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\begin{document}

\title{a case report on an intracranial solitary fibrous tumor}



\author[1]{shivani malik}%
\author[1]{Arun Kumar yadav}%
\author[1]{gaurav dhakre}%
\author[1]{mayank aggarwal}%
\author[1]{ashok arya}%
\author[1]{roopali .}%
\affil[1]{SNMC}%


\vspace{-1em}



  
  \date{May 23, 2024}


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A Case Report on an Intracranial Solitary Fibrous Tumor

Authors : Shivani Malik\textsuperscript{1} , Arun Kumar
Yadav\textsuperscript{2}, Gaurav Dhakre\textsuperscript{3} , Mayank
Aggarwal\textsuperscript{4} , Roopali\textsuperscript{5}~ ,~ Ashok Kumar
Arya\textsuperscript{6}

\textsuperscript{1,2,5,6 - affiliated to Department of Radiation
oncology, Sarojini Naidu Medical College, Agra}

\textsuperscript{3,4 -~ affiliated to Department of Neurosurgery,~}

ABSTRACT

Solitary fibrous tumors (SFT) are very rare, particularly those of the
central nervous system (CNS), and they have mesenchymal origin. Here, we
present the case of a 46-year-old man who, a year after suffering a head
injury, lost consciousness for an hour. He had therapy after developing
paralysis in his left arm and left foot after three months. A month and
a half earlier, he had a bad headache, which triggered an examination.
The right temporal frontal lesion on magnetic resonance imaging seems to
be a sizable, well-defined extra-axial solid lesion with lobulated
edges, predominantly isointense to the white matter with dispersed
patches of hypointensity hole on T1WI. The lesion is isointense to the
gray matter on T2WI, with sporadic hypointensities. Along the right
anterior eminence with the bulk medially, thick, smooth dura mater is
seen. A rise in the choline peak was seen in the MRI spectra. The right
frontal lobe's white matter showed a little hyperintensity but no signs
of angioedema-related diffusion limitation. The pathological diagnostic
of the tumor was a grade 3 solitary fibrous tumor after it was
surgically excised during a right frontal craniotomy with nearly an
entire resection. S100, CD34, STAT Positivity for 6, CK, and KI67 were
found during an immunohistochemistry study, and it was done since SFT is
challenging to differentially detect through imaging. The patient had
extra adjuvant therapy in the form of whole-brain external beam
radiation (54 Gy/30\#@1.8Gy/\#@5\#/week) due to the tumor's grade 3
status. Additional research and observation are needed for the
prognosis.

Keywords: solitary fibrous tumor, central nervous system.

INTRODUCTION

Solitary fibrous tumors (SFT) contribute up to less than 2\% of all soft
tissue masses. They are uncommon, collagen-rich, spindle cell tumors
belonging to mesenchymal origin. It was initially described by Wagner in
1870. Pleural SFT was initially described by Klempere and Rabin in 1931
{[}1{]}. The pericardium, peritoneum, lung, liver, upper respiratory
tract, mediastinum, thyroid, parotid gland, sinuses, orbits, and
systemic circulation are among the pleural and extrapleural locations
where instances have been described. {[}1, 7{]} As there is no real
connective tissue component in the CNS, extrapleural SFTs, particularly
CNS SFTs, are uncommon. One percent of all primary CNS tumors are this
kind. {[}3{]} Cerebellopontine angle, spinal dura mater, parasagittal
region, meninges, and ventral tegmental area SFTs have all been
documented. {[}1{]} The disease often affects individuals between the
ages of 20 and 70, and both men and women have equal chances of
contracting it. {[}4{]} SFTs must be distinguished from certain cancers,
including fibrous meningiomas and hemangiopericytomas, as well as myxoid
forms, including meningiomas, myxochordoid tumors, and myxoid peripheral
nerve sheath tumors. Rare mesenchymal tumors called hemangiopericytomas
(HPC) have SFT's clinical, radiological, and pathological
characteristics {[}5{]}.

NGFI-A binding protein (NAB2) and signal transducer and activator of
transcription 6 (STAT6) gene fusions are driver mutations of SFT {[}1,
6{]}. The World Health Organization (WHO) classified SFT and HPC as a
new combined entity in 2016 {[}2, 7{]} as a result of previous pathology
results showing that these tumor types share the same genetic defects.
Three levels of SFT/HPC, specifically levels I, II, and III, are
described by this classification. It should be underlined that while
there is a clear clinical and histological overlap, the difference
between the two is no longer clinically meaningful. The term
''perivascular hemangioma'' was eliminated from the 2021 WHO
classification of CNS malignancies and replaced with SFT {[}8{]}.

