A malignant tumor of the adrenal gland is a cancer that begins in one of the two small glands that sit on top of the kidneys. Each adrenal gland has two parts. The cortex makes steroid hormones (like cortisol, aldosterone, and androgens). The medulla makes stress hormones (like adrenaline and noradrenaline). When cells in either part grow in an uncontrolled way and can spread to other parts of the body, the tumor is called malignant. These cancers can cause symptoms by pressing on nearby tissues or, very often, by making too much hormone, which upsets the body’s balance.
A malignant tumor of the adrenal gland is a cancer that starts inside one of the two small glands that sit on top of your kidneys. These glands make many hormones that control blood pressure, stress response, salt-water balance, blood sugar, and sex hormones. When cells in the adrenal gland become abnormal and grow without control, they can form a cancer. Two main kinds exist: adrenocortical carcinoma (ACC), which starts in the hormone-making outer layer (cortex), and malignant pheochromocytoma/paraganglioma, which starts in the inner part (medulla) or related nerve tissue and can make adrenaline-type hormones. These cancers may make too much hormone, cause high blood pressure or Cushing-like symptoms, invade nearby tissues, and spread to other body parts. Treatment often combines surgery, medicine (including chemotherapy, hormone-blocking drugs, or immunotherapy), and supportive care by a specialist team.
Other names
Doctors use several names for malignant adrenal tumors. Adrenocortical carcinoma (ACC) means a cancer that starts in the outer layer (cortex) and often makes too much cortisol, aldosterone, or sex hormones. Malignant pheochromocytoma means a cancer arising from the inner layer (medulla) that produces adrenaline-type hormones. In children, a neuroblastoma can arise from adrenal medulla cells and act as a malignant tumor. You may also hear primary adrenal cancer (starts in the adrenal) and secondary or metastatic adrenal cancer (cancer that has spread to the adrenal from somewhere else, like lung or breast). Each name points to the cell of origin and the hormones it may release.
Types
Adrenocortical carcinoma (ACC). A rare cancer from the adrenal cortex. It may secrete cortisol (Cushing’s syndrome), aldosterone (salt and potassium imbalance), and/or androgens or estrogens (sex-hormone changes). It can grow large and spread to liver, lungs, or lymph nodes.
Malignant pheochromocytoma. A cancer from chromaffin cells in the adrenal medulla. It produces excess adrenaline-type hormones, causing sudden high blood pressure, headaches, sweating, and palpitations. Malignancy is defined by spread to sites where chromaffin cells are not normally found.
Adrenal neuroblastoma (mainly in children). A malignant tumor of immature nerve cells of the adrenal medulla. It can cause a belly mass, weight loss, or hormone problems.
Primary adrenal lymphoma (rare). A cancer of lymphoid cells that involves one or both adrenals, often with fatigue, weight loss, and low adrenal function.
Primary adrenal sarcoma (very rare). Cancer from connective tissue in the adrenal region.
Secondary or metastatic tumors to the adrenal. These are common and come from cancers like lung, breast, kidney, melanoma, or colon that spread to the adrenal. They are “adrenal malignancies” but not primary adrenal cancers.
Causes
Li-Fraumeni syndrome (TP53 gene change). A strong inherited risk for many cancers, including adrenocortical carcinoma. The TP53 change weakens the cell’s ability to repair DNA damage.
Beckwith–Wiedemann syndrome. An imprinting change on chromosome 11p15 that drives overgrowth and raises ACC risk in children.
Multiple Endocrine Neoplasia type 2 (RET gene). Increases risk of pheochromocytoma; some can behave malignantly.
Von Hippel–Lindau disease (VHL gene). Raises risk of pheochromocytoma and other tumors.
Neurofibromatosis type 1 (NF1 gene). Increases risk of pheochromocytoma; malignant behavior is possible.
SDHB gene mutation. A hereditary paraganglioma-pheochromocytoma syndrome with higher risk of malignant spread.
SDHD gene mutation. Similar pathway risk, though SDHB is more strongly linked to malignancy.
