(q13;q26) [letter]. Histopathology.
1999;35:94-95.

970
970

Am J Clin Pathol 2012;137:963-970

DOI: 10.1309/AJCPQEG6YNN6CNAL

32. Dal Cin P, Sciot R, Fletcher CD, et al. Trisomy 21 in solitary

fibrous tumor. Cancer Genet Cytogenet. 1996;86:58-60.
33. de Leval L, Defraigne JO, Hermans G, et al. Malignant
solitary fibrous tumor of the pleura: report of a case with
cytogenetic analysis. Virchows Arch. 2003;442:388-392.
34. Debiec-Rychter M, de Wever I, Hagemeijer A, et al. Is 4q13
a recurring breakpoint in solitary fibrous tumors? Cancer
Genet Cytogenet. 2001;131:69-73.
35. Donner LR, Silva MT, Dobin SM. Solitary fibrous tumor
of the pleura: a cytogenetic study. Cancer Genet Cytogenet.
1999;111:169-171.
36. Fletcher CD, Cin PD, de Wever I, et al. Correlation between
clinicopathological features and karyotype in spindle cell
sarcomas: a report of 130 cases from the CHAMP study
group. Am J Pathol. 1999;154:1841-1847.
37. Hanau CA, Miettinen M. Solitary fibrous tumor: histological
and immunohistochemical spectrum of benign and
malignant variants presenting at different sites. Hum Pathol.
1995;26:440-449.
38. Havlik DM, Farnath DA, Bocklage T. Solitary fibrous tumor
of the orbit with a t(9;22)(q31;p13). Arch Pathol Lab Med.
2000;124:756-758.
39. Horton ES, Dobin SM, Donner LR. A clonal t(8;12)
(p11.2;q24.3) as the sole abnormality in a solitary fibrous
tumor of the pleura. Cancer Genet Cytogenet. 2007;172:77-79.
40. Hoshino M, Ogose A, Kawashima H, et al. Malignant
solitary fibrous tumor of the soft tissue: a cytogenetic study.
Cancer Genet Cytogenet. 2007;177:55-58.
41. Krismann M, Adams H, Jaworska M, et al. Benign solitary
fibrous tumour of the thigh: morphological, chromosomal
and differential diagnostic aspects. Langenbecks Arch Surg.
2000;385:521-525.
42. Krismann M, Adams H, Jaworska M, et al. Patterns of
chromosomal imbalances in benign solitary fibrous tumours
of the pleura. Virchows Arch. 2000;437:248-255.
43. Mandahl N, Orndal C, Heim S, et al. Aberrations of
chromosome segment 12q13-15 characterize a subgroup of
hemangiopericytomas. Cancer. 1993;71:3009-3013.
44. Manor E, Bodner L. Chromosomal aberrations in oral solitary
fibrous tumor. Cancer Genet Cytogenet. 2007;174:170-172.
45. Mertens F, Willn R, Lillo-Gil R, et al. Translocation (2;3)
(p21;p26) as the sole anomaly in a benign localized fibrous
mesothelioma [letter]. Cancer Genet Cytogenet. 1996;92:9091.
46. Ness GO, Lybaek H, Arnes J, et al. Chromosomal imbalances
in a recurrent solitary fibrous tumor of the orbit. Cancer
Genet Cytogenet. 2005;162:38-44.
47. Rakheja D, Wilson KS, Meehan JJ, et al. Extrapleural benign
solitary fibrous tumor in the shoulder of a 9-year-old girl:
case report and review of the literature. Pediatr Dev Pathol.
2004;7:653-660.
48. Sreekantaiah C, Bridge JA, Rao UN, et al. Clonal
chromosomal abnormalities in hemangiopericytoma. Cancer
Genet Cytogenet. 1991;54:173-181.
49. Torabi A, Lele SM, DiMaio D, et al. Lack of a common or
characteristic cytogenetic anomaly in solitary fibrous tumor.
Cancer Genet Cytogenet. 2008;181:60-64.

American Society for Clinical Pathology