A 46-year-old guy who was the patient in this instance had CNS SFT.

CASE REPORT

A 46-year-old male patient presented to the hospital 1.5 months ago with
a severe headache for 2 days. He had a history of trauma to the right
side of his head from 1 year ago, following which he had lost
consciousness for 1 hour. Then he recovered spontaneously. Three months
later, he suffered from hemiparesis of the left hand and left foot, for
which he had been taking treatment for six months in the form of oral
medications. He did not have any significant past illnesses or family
history. A neurological examination was normal when the patient
presented to the radiation oncology department. The patient was
investigated, and a brain MRI was performed.

The contrast-enhanced MRI brain study suggested a large, well-defined
extra-axial solid region with lobulated margins in the right
fronto-temporal region, which appeared predominantly isointense to white
matter with patchy areas of hypointensity on T1WI. On T2WI, the lesion
is isointense to gray matter with patchy areas of hypointensity. Patchy
areas of diffusion restriction noted on DWI correspond to a low value on
ADC. In the post-contrast study, the lesion shows a tense homogenous
enhancement. On MRS, an increase in choline peak is seen, and a few
small cystic areas are also seen within the lesion. Smooth dural
thickening is seen along the right frontal convexity. Medially, the
lesion is causing a mass effect, as evidenced by the buckling of the
right fronto-temporal lobes, effacement of the sulci of the right
frontal and anterior temporal lobes, the ipsilateral sylvian cistern,
the body, atria, and temporal horn of the right lateral ventricle, the
third ventricle, the ipsilateral crural cistern, the ventral midline
shift of 6.5mm to the contralateral side, and subfalcine herniation.
T2/FLAIR hyperintensity was noticed in the white matter of the right
frontal lobe, showing no diffusion restriction suggestive of vasogenic
edema. Features were suggestive of atypical meningioma.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Picture1/Picture1}

\end{center}
\end{figure}

Figure 1: T1WI Post-contrast image showing a large, well-defined
extra-axial solid lesion with lobulated margins in the right
fronto-temporal region, appearing predominantly isointense to white
matter with patchy areas of hypointensity with associated dural
thickening and mass effect as described already above.

Then the patient underwent surgery in the form of a right frontotemporal
parietal craniotomy with near total excision of the space-occupying
lesion, and the tissue was sent for histopathological examination, in
which it came out to be a solitary fibrous tumor of grade 3. Just after
surgery, the patient starts developing a bullous lesion on the bilateral
foot at the Achilles tendon, which gradually increases in size and
bursts after 3 days, following which the patient has had a chronic ulcer
for 1 month.

On post-op NCCT head, an ill-defined hypodense area with blood
attenuating density interspersed multiple extra-axial and intra-axial
foci in the right lateral ventricle along with mild surrounding edema,
resulting in a mass effect in the form of an effacement of nearby sulcal
spaces and the right lateral ventricle. A contralateral midline shift of
13.6mm was also seen. Subsequent adjuvant therapy in the form of
whole-brain external beam radiotherapy (54Gy/30\#@1.8Gy/\#@5\#/wk) was
given to the patient.

On the Doppler of the bilateral lower limb, a few enlarged necrotic
lymph nodes are seen in the left inguinal region, with the largest
measuring approximately 2.5x2 cm in size. Arterial systems, venous
systems, superficial venous systems, and perforators seem to be
completely normal. The patient did not complain of inguinal lymph nodes.
On USG-guided Fnac, it was cited that previous inguinal lymph nodes were
likely reactive.

The right FTP mass excision biopsy specimen underwent
immunohistochemistry analysis since SFT is challenging to properly
identify using imaging. Lesional cells exhibited immunoreactivity for
S100 with a score of 1+, CD34 with a score of 3+, and STAT 6 with a
score of 3+. In the cells of the lesions, there was immunoreactive
patchy positivity for CK. In 6--7\% of the lesional cells with INI-1
retention, KI67 was increased. SMA, DESMIN, EMA, SOX 10, or TLE-1 were
not reactive.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/ihc2/ihc2}

\end{center}
\end{figure}

Figure 2: Immunohistochemistry final diagnosis panel {[}immunoreactivity
seen with CD34 and STAT6 with score 3+, i.e., 51--75\% of lesional cells
were immunoreactive{]}

\par\null

DISCUSSIONS

The parasagittal sinus and spinal canal are the most prevalent locations
for the bulk of intracranial SFTs, which are dural masses made up mostly
of very thick collagen bands that are produced by fibroblasts. This
patient exhibited SFT coming from the right frontal lobe of the brain.