MAX gene mutation. Predisposes to pheochromocytoma; some tumors can be malignant.
TMEM127 gene mutation. Another inherited cause of pheochromocytoma.
MEN1 (MEN1 gene). Can be associated with adrenal tumors; rarely these can be malignant.
Somatic CTNNB1 (β-catenin/Wnt) pathway changes in ACC. Drive cell growth in sporadic (non-inherited) ACC.
IGF-2 overexpression in ACC. A growth factor that pushes cell proliferation in many adrenocortical cancers.
Chronic hormonal stimulation. Long-standing signals that push adrenal cells to divide may raise the chance of a malignant change in rare cases.
Prior radiation in childhood. Radiation can damage DNA and increase lifetime cancer risk, including rare adrenal primaries.
Family history of pheochromocytoma/paraganglioma. Suggests an inherited gene change.
Age extremes. ACC has peaks in very young children and in adults in mid-life; neuroblastoma occurs mainly in young children.
Female sex (for ACC). ACC slightly more common in women.
Smoking and environmental carcinogens. General cancer risks; evidence for direct adrenal causation is limited but plausible as contributors.
Secondary spread from other cancers. Not a cause of primary adrenal cancer, but a common reason for a malignant mass in the adrenal.
Unknown/idiopathic mutations. Many adrenal cancers arise without a known inherited syndrome; random DNA errors accumulate and drive malignancy.
Symptoms
High blood pressure. Tumors that make adrenaline or aldosterone can raise blood pressure. It may be constant or come in sudden spikes.
Pounding headache. Sudden surges of stress hormones can cause severe headaches, often with palpitations and sweating.
Heavy sweating. Adrenaline-type hormones trigger sweating, even at rest.
Fast or irregular heartbeat. Extra stress hormones stimulate the heart, causing palpitations or a racing pulse.
Anxiety or panic-like episodes. Hormone bursts can mimic panic attacks, with trembling and a sense of dread.
Weight gain with round face and central fat. Too much cortisol from ACC can cause Cushing’s syndrome, with fat around the belly and neck.
Purple stretch marks and easy bruising. Cortisol weakens skin and blood vessels.
Muscle weakness, especially in hips and shoulders. Cortisol breaks down muscle proteins, making it hard to climb stairs or lift objects.
High blood sugar and thirst. Cortisol increases sugar levels and insulin resistance, sometimes causing new diabetes.
Low potassium, cramps, and fatigue. Excess aldosterone wastes potassium and retains sodium, causing weakness and muscle cramps.
Hirsutism in women (more facial/body hair). Excess androgens from ACC push male-pattern hair growth.
Deepened voice or acne in women. Extra androgens alter skin and voice.
Irregular or absent periods. Hormone imbalance disrupts the menstrual cycle.
Breast enlargement or low sex drive in men. If the tumor makes estrogens, men can develop gynecomastia and reduced libido.
Abdominal or back pain, fullness, or unintentional weight loss. A growing mass or spread of cancer can cause pain, blockage, or general decline.
Diagnostic Tests
Physical Exam
General inspection for Cushingoid features. The clinician looks for round face, central weight gain, thin limbs, purple stretch marks, and bruises. These signs suggest cortisol excess from an adrenal cortex tumor.
Vital signs (blood pressure, pulse). Very high or fluctuating blood pressure and a rapid pulse raise suspicion for pheochromocytoma or aldosterone-secreting tumors.
Abdominal and back palpation. Gentle pressing may reveal a deep, firm mass or tenderness. Large adrenal tumors can be felt indirectly or cause flank fullness.
Sex-hormone effects on exam. The clinician checks for hirsutism, acne, deepened voice, gynecomastia, or testicular changes, which point to tumors making androgens or estrogens.
Manual Tests
Orthostatic blood pressure measurement. BP and pulse are checked lying, then standing. Big drops or spikes suggest hormone-driven instability, common in pheochromocytoma.
Waist circumference and BMI. Central obesity supports cortisol excess; tracking these helps follow response to treatment.
Manual muscle strength testing. Testing hip and shoulder girdle strength detects proximal weakness seen with high cortisol or low potassium.
