Annals of Diagnostic Pathology 54 (2021) 151783

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Annals of Diagnostic Pathology

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Clinical, morphological and immunohistochemical analysis of 13 cases of

phosphaturic mesenchymal tumor - A holistic diagnostic approach
Debajyoti Chatterjee a, Anand Bardia a, Rimesh Pal b, Uma Nahar Saikia a, *,
Sanjay Kumar Bhadada b, Bishan Dass Radotra a
a
Department of Histopathology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India
b
Department of Endocrinology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India

A R T I C L E I N F O A B S T R A C T

Keywords: Background: Phosphaturic mesenchymal tumor-mixed connective tissue (PMT-MCT) is a rare tumor characterized
Phosphaturic mesenchymal tumor clinically by presence of tumor-induced osteomalacia (TIO), subsequent to elevated fibroblastic growth factor 23
Tumor induced osteomalacia (FGF23) levels. This study aims to analyse the morphological spectrum of PMT along with clinico-pathological
FGF-23
correlation and immunophenotype profile of this rare tumor.
SATB2
Materials and methods: Detailed histological analysis of all tumors presenting with TIO over past 7 years was done
retrospectively. Immunohistochemistry was performed in all cases for SATB2, STAT6, CD34, FGF23, ERG, S100
and smooth muscle actin (SMA).
Results: A total of 13 cases were analysed (8 female and 5 male) with mean age of 39.8 years. Five cases were
arising from bone while 4 each from soft tissue and nasal cavity/paranasal sinus. All presented with hypo­
phosphatemia, hyperphosphaturia, elevated serum FGF23 and features suggestive of osteomalacia. Histological
examination revealed basophilic ‘grungy’ calcification seen in 7 (53.8%), osteoid formation in 8 (61.5%),
chondroid matrix in 4 (30.8%), adipose tissue in 6 (46.2%), osteoclast-like giant cells in 9 (69.2%) and
hemangiopericytomatous (HPC like) blood vessels in 7 cases (53.8%). HPC like vessels and adipose tissue were
more common in nasal tumors while calcification was more common in tumors arising from bone. All cases
showed immunoreactivity for SATB2 and clinical improvement following resection except one case with residual
tumor.
Conclusion: PMT shows varied histological pattern with various matrix components depending on the site of the
tumor. Serum FGF-23 is a useful adjunctive marker for diagnosis.

1. Introduction distinct lesions and comprising of unusual admixture of bland spindled

Phosphaturic mesenchymal tumor-mixed connective tissue (PMT-
MCT) is a rare variant of soft tissue tumor with uncertain histogenesis. It
is characterized clinically by the presence of tumor-induced osteoma­
lacia (TIO). The neoplastic cells produce fibroblastic growth factor 23
(FGF23), which causes renal phosphate wasting, resulting in phospha­
turic hypophosphatemia, which leads to TIO [1]. Because of its varied
clinical presentation and morphology, PMT has struggled for decades to
establish itself as a distinct entity as it was often confused with other
similar tumors causing TIO.
The term ‘phosphaturic mesenchymal tumor’ was coined by Weidner
and Santa Cruz in their landmark study in 1987 describing these as
cells in a heterogenous highly vascular stroma often with microcystic
change, grungy calcified matrix with occasional osteoclast-like giant
cells and adipose tissue [2]. They also stressed that the majority of TIO
are a result of a distinct mesenchymal neoplasm, which is largely
ignored. A study of 32 cases by Folpe et al. in 2004 reinforced the
findings of Weidner and Santa Cruz [3]. But it was only in 2013 that the
World Health Organisation (WHO) accepted it as a distinct entity and
included it in its classification of tumors of soft tissue and bone [4]. Still,
it remains an under-recognized entity with no knowledge of overall
incidence because even after decades, only around 450 cases have been
reported worldwide which mainly comprise scattered case reports and a
handful of case series. Unfortunately, while most of the literature

* Corresponding author at: Department of Histopathology, Room no 512, 5th floor, Research block A, Postgraduate Institute of Medical Education and Research
(PGIMER), Chandigarh 160012, India.
E-mail address: umasaikia@gmail.com (U.N. Saikia).

