Hemangiopericytoma

Types
Causes
Common symptoms
Diagnostic tests
Non-Pharmacological Treatments
Drug Treatments
Dietary Molecular & Herbal Supplements
Regenerative & Stem-Cell-Related Drugs
Surgical Procedures
Prevention Strategies
When to See a Doctor
Diet: What to Eat and What to Avoid
Frequently Asked Questions

Hemangiopericytoma (HPC) is a rare vascular tumor that arises from pericytes—cells that wrap around small blood vessels. Recent studies classify it within the spectrum of solitary fibrous tumors due to shared genetic markers (NAB2–STAT6 fusion) and similar behavior. HPCs can occur anywhere in the body but most often affect limbs, the pelvis, and the head and neck region. They tend to grow slowly but may invade nearby tissues and rarely spread (metastasize) to lungs or bones.

Hemangiopericytoma (HPC)/Solitary Fibrous Tumor (SFT) is a rare tumor that grows from cells in connective tissue (the “support” tissue of the body) and often has many small, branching blood vessels that look like deer antlers under the microscope—doctors call these “staghorn” vessels. The tumor can happen almost anywhere (head and neck, chest, abdomen, arms/legs, or inside the skull on the meninges). Today, doctors diagnose it mainly by tissue testing, where a pathologist (a doctor who studies tissue) looks for a NAB2–STAT6 fusion (a specific joining of two genes) and for STAT6 protein inside the cell nucleus using a stain called immunohistochemistry. These tests help confirm the tumor type and guide care. BioMed CentralNature

Connective tissue: the body’s scaffolding (fat, fascia, ligaments, lining of organs).
Staghorn vessels: thin-walled, sharply branching blood channels seen in this tumor.
Gene fusion: two genes (NAB2 and STAT6) become abnormally joined; this drives the tumor’s behavior.
Immunohistochemistry (IHC): special stains that light up certain proteins; STAT6 in the nucleus is a strong clue the tumor is an SFT/HPC. Nature

Why the name changed: Earlier, doctors separated “SFT” and “HPC.” Research showed they share the same genetic hallmark (NAB2–STAT6) and form a single disease spectrum. WHO now uses SFT for soft-tissue and CNS (brain/meningeal) tumors; “hemangiopericytoma” is largely historical. Recent CNS classifications also changed how grades are assigned (now CNS WHO grade 1–3 for SFT), which helps estimate risk. PMCThe Journal of Neuroscience

Types

Doctors describe this tumor in three practical ways: by location, by pathology pattern, and by grade/risk.

1) By location (where it starts)

Meningeal (inside the skull or spine coverings): Presents as a firm mass attached to the dura (the tough brain covering). It may mimic a meningioma but behaves differently and can come back or spread years later. The Journal of Neuroscience
Pleural/thoracic (lining of lungs/chest): Sometimes pedunculated (on a stalk) and found by chest imaging or cough/shortness of breath. MDPI
Head & neck/orbit: Can cause bulging eye (proptosis), visual or sinus symptoms. BioMed Central
Abdominal/retroperitoneal/pelvic: May grow large before causing pressure or pain. SpringerOpen
Extremities/soft tissue or rare in bone: Presents as a deep, slowly enlarging lump; bone involvement is rare. SpringerOpenMDPI

2) By pathology pattern (how it looks under the microscope)

Typical/classic SFT: Spindle-shaped cells, “patternless pattern,” and staghorn vessels; usually slower-growing. BioMed Central
Cellular SFT (historically called “HPC”): More densely packed cells and prominent vessels. BioMed Central
Malignant SFT: Many dividing cells (high mitotic count), cellular crowding (hypercellularity), dead areas (necrosis), and more aggressive behavior. BioMed Central
Dedifferentiated SFT: A portion transforms into a frankly high-grade sarcoma; prognosis is worse. Meridian
Epithelioid or other rare variants: Uncommon patterns that can make diagnosis tricky, but still within SFT. PMC

3) By grade/risk (how likely it is to come back or spread)