Ferriman–Gallwey scoring for hirsutism. A simple visual scoring of hair growth in women helps grade androgen excess from a cortical tumor.
Lab & Pathological
Serum electrolytes and kidney function. Low potassium with high bicarbonate suggests aldosterone excess; lab values also guide safe care.
Morning serum cortisol and ACTH. High cortisol with low ACTH suggests an adrenal source; if ACTH is high, the source may be elsewhere.
Overnight 1-mg dexamethasone suppression test. A pill at night should suppress morning cortisol; failure to suppress points to autonomous cortisol production by a tumor.
24-hour urinary free cortisol or late-night salivary cortisol. These confirm sustained cortisol excess and help stage its severity.
Aldosterone-to-renin ratio. A high ratio suggests primary aldosteronism from an adrenal tumor that makes aldosterone.
Plasma free metanephrines or 24-hour urinary fractionated metanephrines. Very sensitive tests for pheochromocytoma; high values strongly suggest a catecholamine-secreting tumor.
Adrenal androgens (DHEA-S, androstenedione, testosterone) and estradiol. Abnormal levels identify tumors making sex hormones and help track treatment response.
Surgical pathology with tumor markers (e.g., Weiss criteria, Ki-67, SF-1). After removal, a pathologist examines the tumor under a microscope. Features like invasion, mitoses, and Ki-67 index confirm malignancy and help predict behavior.
Electrodiagnostic
Electrocardiogram (ECG). Detects rhythm problems from high catecholamines or low potassium (prolonged QT, arrhythmias), guiding urgent care.
Ambulatory blood pressure monitoring (ABPM) or 24-hour Holter (for pulse). Captures spikes of BP or heart rate that brief clinic checks can miss, supporting the diagnosis of hormone surges.
Imaging
Adrenal protocol CT scan with contrast. Measures size, shape, density (Hounsfield units), and contrast “washout.” ACC often appears large and heterogeneous; pheochromocytoma can be very vascular. CT also looks for spread to liver, lungs, or nodes.
Adrenal MRI (with chemical-shift and diffusion sequences). Helps tell benign from malignant tissue and is useful if CT contrast is not allowed. MRI can better define invasion into blood vessels or the liver. In selected cases, functional imaging (like FDG-PET/CT or MIBG for pheochromocytoma) maps active tumor sites throughout the body.
Non-pharmacological treatments
Physiotherapy
Energy-conserving activity pacing
Description: Break tasks into smaller steps, plan rest before fatigue, and spread chores across the day. Use timers and sit-to-stand strategies.
Purpose: Reduce exhaustion from cancer, hormones, or chemo.
Mechanism: Lowers physiologic strain and cortisol spikes; preserves ATP stores in muscles; prevents “boom-and-bust” cycles.
Benefits: More steady energy, fewer crashes, better ability to attend appointments and rehab.Progressive walking program
Description: Start with short, slow, flat walks (5–10 minutes), add 1–2 minutes every 2–3 days as tolerated.
Purpose: Rebuild stamina safely after surgery or during treatment.
Mechanism: Gradual aerobic conditioning improves mitochondrial efficiency and endothelial function; reduces resting heart rate and stress hormones.
Benefits: Better fitness, mood, sleep, and blood pressure control (especially helpful in pheochromocytoma after tumor control).Resistance training with bands
Description: 2–3 days/week: major muscle groups, 1–2 sets of 8–12 reps at light-to-moderate load.
Purpose: Fight muscle loss from cortisol excess or chemotherapy.
Mechanism: Muscle protein synthesis via mTOR signaling; improves insulin sensitivity.
Benefits: Stronger muscles, less fatigue, better bone support.Post-operative breathing exercises (incentive spirometry + diaphragmatic breathing)
Description: Use an incentive spirometer hourly while awake for several days after surgery; practice slow nasal diaphragmatic breathing.
Purpose: Prevent pneumonia and atelectasis after adrenal surgery.
Mechanism: Increases lung expansion and clears secretions.