https://doi.org/10.1016/j.anndiagpath.2021.151783

Available online 2 July 2021

1092-9134/© 2021 Elsevier Inc. All rights reserved.
D. Chatterjee et al. Annals of Diagnostic Pathology 54 (2021) 151783

focuses on the clinical aspects of PMT, only a few studies have stressed
on the pathological aspects of this tumor. Because of wide variation in its
morphology, PMT is often misdiagnosed as other close histological
mimickers. However, it is important to diagnose PMT accurately, as it
has treatment implications. In a previous study by Agami et al., the
authors observed that all tumors presenting with TIO show similar
immunophenotype, irrespective of their histological pattern, suggestive
of a unifying disease entity [5].
The present study is an attempt to expand the knowledge of this rare
tumor and entails a detailed analysis of the clinico-pathological,
morphological spectrum and immunohistochemical profile, which so
far has been lacking from the Indian subcontinent.
2. Materials and methods
We conducted a retrospective analysis of the resected samples of
tumors presenting at our institution with TIO, diagnosed from January
2013 to December 2019. Samples were retrieved from the archives of
Histopathology department of our institute. A total of 13 cases were
collected including 5 new cases in addition to the 8 cases previously
reported in a clinical journal [6]. Out of these cases, 11 were operated in
our institute. The remaining two cases were operated outside and the
blocks were referred to our institute for opinion. The clinical details
were retrieved from the patient's records. The following information
were noted wherever available: age and sex, tumor location and size, the
pre-biopsy duration of osteomalacia, the presence of hypophosphatemia
and hyperphosphaturia. The initial histological diagnosis was PMT in 9
cases, hemangiopericytoma in 2 cases, vascular malformation in 1 case,
mesenchymal tumor, not otherwise specified in 1 case.
Hematoxylin and eosin stained sections of all the cases were
reviewed with detailed morphological analysis. The points specifically
noted were: tumor cellularity, nuclear atypia, mitotic figures per 10 high
powered (x40) fields (HPF), necrosis, type and quality of matrix, intra­
lesional fat, vascular pattern, osteoclast-like giant cells, aneurysmal
bone cyst-like areas, “grungy” or flocculent calcifications, and woven
bone formation.
Immunohistochemistry (IHC) was carried out in all cases for the
following antibodies: SATB2 (Cell Marque, EP281, 1:50), STAT6 (Cell
Marque, EP325, 1:50), CD34 (Dako, QBend10, 1:50), FGF-23 (Abnova
Catalog, MAB16059, 1:50), ERG (Cell Marque, EP111, 1:50), S100 (Cell
Marque, EP32, 1:200) and smooth muscle actin (SMA, Dako, IA4,
1:200). Five micron sections from blocks were deparaffinised and
rehydrated. All IHCs were done in Ventana automated immunostainer
(BenchMark). The immunostaining was considered positive if more than
5% tumor cells were positive for the antibody.
3. Results
3.1. Clinical findings
The clinical and demographic data of all patients has been shown in
Table 1. The age range of cases varied from 13 years to 54 years with a
mean of 39.8 years. There was a female preponderance (8 female and 5
male patients). All cases initially presented with osteomalacia and tumor
was only subsequently detected on imaging. On radiological assessment,
all tumors were well circumscribed. The size of tumor varied from 0.8 to
5 cm with a mean of 2.29 cm.
Tumors were mainly divided into three categories based on the
location viz. soft tissue/skin, bone and nasal cavity/paranasal sinus. Out
of a total of 13 cases, five were those arising from bone while four each
were arising in soft tissue and nasal cavity/paranasal sinus. All the cases
were diagnosed as osteomalacia based on clinical, biochemical and
imaging findings. All cases had low serum levels of phosphate with
hyperphosphaturia. Serum FGF-23 level was available in 8 cases which
were raised. All cases showed recovery of serum phosphate levels post
resection except one with residual tumor in femur.
3.2. Histopathological findings
In most of the cases, the tumor was removed by curettage and the
tumor was received in multiple fragments for histological evaluation. All
cases showed circumscribed, pushing margin, without evidence of
infiltration to the adjacent normal tissue. A prototypical case of PMT
showed spindled tumor cells, which were arranged in sheets of short
fascicles and focal storiform pattern (Fig. 1A). Cellularity was usually
low except for focal areas exhibiting high cellularity. Some cases showed
alternating hypo and hypercellular areas, resembling schwannoma
(Fig. 1B). The cells were elongated with bland, small nuclei, indistinct
nucleoli and moderate cytoplasm (Fig. 1C). Some cases showed dark
nuclei in the tumor cells (Fig. 1D). All cases showed very low mitosis
(<1/10 high power field). No atypical mitosis was seen except for a
single case arising from nasal sinus.
The matrix of PMT comprised of variable components. Basophilic
flocculent or ‘grungy’ calcification (Fig. 1E) was seen in 7 cases (53.8%),
of which 4 were arising from bone (4 out of 5, 80%) and 2 from soft
tissues (2 out of 4, 50%). Only one case arising from the nasal cavity/
paranasal sinus showed such calcification (1 out of 4, 25%). Osteoid
formation, seen in 8 cases (61.5%), was a common finding in PMT which
was associated with bland spindled shaped tumor cells (Fig. 1F). Half of
these cases were from bone (4 out of 5, 80%) and 2 each from soft tissue
(50%) and nasal sinus (50%). A total of 9 cases (69.2%) showed presence
of osteoclast-like giant cells (Fig. 2A), 3 each from bone (60%), soft
tissue (75%) and nasal sinus (75%). Other matrix components included