For CNS SFT, grading uses CNS WHO grades 1–3; higher grade means higher risk. In soft tissue, SFT is generally labeled “intermediate—rarely metastasizing,” but some are malignant. Risk models consider size, mitotic rate, age, and necrosis. The Journal of NeuroscienceBioMed CentralScienceDirect

Causes

Honest note: The exact cause—why one person develops SFT/HPC and another does not—is unknown. There is, however, one well-established genetic driver and several molecular changes linked to how aggressive the tumor is. Below are 20 items summarizing what causes the tumor to form or to behave more aggressively. Where items are risk modifiers (not root causes), I label them clearly.

NAB2–STAT6 gene fusion (root cause/driver): A defining gene join that activates abnormal growth programs. It is present in the vast majority of SFT/HPC and is considered the hallmark of this tumor. BioMed Centralajp.amjpathol.org
Nuclear STAT6 protein (marker of the fusion’s effect): The fusion drives STAT6 into the cell nucleus; pathologists detect this with IHC and it strongly supports the diagnosis. (Marker, not a separate cause.) Nature
Different fusion variants (e.g., NAB2 exon 4–STAT6 exon 2 or exon 6–exon 16/17) may correlate with site and behavior—an ongoing research area. ScienceDirectSpringerLink
EGR1-dependent transcription changes: Lab work suggests the fusion can hijack EGR1, a growth-control pathway, changing many downstream genes. eLife
Angiogenesis (new blood vessel growth) signaling—especially VEGF: These tumors are very vascular; studies and clinical responses to anti-angiogenic drugs support a VEGF-driven biology. (Biology driver and therapy target.) PMCMDPI
PDGFR and related growth signals: Platelet-derived growth factor pathways may contribute to tumor cell survival and blood-vessel support. (Mechanistic contributor; evidence mostly indirect.) Taylor & Francis Online
TERT promoter mutations (risk modifier for aggressive behavior): Not the basic cause of SFT, but associated with larger size, necrosis, older age, and higher risk tumors. PMCPubMed
TP53 alterations (risk modifier for aggressiveness): Changes in this tumor-suppressor gene correlate with more aggressive SFT in some cohorts. PMCNature
mTOR pathway alterations (possible risk modifier/target): Low-frequency changes linked to shorter progression-free survival in one analysis. Nature
NOTCH pathway alterations (possible risk modifier): Reported associations with patient outcomes in genomic studies. Nature
Loss of apoptotic regulators (e.g., APAF1) and high Ki-67 (risk features in pathology): Associated with malignant transformation in some series. SpringerLink
Large primary tumor size (risk modifier): Larger tumors are more likely to behave aggressively or recur. ScienceDirect
High mitotic rate (many dividing cells) (risk modifier): A strong independent predictor of worse outcome. BioMed Central
Tumor necrosis (dead tissue inside tumor) (risk modifier): Often travels with aggressive biology and TERT promoter changes. PubMed
Older patient age (risk modifier): Used in validated risk models for predicting metastasis in SFT. ScienceDirect
Anatomic site (meningeal vs. elsewhere) (risk modifier): CNS SFT tends to recur or metastasize late; lifelong follow-up is recommended. SpringerLink
Cellular/dedifferentiated histology (risk modifier): Cellular (HPC-like) or dedifferentiated areas signal higher risk. Meridian
Poor surgical margins (not a cause, but a recurrence driver): If tumor cannot be fully removed, risk of local return rises. Frontiers
Tumor blood supply patterns (biology contributor): The dense, branching vessels are part of the tumor’s growth strategy and support rapid enlargement. BioMed Central
Paraneoplastic hormone-like activity (IGF-2 production) does not cause the tumor, but explains a key complication—hypoglycemia (Doege-Potter syndrome). It reflects tumor biology and size. PubMedOxford Academic

Common symptoms

Symptoms depend on where the tumor grows and how big it gets. Many SFT/HPC are slow-growing and painless at first.