SFT symptoms can vary, and patients may have a variety of nonspecific
symptoms linked to raised intracranial pressure or the tumor site. There
can be hemiplegia, hearing loss, headaches, nausea, vomiting,
disorientation, and memory issues {[}9{]}.

An 86-year-old man with SFT, localized to the parietal lobe of the right
side and infiltrating the parietal bone, was described by Sugiyama et
al. {[}10{]} as presenting for 1 month with increasing and persistent
motor impairment in the left lower extremities.

In another study, a 30-year-old man was diagnosed with SFT that was
close to the temporal lobe of the right side and thickened the temporal
bone next to it. The patient also exhibited dysarthria and left facial
nerve palsy, as well as lessened muscle power in his left upper and
lower limbs {[}1, 3{]}. This patient experienced hemiparesis of the left
arm and left foot in addition to a significant headache, and the SFT was
found to be in the right frontal region. The main cause of headaches and
vertigo is elevated intracranial pressure. Patients in this trial did
not exhibit dysarthria, impaired vision, or symptoms of paralysis of the
facial nerve.

For SFT diagnosis, MRI and CT imaging are crucial. Due to MRI's
fluctuating signal intensity, differential diagnosis of SFT is
challenging. It's crucial to distinguish between lymphoma, metastases,
neurofibromas, meningiomas, and schwannomas. Important imaging methods
for diagnosing SFT include CT and MRI.

Intracranial SFTs imaging exhibits a variety of characteristics, and
earlier images have shown that intracranial SFTs are most likely to
develop in or around the venous sinuses, the base of the skull, the
sagittal sinus, the falx cerebri, and the peritentorium cerebelli.
Extraaxial tumors with lobulated or irregular shapes, some of which are
oval or dumbbell-shaped, further identify intracranial SFTs {[}11{]}.
When compared to gray matter, the SFT generally has isointensity to
slight hyperintensity on T1WI and isointensity on T2WI. In cystic
degeneration and necrosis, T1WI exhibits an isointense mixed signal and
an isointense signal with modest hyperintensity {[}10{]}. Additionally,
in situations of necrotic areas and cystic degeneration, T2WI exhibits
slight hyperintensity or mixed signals of isointensity {[}10{]}.

The tumor looked markedly increased after enhanced MRI, and those who
had cystic degeneration had heterogeneous enhancement {[}12{]}.
Peritumoral edema is often not harmful.

SFT and meningiomas have comparable imaging characteristics; SFT may be
distinguished from meningiomas using MRS. In SFT, compared to
meningiomas, the relative amounts of choline and myo-inositol are
higher. In addition, Chen et al. {[}13{]} demonstrated that SFT/HPC
could be distinguished from meningiomas using the normalized ratio of
apparent diffusion coefficient and sensitive signal intensity in the
tumor. The right fronto-temporal area of the brain experienced SFT in
the currently reported instance, along with signal hyperintensity, dural
thickening, and mass effect as previously documented with an elevated
choline peak on MRI spectroscopy.

SFT is mostly diagnosed by pathological investigation. The tumor tissue
had a high concentration of spindle or polygonal cells, as seen by
histological staining. Typically, there are many blood vessels and
collagen fibers that resemble antlers. Around blood vessels, tumor cells
are organized in concentric rings and can either form depleted or rich
areas {[}14{]}. IHC revealed that CD34, vimentin, and STAT6 were
positive for SFT tissues. However, the prognosis of a patient is
frequently predicted by the Ki-67 proliferation index. In the prognosis
assessment of CNS SFT, it has been suggested by several studies that
elevated Ki-67 levels (\textgreater{}5\%) lead to adverse prognoses.

Currently, CD34 is thought to be the best marker for SFT. Positive
staining has been observed in 95--100\% of patients, yet this tumor can
still exist without CD34. Most individuals with intracranial SFT have
positive STAT6. Due to a rearrangement on chromosome 12q, STAT6 could be
connected to the NAB2-STAT6 gene fusion. Therefore, it is advised that
intracranial SFT be diagnosed by looking for the STAT6 or NAB2-STAT6
fusion gene {[}1{]}. On the long arm of chromosome 12, NAB2 and STAT6
are adjacent genes that are transcribed in opposing ways {[}9{]}. In
SFT, an intrachromosomal inversion aligns the genes so that they are
transcribed from the NAB2 promoter in the same direction {[}5{]},
resulting in nuclear expression of STAT6 that can be seen by IHC
{[}15{]}.