Table 1
Clinical characteristics of all cases.
S. Age Sex A broad Site Size Serum phosphate Serum FGF-23 Post-operative serum Post-operative serum FGF-
No. category (mg/dl) (RU/ml) Phosphate (mg/dl) 23 (RU/ml)

1. 37 F Bone Tibia 2.5 NA NA NA NA

2. 28 M Bone Mandible 2 1.3 201 2.1 307.8
3. 13 F Bone Sacrum 4 NA NA NA NA
4. 51 M Bone Femur 1 1.6 263.5 3.7 191
5. 29 F Bone Vertebra D6-D10 1 NA NA NA NA
6. 40 M Sinus Nasal cavity left 1.5 NA NA NA NA
7. 36 F Sinus Maxillary sinus 3 1.5 1239 3.7 174
8. 53 F Sinus Nasal cavity middle 1.5 1.8 814.4 3.4 63.4
turbinate
9. 58 M Sinus Nasal cavity sphenoid 4 1.2 513.2 3.2 56
10. 54 M Soft tissue Thigh 2 1.7 288 NA 68.1
11. 35 F Soft tissue Inguinal region right 1.5 NA NA NA NA
12. 40 F Soft tissue Thigh 5 1.3 522.9 3.1 102.2
13. 44 F Soft tissue Leg right 0.8 1.5 349 3.8 101

FGF-23 - fibroblast growth factor 23; normal range of serum FGF-23: 5 to 210RU/ml; normal range of serum phosphate: 3.4 to 4.5 mg/dl.

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D. Chatterjee et al. Annals of Diagnostic Pathology 54 (2021) 151783

Fig. 1. (A) Photomicrograph showing PMT of paranasal sinus arranged in sheets, short fascicles and focal storiform pattern (H&E, 20×); (B) A case of PMT showing
alternate hypocellular and hypercellular areas resembling schwannoma (H&E, 40×); (C) Tumor cells in PMT are elongated with little pleomorphism and have
elongated, bland nuclei (H&E, 100×) (D) Some cases showed focally dark nuclei (H&E, 200×) (E) A case of PMT of bone showing basophilic, flocculent or ‘grungy’
calcification (H&E, 100×); (F) A case of PMT of soft tissue showing osteoid formation (H&E, 100×).

chondroid (Fig. 2B) and adipose tissue (Fig. 2C). Chondroid differenti­
ation was seen in 4 cases (30.8%), 2 from bone and 1 each in sinus and
soft tissues. It was seen in the form of lobules of mature hyaline cartilage.
The chondrocytes did not show any significant pleomorphism. Adipose
tissue was seen mostly in tumors arising from sinus cavity (3 out of 4,
75%). However, it was also seen in 2 cases from soft tissue and 1 from
bone (50% and 20% respectively).
Microvasculature was a prominent histological feature of PMT and
varied from capillary sized vascular channels to thick walled, hyalinised
and branching blood vessels in a hemangiopericytoma-like (HPC)
pattern (Fig. 2D). The stag horn-like branching and thick-walled blood
vessels (HPC-like pattern) was seen in 7 cases (53.8%). It was seen in all