A firm, slowly enlarging lump (any soft-tissue site). The skin over it usually looks normal.
Pain or deep ache from pressure on nearby tissues or nerves.
Tingling, numbness, or weakness if the mass presses on a nerve.
Visible pulsation or a whooshing sound (bruit) over the lump because the tumor is very vascular.
Swelling of a limb if the mass blocks veins or lymphatic flow.
Limited joint movement when the tumor sits near a joint.
Unintended weight loss or fatigue in advanced disease (nonspecific).
Chest symptoms (cough, shortness of breath, chest discomfort) if pleural/thoracic. MDPI
Abdominal fullness, early satiety, constipation, or urinary symptoms if pelvic/retroperitoneal. SpringerOpen
Headache with meningeal tumors; can be chronic, worse in the morning. The Journal of Neuroscience
Seizures if the tumor irritates brain tissue. The Journal of Neuroscience
Vision changes or bulging eye (proptosis) when in the orbit. BioMed Central
Facial pain or nasal blockage for head/neck sites. BioMed Central
Back pain or nerve root symptoms if tumor involves spine or paraspinal tissues. The Journal of Neuroscience
Episodes of low blood sugar (hypoglycemia)—sweating, confusion, fainting—caused by IGF-2 secretion from a large SFT (Doege-Potter syndrome). PubMed

Diagnostic tests

A) Physical exam

Inspection and palpation of the mass: The doctor looks and feels for size, depth, mobility, tenderness, and pulsation. A firm, deep, slowly enlarging mass raises concern for SFT/HPC.
Auscultation (listening) over the mass: A bruit (whooshing) suggests high blood flow, which is common in SFT/HPC.
Limb and joint exam: Assesses range of motion and function if the mass is near a joint or muscle.
Neurologic exam: Checks strength, sensation, reflexes, vision, and cranial nerves if symptoms point to CNS or nerve compression. The Journal of Neuroscience
General exam for paraneoplastic hypoglycemia: Looks for confusion, sweating, rapid heartbeat when glucose is low (possible Doege-Potter syndrome). PubMed

B) Manual/bedside tests

These are simple tests done without advanced machines.

Bedside capillary glucose (finger-stick): Low sugar during symptoms suggests a paraneoplastic hypoglycemia pattern; later labs confirm tumor-related IGF-2. PubMed
Palpation for a thrill: A faint vibration over the mass can indicate very high blood flow.
Range-of-motion maneuvers: The examiner moves the nearby joint to see if pain/locking is mechanical from the mass.
Tinel-like percussion over the mass: Tapping the area to see if it reproduces tingling, suggesting nerve compression.
Gait and functional tests: Simple walking, balance, and grip assessments reveal functional impact from limb or spine masses.

These bedside checks do not diagnose SFT/HPC alone. They guide which imaging and tissue tests to do next.

C) Laboratory & pathological tests

Basic metabolic panel (glucose): Documents hypoglycemia if present; during attacks, glucose is low. PubMed
Insulin, C-peptide, β-hydroxybutyrate: In tumor-induced hypoglycemia, insulin and C-peptide are low (unlike insulinoma); ketones may be low because of IGF-2 effects. PubMed
IGF-2 and IGF-2:IGF-1 ratio: High IGF-2 or an elevated ratio supports Doege-Potter syndrome from SFT. Oxford Academic
Core-needle or excisional biopsy (the key test): A pathologist confirms SFT/HPC by the microscopic pattern (spindle cells, staghorn vessels). BioMed Central
Immunohistochemistry (IHC) panel: STAT6 nuclear staining (highly specific), often CD34, BCL-2, CD99 positive; helps distinguish SFT from look-alike tumors. NatureFrontiers
Molecular testing for NAB2–STAT6 fusion: Detected by targeted RNA/DNA tests; confirms the pathognomonic fusion. ajp.amjpathol.org
Ki-67 (MIB-1) proliferation index: Estimates how fast cells are dividing; higher values suggest more aggressive behavior. SpringerLink
TERT promoter mutation testing (selected cases): Helps refine risk in some settings, as these mutations correlate with high-risk features. PubMed