Benefits: Fewer pulmonary complications, faster recovery.Thoraco-lumbar mobility and gentle core work
Description: Pelvic tilts, cat-camel, McGill “big three” (modified), 10–15 minutes/day.
Purpose: Reduce back discomfort from flank incision or tumor-related posture changes.
Mechanism: Improves spinal stability and proprioception.
Benefits: Less pain, easier walking and sitting.Balance and proprioception training
Description: Tandem stance, single-leg support near a counter, eyes-open then eyes-closed progression.
Purpose: Reduce fall risk from weakness, neuropathy, or blood pressure swings.
Mechanism: Trains vestibular and somatosensory systems.
Benefits: Fewer stumbles, safer independence.Pelvic floor and abdominal wall protection
Description: Teach log-rolling in/out of bed, cough support with pillow, avoid strain.
Purpose: Protect incisions after open adrenalectomy.
Mechanism: Keeps intra-abdominal pressure lower during healing.
Benefits: Less pain, reduced hernia risk.Gentle flexibility routine
Description: 20–30 second stretches for hip flexors, hamstrings, calves, chest.
Purpose: Counter stiffness from bed rest and steroids.
Mechanism: Increases muscle length and reduces fascial adhesions.
Benefits: Better stride, posture, and comfort.Neuropathy-safe foot care training
Description: Daily foot checks, proper shoes, moisturizers.
Purpose: Protect feet if chemo causes numbness.
Mechanism: Early detection prevents ulcers/infections.
Benefits: Fewer wounds; maintained mobility.Lymphedema-aware movement (if nodes removed)
Description: Gradual arm/core exercises with compression as advised.
Purpose: Minimize swelling after lymph node dissection.
Mechanism: Muscle pumping improves lymph flow.
Benefits: Swelling control, function preserved.Orthostatic hypotension prevention
Description: Rise slowly, ankle pumps before standing, small salty fluids if advised.
Purpose: Reduce dizziness during medication changes.
Mechanism: Boosts venous return and autonomic stability.
Benefits: Fewer falls and blackouts.Return-to-work conditioning
Description: Task-specific practice (lifting, reaching, computer setup).
Purpose: Safe work re-entry after treatment.
Mechanism: Gradual exposure builds capacity.
Benefits: Confidence and productivity.Scar mobility and desensitization
Description: Once healed, gentle circular massage and texture exposure.
Purpose: Reduce tightness and hypersensitivity.
Mechanism: Remodels collagen and calms nerve endings.
Benefits: Freer movement, less pain.Posture training for cortisol-related weakness
Description: Wall angels, chin tucks, mid-back strengthening.
Purpose: Correct rounded shoulders/back pain.
Mechanism: Restores scapular balance.
Benefits: Less strain, better breathing.Safe blood-pressure exercise monitoring
Description: Home BP/HR checks before/after sessions; defer if dangerously high.
Purpose: Keep exercise safe in hormonally active tumors.
Mechanism: Early detection of surges.
Benefits: Complication prevention.
Mind-Body / Gene-informed supportive care
Cognitive-behavioral therapy (CBT) for cancer stress
Description: Short, structured program to manage worry and treatment burden.
Purpose: Reduce anxiety/depression, improve adherence.
Mechanism: Reframes unhelpful thoughts; lowers sympathetic drive.
Benefits: Better sleep, coping, and quality of life.Mindfulness and paced breathing (4-6 breaths/min)
Description: 10–20 minutes daily, apps or guided sessions.
Purpose: Calm adrenergic symptoms and pain.
Mechanism: Vagal activation; lowers catecholamine output.
Benefits: Lower BP/HR variability, improved focus.Trauma-informed counseling
Description: Addresses fear from emergency hypertension crises or ICU stays.
Purpose: Prevent PTSD-like symptoms.
Mechanism: Exposure + coping skills.
Benefits: Less hypervigilance and better recovery.Sleep optimization program
Description: Fixed wake time, dark cool room, limit naps/caffeine; CBT-I if needed.
Purpose: Restore energy, immune function, glucose control.
Mechanism: Resets circadian rhythm.