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D. Chatterjee et al. Annals of Diagnostic Pathology 54 (2021) 151783

Fig. 2. (A-D) Panel of photomicrographs showing varied matrix components of PMT in the form of osteoclast-like giant cells (A), chondroid areas (B), adipose tissue
(C) and presence of thin to thick walled, branching blood vessels in hemangiopericytoma-like (HPC-like) pattern (D) (H&E, 100×); (E) PMT showing strong and
diffuse nuclear SATB2 immunoreactivity (100×) while being negative for CD34 which highlights the microvasculature (F, 100×).

tumors arising in sinus cavities (4/4, 100%) and most of soft tissue (3 out
of 4 cases, 75%). However, tumor arising in bone did not show such
vascular pattern. One case arising from sinus cavity also showed thick-
walled anastomosing vessels, which was mistaken as vascular malfor­
mation. The histopathological findings have been summarized in
Table 2.
3.3. Immunohistochemical findings
All the cases including bone, sinus and soft tissue showed diffuse,
positive nuclear immunoreactivity with SATB2 immunostain in the
spindled tumor cells (Fig. 2E). However, no immunoreactivity was
observed in the non-neoplastic skeletal muscle, smooth muscle and fat.
ERG was evaluated in 11 cases, out of which 9 (82%) showed positivity.