D) Electrodiagnostic tests

EMG/Nerve Conduction Studies: If a limb mass causes numbness/weakness, these tests show nerve compression or injury and help plan surgery.
EEG (electroencephalogram): If meningeal SFT causes seizures, EEG helps document seizure activity and guide anti-seizure treatment. The Journal of Neuroscience

E) Imaging tests

MRI with contrast (soft tissue or brain): Best detail for soft tissues and the meninges; SFT/HPC often shows a well-defined, intensely enhancing mass with flow voids (signs of fast blood flow). In the brain, it may be dural-based but not a typical meningioma. SpringerOpen
CT scan (chest/abdomen/pelvis or head): Maps size, relation to bone or lung; chest CT is commonly used for pleural tumors and for staging the lungs for spread. MDPI
Doppler ultrasound (for superficial masses): Shows high vascularity and guides biopsy safely. SpringerOpen
Catheter angiography (DSA): Outlines the feeding arteries; sometimes used right before surgery to embolize (block) blood flow to reduce bleeding risk. SpringerOpen
FDG PET-CT (selected cases): Can help in staging or looking for recurrence/metastasis; uptake varies with tumor grade. SpringerOpen

Non-Pharmacological Treatments

Each approach is described with its Description, Purpose, and Mechanism.

Surgical Resection with Wide Margins
- Description: Removing the tumor plus a rim of healthy tissue.
- Purpose: Achieve complete local control and reduce recurrence.
- Mechanism: Physically excising all tumor cells under the microscope.
Radiation Therapy
- Description: High-energy X-rays directed at the tumor bed.
- Purpose: Kill residual cells after surgery or shrink tumors pre-operatively.
- Mechanism: Damages DNA in proliferating tumor cells, preventing repair.
Preoperative Embolization
- Description: Blocking feeding blood vessels via catheter.
- Purpose: Reduce tumor blood supply, minimize bleeding during surgery.
- Mechanism: Injects particles or coils to occlude tumor vessels.
Cryoablation
- Description: Freezing tumor tissue using probes.
- Purpose: Destroy small or inoperable lesions.
- Mechanism: Ice crystals disrupt cell membranes and blood flow.
Hyperthermia Therapy
- Description: Local heating of tumor area (42–45 °C).
- Purpose: Enhance effects of radiation and immune response.
- Mechanism: Heat increases tumor blood flow, oxygenation, and protein denaturation.
Photodynamic Therapy (PDT)
- Description: Light activation of injected photosensitizer.
- Purpose: Target and kill superficial or accessible tumors.
- Mechanism: Light triggers reactive oxygen species formation, damaging cells.
Ultrasound-Guided High-Intensity Focused Ultrasound (HIFU)
- Description: Concentrated ultrasound waves heat and ablate tissue.
- Purpose: Non-invasive treatment for deep tumors.
- Mechanism: Ultrasound energy induces rapid temperature rise.
Physical Therapy
- Description: Gentle exercises for affected limbs.
- Purpose: Maintain mobility and function post-treatment.
- Mechanism: Improves muscle strength and joint flexibility.
Occupational Therapy
- Description: Training to perform daily tasks safely.
- Purpose: Enhance quality of life and independence.
- Mechanism: Adapts activities and environment to patient’s abilities.
Pain Management (Non-Drug)
- Description: Techniques like TENS, heat/cold packs.
- Purpose: Alleviate treatment-related or tumor pain.
- Mechanism: Modulates nerve signals and reduces inflammation.
Psychological Support & Counseling
- Description: Therapy sessions to address emotional well-being.
- Purpose: Reduce anxiety, depression, and improve coping.
- Mechanism: Cognitive-behavioral techniques reshape unhelpful thoughts.
Dietary Counseling
- Description: Personalized nutrition plans.
- Purpose: Support healing, maintain weight, and reduce fatigue.
- Mechanism: Optimizes intake of protein and micronutrients.
Mind–Body Therapies (Yoga, Meditation)
- Description: Breathing exercises, guided imagery.
- Purpose: Lower stress, improve sleep and immune function.
- Mechanism: Activates relaxation response, balances hormones.
Acupuncture
- Description: Inserting fine needles at specific points.
- Purpose: Reduce pain, nausea, and fatigue.
- Mechanism: Stimulates endorphin release and modulates nerve pathways.
Massage Therapy
- Description: Gentle soft-tissue manipulation.
- Purpose: Relieve muscle tension and promote relaxation.
- Mechanism: Enhances blood flow and reduces stress hormones.
Music and Art Therapy
- Description: Creative expression sessions.
- Purpose: Improve mood and emotional resilience.
- Mechanism: Provides nonverbal outlet, engages reward centers.
Peer Support Groups
- Description: Regular meetings with survivors and patients.
- Purpose: Share experiences and coping strategies.
- Mechanism: Offers social support, reduces isolation.
Occupational Radiation Safety Measures
- Description: Lead shields and distance protocols for staff.
- Purpose: Protect healthcare teams during radiologic procedures.
- Mechanism: Minimizes stray radiation exposure.
Environmental Modifications at Home
- Description: Installing rails, reducing trip hazards.
- Purpose: Prevent falls and injuries during recovery.
- Mechanism: Creates safer living spaces for mobility-limited patients.
Palliative Care Integration
- Description: Holistic symptom management approach.
- Purpose: Enhance comfort and quality of life at any treatment stage.
- Mechanism: Combines medical, psychological, and spiritual support.