Benefits: Less fatigue, improved mood and BP.Genetic counseling & family testing (when indicated)
Description: Discuss syndromes (e.g., Li-Fraumeni/TP53, Lynch, MEN2, SDHB).
Purpose: Early detection and prevention in families.
Mechanism: Risk stratification → tailored screening.
Benefits: Safer surveillance, informed choices.Guided imagery for procedural pain
Description: Brief imagery scripts before scans/needles.
Purpose: Reduce procedure anxiety.
Mechanism: Competes with pain pathways.
Benefits: Smoother visits, less sedation.
Educational / Practical supports
Medication literacy coaching
Description: Teach what each drug does, how and when to take it, and what to report.
Purpose: Improve adherence and safety.
Mechanism: Increases self-efficacy.
Benefits: Fewer missed doses and side effects.Blood pressure and glucose self-monitoring skills
Description: Home logs, thresholds for calling the team.
Purpose: Early detection of hormone crises or steroid effects.
Mechanism: Real-time feedback.
Benefits: Prevents emergencies.Nutrition counseling during treatment
Description: Registered dietitian sets protein/energy goals and manages salt/potassium per tumor/hormone status.
Purpose: Maintain weight and muscle; manage BP and electrolytes.
Mechanism: Personalized macronutrient/electrolyte planning.
Benefits: Better strength, fewer hospital visits.Care-navigation and financial counseling
Description: Help with referrals, transportation, work notes, and insurance.
Purpose: Reduce barriers to care.
Mechanism: Practical problem-solving.
Benefits: More consistent treatment and less stress.
Drug treatments
Important: Doses below are typical reference ranges for adults and must be individualized by oncology/endocrinology teams. Some uses are off-label due to the rarity of adrenal cancers.
Mitotane
Class: Adrenolytic steroidogenesis inhibitor.
Typical dose/time: Start ~1–2 g/day in divided doses with fatty food; titrate to 3–6 g/day; aim for blood level 14–20 mg/L; long half-life (weeks).
Purpose: Core drug for metastatic or high-risk ACC; also used adjuvantly.
Mechanism: Selectively damages adrenal cortical cells and inhibits 11β-hydroxylase; lowers cortisol/androgen production.
Side effects: Nausea, fatigue, neurocognitive slowdown, liver enzyme rise; adrenal insufficiency requiring steroid replacement.Etoposide
Class: Topoisomerase II inhibitor (chemotherapy).
Dose/time: 100 mg/m² IV days 2–4 in EDP-M cycle every 3–4 weeks.
Purpose: Part of first-line combo for advanced ACC.
Mechanism: DNA strand breaks → apoptosis.
Side effects: Low blood counts, hair loss, mucositis.Doxorubicin
Class: Anthracycline.
Dose/time: 40–50 mg/m² IV day 1 in EDP-M; cumulative lifetime max due to cardiotoxicity.
Purpose: Cytotoxic backbone for ACC.
Mechanism: DNA intercalation and free radicals.
Side effects: Myelosuppression, cardiomyopathy risk, nausea, alopecia.Cisplatin
Class: Platinum agent.
Dose/time: ~40 mg/m² IV day 1 in EDP-M (varies); hydration required.
Purpose: Cytotoxicity in ACC.
Mechanism: DNA crosslinks.
Side effects: Kidney injury, neuropathy, nausea, hearing loss.Carboplatin
Class: Platinum agent.
Dose/time: AUC-based dosing IV every 3–4 weeks (used if cisplatin unsuitable).
Purpose: Alternative platinum in ACC regimens.
Mechanism: DNA crosslinks.
Side effects: Myelosuppression, less nephro/ototoxicity than cisplatin.Streptozocin
Class: Alkylating agent (nitrosourea).
Dose/time: IV days 1–5 every 6 weeks (legacy ACC option).
Purpose: Older option when EDP-M not tolerated.
Mechanism: DNA alkylation.
Side effects: Nausea, kidney toxicity, glucose changes.Gemcitabine ± Capecitabine
Class: Antimetabolites.