4
D. Chatterjee et al.
Table 2
Histopathological comparison of PMTs arising from different sites.
Histopathological feature Bone Soft tissue Nasal sinus
(n = 5) (n = 4) (n = 4)
Grungy calcification 4 (80%) 2(50%) 1(25%)
Osteoid formation 4(80%) 2(50%) 2(50%)
Chondroid differentiation 2(40%) 1(25%) 1(25%)
Osteoclast like giant cells 3(60%) 3(75%) 3(75%)
Intra-lesional adipose tissue 1(20%) 2(50%) 3(75%)
HPC-like blood vessels 0 3(75%) 4(100%)
Aneurysmal bone cyst like changes 1(20%) 0 0
In 5 cases, the staining was strong and diffuse, while in 4, it was patchy.
Immunostain for CD34 highlighted the microvasculature; however,
tumor cells did not show any positivity (Fig. 2F). Tumor cells in all cases
were negative for STAT6, S100 and SMA. In those cases, showing
chondroid differentiation, S-100, however, highlighted the chon­
drocytes. IHC for FGF23 did not give a satisfactory staining pattern
hence not interpreted.
3.4. Follow up data
All cases except one showed improvement of clinical symptoms
following resection of tumor. There was no recurrence of tumor and
follow up serum FGF23 levels were reduced. However, one case (case 2)
showed residual tumor and follow up serum FGF23 level was elevated.
4. Discussion
PMT is an uncommon mesenchymal neoplasm and largely under-
recognized. This can be attributed to several reasons. Firstly, varied
histological features of PMT make it difficult to diagnose and requires
the pathologist to be well aware of the existence of such entity. Further,
lack of clinical, radiological and serological information at the time of
biopsy also adds to delay in diagnosis. Sometimes, in spite of suspicion of
PMT, lack of unifying immunophenotype makes it difficult to exclude
other differential diagnoses. All these factors may play a role in under-
reporting of PMT.
The confusion regarding diagnosis and classification of PMT is re­
flected by the varied terminologies used to describe this entity in pre­
vious reports of literature or terms used in original diagnoses, which
were later reviewed and diagnosed as PMT. This includes mesenchymal
chondrosarcomas, osteosarcoma, osteoblastoma, atypical enchon­
droma, and atypical giant cell tumor of bone for the intraosseous lesions
and spindle cell lipoma, angiolipoma, sclerosing hemangioma, heman­
giopericytoma with osteoclastic giant cells, atypical/tenosynovial giant
cell tumor, and sinonasal hemangiopericytoma-like tumor for soft tissue
and sinonasal cases, respectively [3]. In the current study, 2 cases were
originally diagnosed as hemangiopericytoma and 1 case as arterio-
venous malformation. One case could not be accurately classified and
initially diagnosed as mesenchymal tumor, not otherwise specified.
These were later reviewed and diagnosed as PMT in view of histological
features and supportive clinical and serological data.
PMT have varied histological features with matrix comprising of
several components. The spindled bland neoplastic cells of PMT are
believed to produce smudgy basophilic matrix material which often
calcifies to form a distinctive ‘grungy calcification’. This peculiar
calcification has been described as a characteristic feature of PMT even
in non-phosphaturic type. In a study by Folpe et al., it was reported in
about 2/3rd of cases (20/30) while Agaimy et al. reported it in 50% (11/
22) cases [3,5]. Similarly, we found evidence of grungy calcification
only in half the cases (7/13, 53.8%) with maximum in those arising in
bone (4/5). This points out that although characteristic, calcification is
not a universal finding in PMT and should not be taken as the sole
diagnostic criteria. This calcification is believed to elicit osteoclast-like
giant cell and fibro-histiocytic spindle cell reaction [7]. In the present
5
Annals of Diagnostic Pathology 54 (2021) 151783
study, we did notice osteoclast-like giant cells in 9 cases but only 4 of
these were associated with calcification, unlike in other studies where it
was seen practically in all cases with calcification [3,5,8]. This implies
osteoclast like giant cells are a part of tumor matrix irrespective of the
presence or absence of calcifications.
The tumor from sinus cavities and soft tissues were somewhat
different from those arising in bone. All the cases from sinus cavity
showed presence of prominent HPC-like vasculature. The majority of
these cases also showed adipocytes as part of matrix. One case also
showed thick-walled blood vessels resembling arterio-venous malfor­
mation. One other case revealed storiform pattern with presence of oc­
casional atypical mitosis. However, the total mitotic count was low (2/
10 hpf). Similarly, tumors arising from soft tissues had HPC-like
microvasculature except for one case. Two cases also showed presence
of adipocytes with one case having lipoblasts as well. Most of the tumor
arising from bone showed osteoid formation with giant cells and clas­
sical ‘grungy’ calcification. However, HPC like vessels and stromal fat
were rare findings in PMT arising from bone. These findings reinforce
the importance of evaluating micro-vasculature to aid in diagnosis of
PMT, particularly in those arising from the paranasal sinus and soft
tissue.
Immunohistochemistry (IHC) has limited role in establishing the
diagnosis of PMT in cases showing classical morphology and supportive
clinical findings. Immunohistochemical data on PMT till date, has been
scarce. Folpe et al. studied a number of immunohistochemical stains and
found that the majority of the tumors (16/20) showed granular cyto­
plasmic staining for FGF23 polyclonal antibody while all tumors were
negative for S-100 protein, CD34, desmin, and cytokeratin [3]. Subse­
quent studies also found consistent expression of FGF23 in PMT but it
was found to be of limited specificity [9-11]. FGF-23 staining has been
described in solitary fibrous tumor/hemaingiopericytoma (SFT/HPC),
chondromyxoid fibroma and aneurysmal bone cyst [11]. Occasional
cases showed limited expression for PGP 9.5, smooth muscle actin,
CD34, S100 protein, synaptophysin and dentin matrix protein-1 [5,12-
15]. A recent study by Agaimy et al. demonstrated frequent expression