Drug Treatments

Key medications for HPC management, with Class, Dosage, Timing, Purpose, Mechanism, and Side Effects.

Doxorubicin
- Class: Anthracycline antibiotic
- Dosage/Timing: 75 mg/m² IV every 3 weeks
- Purpose: First-line chemotherapy for advanced disease
- Mechanism: Intercalates DNA, inhibits topoisomerase II
- Side Effects: Cardiotoxicity, nausea, hair loss
Ifosfamide
- Class: Alkylating agent
- Dosage/Timing: 1.8 g/m²/day IV for 5 days, every 3 weeks
- Purpose: Combined with doxorubicin for higher response
- Mechanism: Cross-links DNA strands, preventing replication
- Side Effects: Hemorrhagic cystitis, neurotoxicity
Pazopanib
- Class: Tyrosine kinase inhibitor (TKI)
- Dosage/Timing: 800 mg orally once daily
- Purpose: Targeted therapy for unresectable or metastatic HPC
- Mechanism: Inhibits VEGFR, PDGFR to block angiogenesis
- Side Effects: Hypertension, hepatotoxicity, diarrhea
Trabectedin
- Class: DNA minor-groove binder
- Dosage/Timing: 1.5 mg/m² IV over 24 h every 3 weeks
- Purpose: Second-line for soft-tissue sarcomas including HPC
- Mechanism: Binds DNA and disrupts transcription
- Side Effects: Myelosuppression, elevated liver enzymes
Gemcitabine
- Class: Antimetabolite
- Dosage/Timing: 1,000 mg/m² IV on days 1 and 8 every 21 days
- Purpose: Option for refractory cases
- Mechanism: Incorporates into DNA, halting replication
- Side Effects: Flu-like symptoms, thrombocytopenia
Docetaxel
- Class: Taxane
- Dosage/Timing: 75 mg/m² IV every 3 weeks
- Purpose: Combined regimens to enhance effect
- Mechanism: Stabilizes microtubules, inhibiting cell division
- Side Effects: Fluid retention, neuropathy
Temozolomide
- Class: Alkylating agent
- Dosage/Timing: 150–200 mg/m² orally daily for 5 days per 28-day cycle
- Purpose: Oral therapy for metastatic or recurrent HPC
- Mechanism: Methylates DNA base guanine causing breaks
- Side Effects: Fatigue, myelosuppression
Bevacizumab
- Class: Monoclonal antibody against VEGF
- Dosage/Timing: 10 mg/kg IV every 2 weeks
- Purpose: Anti-angiogenic agent to slow tumor growth
- Mechanism: Binds VEGF, preventing blood vessel formation
- Side Effects: Hypertension, risk of bleeding
Sunitinib
- Class: Multi-target TKI
- Dosage/Timing: 50 mg orally daily, 4 weeks on/2 weeks off
- Purpose: Alternative targeted therapy
- Mechanism: Inhibits multiple receptors (VEGFR, PDGFR)
- Side Effects: Skin discoloration, hypothyroidism
Thalidomide
- Class: Immunomodulatory drug
- Dosage/Timing: 200 mg orally daily
- Purpose: Anti-angiogenic adjunct in refractory disease
- Mechanism: Inhibits new vessel formation, modulates cytokines
- Side Effects: Peripheral neuropathy, constipation

