Adrenal gland cancer means a harmful tumor starts in one or both adrenal glands. These glands sit above the kidneys. They make hormones that control stress, blood pressure, salt balance, sex traits, and metabolism. Cancer can grow from the outer layer (the cortex) or the inner part (the medulla). Tumors may make extra hormones, or they may be “silent” and grow without clear signs. The cancer can stay in the gland or spread to nearby tissues, lymph nodes, liver, lungs, bone, or other organs. Early diagnosis and careful hormone testing help doctors choose the right treatment.
Adrenal gland cancer most often means adrenocortical carcinoma (ACC)—a rare, aggressive cancer that starts in the outer layer (cortex) of the adrenal gland. The cortex makes steroid hormones such as cortisol, aldosterone, and androgens/estrogens. In ACC, cells grow out of control and may also overproduce hormones, causing body-wide changes (for example, Cushing’s syndrome from too much cortisol). ACC can spread (metastasize) to nearby tissues (kidney, liver, vena cava) or distant organs (lung, liver, bone). The main cure, when possible, is complete surgical removal. Many people also need medicines to control hormones and chemotherapy to treat or reduce the tumor. ACC is different from malignant pheochromocytoma, which comes from the inner medulla; this guide focuses on adrenocortical carcinoma.
Another names
Adrenal gland cancer is also called adrenocortical carcinoma (ACC) when it begins in the adrenal cortex. It may be called adrenal cortex carcinoma, adrenal cortical cancer, or primary adrenal cancer. Cancers from the adrenal medulla are usually pheochromocytomas; when they spread, people say malignant pheochromocytoma or adrenal medullary carcinoma. Doctors also use phrases like hormone-secreting adrenal tumor, functional adrenal carcinoma, or nonfunctional adrenal carcinoma depending on whether hormones are overproduced. If cancer from another organ spreads to the adrenal, that is adrenal metastasis, which is different from primary adrenal gland cancer.
Types
By the adrenal part involved
Adrenocortical carcinoma (ACC). A rare cancer of the adrenal cortex. It may produce excess cortisol, aldosterone, androgens, or estrogens, or be non-secreting. It tends to be aggressive and needs prompt care.
Adrenal medulla cancers. The classic tumor is pheochromocytoma. Most are benign; some are malignant and can spread (metastasize). They make extra catecholamines (adrenaline-like hormones) and cause severe blood pressure spikes.
By hormone activity
Functional tumors. These make extra hormones. Subtypes include:
Cortisol-secreting ACC (Cushing syndrome): causes weight gain in trunk, round face, easy bruising, high blood sugar, and weak muscles.
Aldosterone-secreting ACC (primary aldosteronism): causes high blood pressure, low potassium, muscle cramps, and fatigue.
Androgen-secreting ACC: causes hirsutism, acne, deep voice, and menstrual changes in women; early puberty in children.
Estrogen-secreting ACC: causes breast growth and low sex drive in men; abnormal bleeding in women.
Catecholamine-secreting pheochromocytoma: causes episodes of headache, palpitations, sweating, tremor, and sudden high blood pressure.
Nonfunctional tumors. These do not make extra hormones. They may stay silent until they grow large and cause pressure symptoms.
By behavior, cells, or special patterns
Conventional ACC, oncocytic ACC (cells look packed with mitochondria), and myxoid variants (gel-like stroma). Pathologists also grade tumors by Ki-67 index and other features under the microscope.
Primary adrenal lymphoma and sarcomas (very rare) can arise in the adrenal region and may mimic adrenal cancer.
Adrenal metastases (from lung, kidney, melanoma, colon, or breast) are common but are not primary adrenal gland cancers; they change treatment choices.
Causes
Adrenal gland cancer is rare. For many people, the exact cause is unknown. Still, research shows several genetic syndromes, inherited changes, and exposures that raise the risk. Below are 20 important, evidence-based contributors explained in simple terms:
Li-Fraumeni syndrome (TP53 mutation). A strong inherited risk. The TP53 gene repairs DNA damage. When it is faulty, cells can grow into cancer, including ACC, especially in children and young adults.
Beckwith-Wiedemann spectrum (11p15 imprinting defects). Children with this overgrowth syndrome have higher risk of several tumors, including adrenocortical tumors. Abnormal control of growth genes (like IGF2) promotes tumor growth.
Lynch syndrome (mismatch repair gene defects). Best known for colon and uterine cancers. It also slightly raises the risk of adrenal tumors. Faulty “spell-check” for DNA lets mutations build up.
MEN1 (multiple endocrine neoplasia type 1). Usually causes benign endocrine tumors, but the adrenal cortex can form tumors, and rarely a cancer can develop due to long-term growth signals.