Dose/time: Gemcitabine 800–1000 mg/m² IV weekly; capecitabine 1000–1250 mg/m² PO bid days 1–14 q21 days.
Purpose: Later-line ACC; symptom control.
Mechanism: DNA synthesis inhibition.
Side effects: Fatigue, hand-foot syndrome (cape), cytopenias.Pembrolizumab (or Nivolumab)
Class: PD-1 immune checkpoint inhibitors.
Dose/time: Pembro 200 mg IV q3 weeks or 400 mg q6 weeks; Nivo 240 mg q2 weeks or 480 mg q4 weeks.
Purpose: Select patients with advanced ACC or malignant PPGL, especially if MSI-H, high TMB, or after other lines.
Mechanism: Re-activates anti-tumor T-cells.
Side effects: Immune-related: thyroiditis, colitis, hepatitis, rash; needs prompt management.Ipilimumab (± Nivolumab)
Class: CTLA-4 inhibitor (immune checkpoint).
Dose/time: Ipi 1–3 mg/kg IV q3 weeks × 4, often with nivolumab.
Purpose: Some refractory ACC cases or trials in PPGL.
Mechanism: Expands T-cell priming.
Side effects: Higher immune-toxicity risk.Tyrosine kinase inhibitors (Cabozantinib, Sunitinib, Pazopanib)
Class: Multi-target TKIs (VEGFR, MET, etc.).
Dose/time: Cabozantinib 60 mg PO daily (adjust as needed); sunitinib 37.5–50 mg PO (continuous or 4/2 schedule).
Purpose: Later-line ACC and metastatic PPGL in selected cases.
Mechanism: Blocks tumor angiogenesis and signaling.
Side effects: Hypertension, fatigue, diarrhea, hand-foot syndrome.Temozolomide
Class: Alkylating agent (oral).
Dose/time: 150–200 mg/m² PO days 1–5 q28 days; may work better in SDHB-mutated PPGL.
Purpose: Metastatic PPGL or ACC later line.
Mechanism: DNA methylation causing tumor cell death.
Side effects: Cytopenias, fatigue, nausea.Cyclophosphamide + Vincristine + Dacarbazine (CVD)
Class: Combination chemotherapy.
Dose/time: Cycles q3–4 weeks per protocol.
Purpose: Classic regimen for metastatic pheochromocytoma/paraganglioma.
Mechanism: Multi-pathway cytotoxicity.
Side effects: Low counts, neuropathy (vincristine), nausea.Phenoxybenzamine (or Doxazosin) – pre-op alpha blockade
Class: Non-selective (phenoxybenzamine) or selective (doxazosin) α-blockers.
Dose/time: Phenoxybenzamine 10 mg PO bid, titrate; doxazosin 1–16 mg/day.
Purpose: Control severe hypertension and prevent surgical crises in catecholamine-secreting tumors.
Mechanism: Blocks α-adrenergic receptors → vasodilation.
Side effects: Orthostatic hypotension, nasal stuffiness, fatigue.Metyrosine
Class: Tyrosine hydroxylase inhibitor.
Dose/time: 250 mg PO qid, titrate up (often 1–4 g/day).
Purpose: Reduce catecholamine production in malignant PPGL when α-blockade alone is not enough.
Mechanism: Blocks first step in catecholamine synthesis.
Side effects: Sedation, depression, crystalluria (hydrate well).Glucocorticoid and mineralocorticoid replacement (Hydrocortisone ± Fludrocortisone)
Class: Hormone replacement.
Dose/time: Hydrocortisone 10–25 mg/day in divided doses; fludrocortisone 0.05–0.2 mg/day if needed.
Purpose: Treat or prevent adrenal insufficiency due to mitotane or surgery.
Mechanism: Restores deficient hormones.
Side effects: Weight gain, glucose rise, BP changes (monitor closely).
Dietary molecular supplements
Always discuss supplements with your oncology team—interactions are possible.
Protein (whey/pea) 20–30 g per meal
Function/mechanism: Provides leucine to trigger muscle protein synthesis; helps counter catabolism from cortisol or chemo.