Dietary Molecular & Herbal Supplements

Each with Dosage, Function, and Mechanism.

Curcumin (Turmeric Extract)
- Dosage: 500 mg twice daily
- Function: Anti-inflammatory, antioxidant
- Mechanism: Inhibits NF-κB and COX-2 pathways
Green Tea Catechins (EGCG)
- Dosage: 400 mg EGCG daily
- Function: Anti-angiogenic and pro-apoptotic
- Mechanism: Blocks VEGF and activates caspases
Resveratrol
- Dosage: 250 mg daily
- Function: Cell-cycle arrest inducer
- Mechanism: Modulates p53 and cyclin expression
Quercetin
- Dosage: 500 mg daily
- Function: Anti-proliferative
- Mechanism: Inhibits PI3K/Akt signaling
Omega-3 Fish Oil (EPA/DHA)
- Dosage: 2 g daily
- Function: Reduces inflammation
- Mechanism: Converts to anti-inflammatory resolvins
Mushroom Extract (Polysaccharide-K)
- Dosage: 1,000 mg daily
- Function: Immune enhancer
- Mechanism: Stimulates NK cells, macrophages
Melatonin
- Dosage: 3 mg nightly
- Function: Radiosensitizer, antioxidant
- Mechanism: Scavenges free radicals, modulates apoptosis
Vitamin D₃
- Dosage: 2,000 IU daily
- Function: Regulates cell growth
- Mechanism: Binds VDR to influence gene transcription
Silymarin (Milk Thistle)
- Dosage: 420 mg daily
- Function: Protects liver during chemo
- Mechanism: Stabilizes hepatocyte membranes, antioxidant
Ginger Extract
- Dosage: 500 mg daily
- Function: Nausea relief, anti-inflammatory
- Mechanism: Inhibits COX and 5-LOX enzymes
Astragalus
- Dosage: 1,000 mg twice daily
- Function: Immunostimulant
- Mechanism: Enhances T-cell and macrophage activity
Ashwagandha
- Dosage: 600 mg daily
- Function: Stress reduction, immune support
- Mechanism: Modulates cortisol, NK cells
Reishi Mushroom
- Dosage: 1,500 mg daily
- Function: Anti-tumor, immune modulator
- Mechanism: Activates dendritic cells, T-cells
Coenzyme Q10
- Dosage: 100 mg daily
- Function: Mitochondrial protector
- Mechanism: Enhances ATP production, antioxidant
L-Glutamine
- Dosage: 5 g twice daily
- Function: Gut mucosa support during chemo
- Mechanism: Serves as fuel for enterocytes, decreases mucositis

Regenerative & Stem-Cell-Related Drugs

Focused on immunity and tissue repair.