IHC labeling was used to identify STAT6 expression in cerebral SFT
tissue, and the NAB2-STAT6 fusion gene was successfully identified to be
excellently specific and sensitive. Nuclear STAT6's have 100\%
specificity and 96.6\% sensitivity, making STAT6 IHC a highly sensitive
and specific alternative for the NAB2-STAT6 fusion gene.

In the current work, lesional cells showed STAT6 expression. Clinical
pathology and prognosis may be related to various NAB2-STAT6 fusion
mutations. The patient profiled in this study's SFT tissue was
discovered to be STAT6, CD34, S100, and CK positive, with a KI 67 INDEX
of 6-7\%. After surgery, the patient's tumor did not return.

A high incidence of extracranial and local metastases is a feature of
SFT {[}15{]}. Previous research has shown that there is a risk of
recurrence in people with long-term SFT, even ten years after the first
resection. As a result, SFT patients need careful care and continuous
observation. The prognosis and therapy of the tumor presented in this
article need more research because it is an uncommon malignancy.

Retrospective research was conducted on patients who got SFT of the
brain between January 2009 and June 2019 by Yu et al. {[}15{]}.
According to their findings, the WHO classification was lowered, and
patients who received complete resection along with adjuvant therapies
such as Gamma Knife surgery had longer progression-free survival (PFS).
It should be emphasized that the prior study, which was previously
stated, was done retrospectively, had a limited sample size, and that
its conclusions were skewed due to selection bias. According to the
findings of a multicenter study, postoperative radiotherapy, such as 2D
conventional radiotherapy, 3D conformal radiotherapy, and intensity
modulated radiotherapy, can increase the PFS of patients with SFT very
significantly, regardless of the extent of surgery {[}15{]}.

It should be emphasized that the current study did not look at how
various radiotherapy procedures affected SFT. Currently, no accepted
treatment standards exist for malignant intracranial SFT.

Malignant intracranial SFT cannot be treated with surgical excision or
postoperative radiation. Tumor angiogenesis and proliferation are
inhibited by Anlotinib, a new multitargeted tyrosine kinase inhibitor
with anticancer and antiangiogenic action {[}1{]}. SFT may benefit from
anti-angiogenesis as a possible therapy. Malignant intracranial SFT can
be effectively treated with surgery, radiation, and anlotinib alone
{[}6{]}. The current work only covers one instance; thus, more
investigation and bigger RCTs are required to confirm its findings.
Advanced renal carcinoma and a few subtypes of advanced sarcomas of soft
tissue are both approved to be treated with Pazopanib, which is a strong
inhibitor of tyrosine kinase {[}17{]}. It should be noted that patients
with metastatic or unresectable SFT are successfully treated with
pazopanib.

The results of the current study revealed that surgical resection is the
best option for treating SFT and that postoperative radiation can
considerably increase patient PFS. For aggressive, incurable, or
metastatic SFT, molecule-targeting therapies like the tyrosine kinase
inhibitors anlotinib and pazopanib are potential options.

Conclusion

SFT is an uncommon tumor. As it is rare but very similar to other common
brain tumors, SFT has a heavy chance of misdiagnosis after imaging. It
should be noted that histopathological examination is essential to
differentiate SFT from other diseases of the CNS. Furthermore, resection
of the complete tumor is the preferred treatment modality for SFT.
Postoperative adjuvant treatment indications have not yet been
clarified. Because of the risk of recurrence, careful follow-up for the
long term, including periodic imaging along with surveillance, is
recommended.

Patient's ~perspective

I was very worried, firstly, when I learned that I have a rare type of
cancer, due to which I was having problems. But after surgery, my
symptoms resolved, and I got better. During radiotherapy, I was getting
much better, and after that, I felt myself being normal, and I improved
very much. and I am very thankful to the doctors.

Authors' contributions

S.M. is a major contributor to concept design, defining intellectual
content, literature search, data acquisition, data analysis, statistical
analysis, manuscript preparation, and manuscript review. A.K.Y. and G.D.
helped in concept, literature search, clinical studies, data
acquisition, data analysis, and manuscript preparation. M.A., R., and
A.K.A. contributed to the definition of intellectual content, data
acquisition, and manuscript review.

Ethical Approval

All procedures performed were according to the ethical standards of the
institutional and/or national research committee and the 1964 Helsinki
Declaration, along alongwith ~its later amendments or comparable ethical
standards.

Patient consent for publication

Informed consent in written form was obtained from the patient for
publication of the present manuscript, including all data and
accompanying images.

Conflicts of interests

The authors declare that they have no conflicts of interest.

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