of SATB2, CD56, ERG and somatostatin receptor 2A (SSTR2A) in PMT
[5]. While SATB2 was consistently expressed irrespective of histologic
variant, ERG expression was seen in 19/21 (90.5%) cases. They found
ERG expression in the tumor cells was weak compared to the endothelial
cells. Similar to Agaimy et al., we found uniform nuclear expression of
SATB2 in tumor cells in all the cases while being consistently negative
for CD34, STAT6 and SMA. We found strong and diffuse SATB2
expression by PMTs irrespective of the site of origin and the morpho­
logical pattern. SATB2 expression by tumor cells further substantiates
the belief regarding osteocytic differentiation in these tumors, which
correlates with increased serum FGF23 level [16]. In a recent study, Sun
et al. found strong and diffuse ERG expression in 5 out of 6 cases (83.3%)
[17]. We also found ERG expression in majority (82%) of our cases. The
intensity of ERG staining in PMT can be variable, which may be
attributed to different clones used by different authors. This unique
immunophenotype of PMT (SATB2+/ERG+/CD56+/S-100-/STAT6-)
helps to distinguish PMT from many of its histologic mimics and further
confirms the hypothesis that all tumors associated with TIO falls under
same category irrespective of their morphological pattern. SFT/HPC is a
close differential diagnosis for PMT particularly in sinus cavities. A
combination of the immunohistochemical markers used in this study can
help in such cases as STAT6 is frequently expressed in SFT/HPC while
being consistently negative in PMT.
Some rare cases of PMT exist, which show typical morphology,
however, do not produce TIO (known as nonphosphaturic PMT) [8].
These cases are not associated with increased serum FGF23, thus require
further confirmation. Chromogenic in situ hybridization (CISH) for
FGF23 mRNA is useful to identify PMT, including nonphosphaturic cases
[8,10]. It shows a remarkably very high sensitivity to detect PMTs. A
subset of PMT cases show novel FN1-FGFR1 and FN1-FGF1 gene fusion
[8,18]. FN1-FGFR1 gene fusion is seen in around 40–47% cases, while a
D. Chatterjee et al.
small subset (around 6%) shows FN1-FGF1 gene fusion [5,17]. It can be
detected by fluorescence in situ hybridization (FISH) or next generation
sequencing. However, the genetic alterations of majority of PMT cases
still remain unknown.
Besides, hemangiopericytoma, PMT may be confused with other
entities as well and thus, require careful microscopic examination along
with clinical and radiological correlation. Sinonasal glomangioper­
icytoma can show HPC-like blood vessels but have uniform myoid
appearing cells and express smooth muscle actin, which is not seen in
PMT. PMT can resemble giant cell tumor, which show numerous giant
cells in a background of fibrohistiocytic spindle cell proliferation. But
these tumors lack the characteristic calcification and varied matrix
along with distinctive spindle cell population of PMT. Chondromyxoid
tenosynovial giant cell tumor may form matrix that closely resembles
that of PMT but presence of small histiocytes, hemosiderin pigment
containing large synoviocytes and foamy macrophages favour more
tenosynovial giant cell tumor. Occasionally PMT in bone may warrant
exclusion of osteosarcoma, however, it is not that difficult because PMT
has indolent radiological features with uniform bland spindled cell
proliferation. Other differential diagnoses may include non-ossifying
fibroma, chondroma of soft part, chondromyxoid fibroma and mesen­
chymal chondrosarcoma. However, these tumors have typical radio­
logical features and lack the typical bland spindle cells in a basophilic
matrix as seen in PMT. In bone, distinguishing PMT from chon­
dromyxoid fibroma could be very difficult, as both share common his­
tologic features. However, chondromyxoid fibroma shows lobulated
growth pattern with hypercellular areas at the periphery. The centre of
the lobules shows chondromyxoid differentiation while the cells in the
periphery show myofibroblastic differentiation and express smooth
muscle actin. However, PMT does not show a lobulated growth pattern
and does not express SMA in the spindle cell component. Still some cases
remain indistinguishable on morphological grounds. In addition, PMT
may have features similar to spindle cell lipoma with presence of adi­
pose tissue and spindle cells. But, unlike spindle cell lipoma, it lacks wiry
collagen and CD34 expression apart from the unusual matrix seen in
PMT.
In the current study, we found a significant reduction in serum FGF-
23 levels and restoration of serum phosphate levels post-operatively
within 3–6 months. Only 1 case had increased levels of serum FGF-23
following resection due to residual disease. These serum markers can
be used as useful indicators for recurrence or presence of any residual
disease.
One of the limitations of this study is small number of cases. Further,
correlation of the pathological diagnosis of PMT with serum phosphate
and FGF23 levels was not available in all cases. However, the remaining
cases were diagnosed as PMT based on the classical PMT morphology as
described in the literature [6] and immunohistochemical expression,
which was uniform in all the cases irrespective of the site of lesion.
5. Conclusion
This study highlights the varied morphological features and the
importance to carefully evaluate the various matrix components and
micro-vasculature to aid in diagnosis of PMT. A high clinical suspicion
and serological data are necessary to correctly establish the diagnosis.
PMT shows unique immunophenotype (SATB2+/ERG+/CD56+/S-
Annals of Diagnostic Pathology 54 (2021) 151783
100-/STAT6-), that helps to distinguish PMT from many of its histologic
mimics and further confirms the hypothesis that all tumors associated
with TIO falls under same category irrespective of their morphological
patterns. In cases lacking phosphaturia or typical morphology, CISH for
FGF-23 mRNA can be a useful diagnostic tool.
Source of funding
None.
Declaration of competing interest
Nil.
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