Filgrastim (G-CSF)
- Dosage: 5 mcg/kg/day subcutaneously
- Function: Boosts white cell count after chemo
- Mechanism: Stimulates neutrophil progenitor proliferation
Pegfilgrastim
- Dosage: 6 mg single dose per chemo cycle
- Function: Long-acting G-CSF support
- Mechanism: Sustained neutrophil growth factor release
Erythropoietin-Alpha
- Dosage: 40,000 IU weekly
- Function: Prevents anemia and fatigue
- Mechanism: Stimulates red blood cell production
Thymosin Alpha-1
- Dosage: 1.6 mg subcutaneously twice weekly
- Function: Immunomodulation in refractory cases
- Mechanism: Enhances T-cell and dendritic cell function
Mesenchymal Stem Cell-Derived Exosomes
- Dosage: 1 × 10⁹ particles IV monthly (investigational)
- Function: Tissue repair and immune regulation
- Mechanism: Delivers growth factors, anti-inflammatory cytokines
Autologous Dendritic Cell Vaccines
- Dosage: Customized schedule post-resection
- Function: Stimulates patient’s immune response to tumor
- Mechanism: Presents tumor antigens to T-cells

Surgical Procedures

Procedure and Why It’s Done.

Wide Local Excision
- Removes tumor with margin to prevent local recurrence.
Amputation
- For limb HPCs when margins cannot be achieved safely.
Pelvic Resection
- En bloc removal of pelvic bone segments for deep pelvic HPCs.
Cranial Craniotomy
- For intracranial HPCs, to decompress brain and achieve control.
Laparoscopic Resection
- Minimally invasive removal of abdominal HPCs to reduce recovery time.

Prevention Strategies

Simple steps to lower risk or detect early.

Regular Health Screenings
Imaging Follow-Up After Benign Vascular Lesions
Genetic Counseling if Family History
Protective Equipment in Radiation-Occupational Settings
Healthy Weight Maintenance
Sun Protection for Skin Lesions
Prompt Evaluation of New Masses
Balanced Diet Rich in Antioxidants
Avoiding Tobacco and Excess Alcohol
Stress Management and Adequate Sleep

When to See a Doctor

Seek evaluation if you notice:

A growing lump anywhere on the body
Persistent pain, swelling, or numbness
Unexplained weight loss or fatigue
New headaches or vision changes (for head/neck lesions)
Shortness of breath or bone pain (possible metastasis)

Diet: What to Eat and What to Avoid

Eat:

Lean proteins (chicken, fish) for tissue repair
Fruits and vegetables high in antioxidants
Whole grains for steady energy
Healthy fats (olive oil, nuts) to support immunity
Hydrating fluids and broths

Avoid:

Processed foods high in sugar and trans fats
Excess red meat which may increase inflammation
Alcohol, which can worsen liver function during chemo
Unverified herbal concoctions without medical advice
High-salt snacks that can exacerbate swelling

Frequently Asked Questions

What causes hemangiopericytoma?
Abnormal growth of pericytes around blood vessels, often due to genetic fusions in tumor cells.
Is HPC benign or malignant?
Most behave indolently but have malignant potential; they can recur or metastasize in 20–30% of cases.
How is HPC diagnosed?
Via imaging (MRI/CT) and confirmed by biopsy with immunohistochemistry (STAT6 marker).
Can HPC come back after treatment?
Yes—regular imaging follow-up every 6–12 months is essential.
What is the role of radiation therapy?
It targets residual cells post-surgery or shrinks unresectable tumors.
Are there targeted therapies?
Yes—TKIs like pazopanib and sunitinib inhibit tumor angiogenesis.
How long is recovery after surgery?
Depends on location; minor resections may take weeks, major pelvic or cranial surgery can take months.
Can lifestyle affect outcomes?
Good nutrition, exercise, and stress management support healing and immunity.
Is there a genetic test for HPC?
Molecular testing for NAB2–STAT6 fusion confirms diagnosis but not susceptibility.
What are common side effects of chemotherapy?
Nausea, hair loss, fatigue, risk of infection, and organ toxicities.
Are herbal supplements safe?
Many can support health, but always discuss with your oncologist to avoid interactions.
How often should I have scans?
Typically every 6 months for the first 2 years, then annually if stable.
Can children develop HPC?
It is rare but can occur at any age; pediatric cases follow similar treatment protocols.
What is the survival rate?
Five-year survival ranges from 70% to 90% for localized disease when treated early.
Are there clinical trials for HPC?
Yes—investigate trials at major cancer centers for access to novel therapies.

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