Note: Adjust if kidney issues.Omega-3 fatty acids (EPA+DHA 1–2 g/day)
Mechanism: Anti-inflammatory eicosanoid shift; may help appetite and weight.
Note: Watch bleeding risk with TKIs/anticoagulants.Vitamin D3 (target 25-OH D 30–50 ng/mL; typical 1000–2000 IU/day)
Mechanism: Bone, muscle, and immune support; steroid-related bone loss prevention.
Note: Check levels; avoid excess.Calcium (1000–1200 mg/day from food; supplement if needed)
Mechanism: Bone health with steroids/mitotane.
Note: Split doses; avoid with certain TKIs near dosing time.Magnesium (200–400 mg/day)
Mechanism: Supports muscle/nerve function; helpful if cisplatin lowers Mg.
Note: Separate from thyroid meds and some TKIs.Soluble fiber (psyllium 5–10 g/day)
Mechanism: Improves bowel regularity and cholesterol; stabilizes glucose.
Note: Take with water; separate from oral chemo.Probiotics (evidence-based strains, e.g., Lactobacillus rhamnosus GG)
Mechanism: Gut barrier support, may reduce antibiotic-related diarrhea.
Note: Avoid if severely immunosuppressed without doctor approval.Curcumin (Meriva/BCM-95 forms 500–1000 mg/day)
Mechanism: Anti-inflammatory signaling (NF-κB).
Note: Interaction potential with chemo/TKIs; confirm.Green tea extract (EGCG 200–400 mg/day)
Mechanism: Antioxidant and metabolic support.
Note: Space away from bortezomib-like drugs (not typical here) and from TKI doses.Coenzyme Q10 (100–200 mg/day)
Mechanism: Mitochondrial support; may help fatigue during anthracyclines.
Note: Discuss if on anticoagulants.
Immunity-booster / Regenerative / Stem-cell” drug concepts
There are no approved “stem-cell drugs” to cure adrenal cancer. Below are clinically used or studied immune-supportive or immunotherapy options; use only under specialist care.
G-CSF (filgrastim/pegfilgrastim) – Dose: per chemo protocol. Function: Stimulates neutrophil production to prevent infections during cytotoxic chemo. Mechanism: Binds G-CSF receptor in marrow to speed neutrophil maturation.
IVIG (selected cases) – Dose: individualized. Function: Temporary immune support in hypogammaglobulinemia or autoimmune complications. Mechanism: Provides pooled antibodies; modulates Fc receptors.
Interferon-alpha (legacy/selected PPGL cases) – Function: Anti-proliferative and immune-modulating effects. Mechanism: JAK-STAT–mediated antiviral/cell-cycle signals.
Checkpoint inhibitors (PD-1/CTLA-4) – Function: Reactivate T-cells against tumor antigens. Mechanism: Remove inhibitory signals on T-cells. Note: Benefits in a subset; immune toxicities require expertise.
Cancer vaccines / adoptive T-cell trials – Function: Experimental options creating/expanding tumor-specific immunity. Mechanism: Ex vivo T-cell priming or neoantigen vaccination. Note: Clinical trial only.
Erythropoiesis-stimulating agents (ESAs) – Function: Treat chemo-induced anemia to reduce transfusions. Mechanism: Stimulates red cell production. Note: Use follows strict oncology guidelines.
Surgeries
Open adrenalectomy (preferred for suspected ACC)
Procedure: Large incision to remove the adrenal gland and tumor en bloc, sometimes with nearby tissue.
Why: Better margin control and safety when tumors are large or invasive.Laparoscopic adrenalectomy (selected, smaller non-invasive tumors)
Procedure: Keyhole removal with camera tools.
Why: Faster recovery for small, localized lesions without invasion.En bloc resection with adjacent organs
Procedure: Remove adrenal plus involved kidney, liver segment, or diaphragm if invaded.
Why: Achieve clear margins to reduce recurrence.Lymph node dissection
Procedure: Remove regional nodes.
Why: Staging and potential local control.Metastasectomy / Cytoreductive (debulking) surgery
Procedure: Remove solitary or limited metastases (e.g., lung/liver).
Why: Symptom relief, hormone control, and in selected cases, improved outcomes.
Preventions
Genetic counseling/testing if family history or young age at diagnosis.
Syndrome-specific surveillance (e.g., MEN2, Li-Fraumeni, SDHB) per guidelines.
Do not ignore “adrenal incidentalomas”—complete hormonal testing and risk imaging.
Manage hypertension and diabetes—lowers surgical risk and complications.
Avoid unnecessary radiation exposure; use ultrasound/MRI when suitable.
Healthy body weight and regular activity—general cancer-risk reduction.
No tobacco; limit alcohol—supports overall cancer and heart health.
Adequate sleep and stress management—stabilizes autonomic responses.
Medication review—avoid interactions that raise BP or cortisol without monitoring (e.g., decongestants, high-dose steroids).
Vaccinations up to date—especially before chemo/immunotherapy.
When to see a doctor
Severe headache, pounding heartbeat, sweating attacks, or sudden very high blood pressure—possible catecholamine crisis.
Rapid weight gain, purple stretch marks, easy bruising, new diabetes or blood pressure hard to control—possible cortisol excess.
Muscle weakness, severe fatigue, salt craving, low blood pressure, vomiting—possible adrenal insufficiency (medical emergency if severe).
Any adrenal mass >4 cm, or fast-growing mass on imaging.
After adrenal surgery or on mitotane with fever, vomiting, or fainting—possible adrenal crisis; use emergency steroid plan.
Diet: “what to eat” and “what to avoid”
Eat more of:
Lean proteins (fish, eggs, poultry, tofu) to protect muscle.
High-fiber whole grains (oats, brown rice) for glucose and bowel health.
Colorful vegetables and fruits for antioxidants and potassium (adjust if potassium restricted).
Healthy fats (olive oil, nuts, seeds) for energy and satiety.
Fermented foods (yogurt, kefir, tempeh) for gut health if safe.
Limit/avoid:
- Very salty processed foods if hypertension problematic (exceptions if advised to increase salt pre-op pheo—follow your doctor).
- Excess caffeine/energy drinks—can worsen palpitations/BP.
- Alcohol—can interact with chemo and BP meds.
- Licorice (glycyrrhizin)—can raise BP and lower potassium.
- Grapefruit with certain TKIs—alters drug metabolism (ask your team).
Frequently asked questions
Is every adrenal tumor cancer?
No. Many are benign. Hormone tests and imaging help decide if surgery is needed.What is the main cancer of the adrenal cortex?
Adrenocortical carcinoma (ACC). It can make cortisol, androgens, or none.What is malignant pheochromocytoma?
A catecholamine-producing tumor that has spread or shows aggressive behavior.How is ACC usually treated first?
Surgery when possible. If high-risk or metastatic, mitotane and/or combination chemotherapy are considered.Why do I need alpha-blockers before pheochromocytoma surgery?
To prevent dangerous blood-pressure spikes during surgery.Can immunotherapy help?
Sometimes. A subset of patients benefit, especially with certain tumor features. Your oncologist will check eligibility.Will I need hormone pills after surgery?
Possibly, especially if both glands are affected or you take mitotane. Many people carry an emergency steroid card.How often will I need scans?
Regular imaging and hormone labs for years; schedule depends on tumor type and stage.What are red flags after discharge?
Fever, vomiting, severe weakness, very low BP or confusion—call urgently.Can lifestyle changes cure the cancer?
Lifestyle supports treatment and recovery but does not replace medical therapy.Are there approved stem-cell cures?
No. Consider clinical trials only through accredited centers.Can I exercise during treatment?
Yes, with guidance. Start low, go slow, monitor BP/HR, and stop for warning signs.What if my tumor was found by accident?
Adrenal incidentalomas are common. Your team will check hormone activity and cancer risk.Should my family be tested?
If you have features suggesting a hereditary syndrome, genetic counseling is recommended.What is the outlook?
It varies by stage, tumor biology, and response to treatment. Early complete surgery gives the best chance.
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: September 09, 2025.