MEN2 (RET mutations). Strongly linked to pheochromocytoma. While most pheochromocytomas are benign, RET mutations increase the chance of bilateral tumors and, rarely, malignancy.
Von Hippel–Lindau (VHL). Raises risk of pheochromocytoma and other tumors. Mutant VHL fails to control cell responses to low oxygen, allowing growth pathways to stay “on.”
Neurofibromatosis type 1 (NF1). Increases risk of pheochromocytoma. NF1 gene loss activates growth pathways in nerve-related cells that can exist in the adrenal medulla.
SDHx mutations (SDHB, SDHC, SDHD). Affect mitochondrial energy enzymes. These mutations raise risk of pheochromocytomas and paragangliomas; SDHB is linked with higher risk of malignancy.
Carney complex (PRKAR1A). Commonly causes adrenal nodules and cortisol excess. While ACC is rare here, dysregulated cAMP signaling can drive abnormal adrenal growth.
Family history of ACC or adrenal tumors. Suggests a heritable predisposition. Genetic counseling and testing may be recommended.
Childhood age peak (for ACC). ACC has a small peak in very young children, reflecting developmental windows when growth pathways are more active and vulnerable.
Adult age (40–60 years). A second peak occurs in mid-life, when cumulative DNA damage and hormonal influences may permit malignant transformation.
Prior radiation exposure to abdomen/retroperitoneum. Radiation can injure DNA and raise long-term cancer risk in exposed tissues, including the adrenal area.
Certain environmental exposures (probable). Long-term exposure to some pesticides or industrial chemicals may increase risk, though data are mixed. Mechanisms may include endocrine disruption and DNA injury.
Tobacco smoke (general carcinogen). Smoking increases many cancer risks. While evidence is stronger for other organs, carcinogens can affect adrenal tissue as well.
Chronic hormonal stimulation (theory). Long-standing ACTH drive or other trophic signals may encourage growth of abnormal adrenal cells, though direct proof in humans is limited.
Obesity and metabolic stress (possible). Insulin resistance and chronic inflammation may support tumor growth signals. Evidence is suggestive rather than definitive for ACC.
Immunosuppression (possible). Reduced immune surveillance can allow abnormal adrenal cells to escape detection and expand.
High birth weight / overgrowth states in infancy. Seen in Beckwith-Wiedemann and some non-syndromic cases; excessive growth signals can raise tumor risk early in life.
Random (sporadic) DNA errors. Even without known risks, cells sometimes acquire harmful mutations by chance over time, leading to cancer.
Note: Some items above are risk factors or syndromic drivers, not direct “causes” in every person. Most people with these risks do not develop adrenal cancer, but their odds are higher than average.
Symptoms
A growing belly lump or deep flank fullness. A large adrenal tumor can press on nearby organs, causing a sense of fullness, early satiety, or a palpable mass.
Persistent back or side pain. Tumor pressure on muscles, nerves, or the diaphragm can cause dull, constant pain behind the ribs.
Unexplained weight loss. Cancer uses energy and changes metabolism, leading to gradual weight loss even without dieting.
Severe or resistant high blood pressure. Aldosterone-secreting tumors and pheochromocytomas often cause hard-to-control hypertension.
Sudden blood pressure spikes with headache, palpitations, and sweating. Classic “spells” of catecholamine excess point to pheochromocytoma or a medullary tumor.
Muscle weakness and cramps. Low potassium from aldosterone excess weakens muscles and may trigger cramps or tingling.
New-onset or worsening diabetes and easy bruising. Cortisol-secreting tumors raise blood sugar and thin skin, causing purple stretch marks and bruises.
Central weight gain with thin limbs and round face. Typical of excess cortisol (Cushing features), often with fragile skin and poor wound healing.
Infections that occur more often than usual. High cortisol suppresses the immune system, making infections more likely.
Hirsutism, acne, deepened voice, or menstrual changes in women. Excess androgens from an adrenal tumor can cause male-pattern hair growth and cycle disruption.
Early puberty in children. Androgen-secreting tumors may trigger rapid growth, acne, and pubic hair at a very young age.
Breast enlargement and low libido in men. Estrogen-secreting tumors can cause gynecomastia, erectile dysfunction, and reduced facial hair.
Nausea, tremor, and anxiety episodes. Catecholamine surges can cause shaking, pale skin, and a sense of panic.
Shortness of breath or cough. If cancer spreads to the lungs or presses on the diaphragm, breathing symptoms can appear.
Bone pain or fractures. Metastases or severe cortisol excess (which thins bone) can lead to aches and breaks after minor injury.
Diagnostic tests
The exact test set is tailored to the person’s symptoms, hormone findings, and imaging. Doctors often start with hormone screening and a dedicated adrenal CT or MRI. Below are 20 key tests explained clearly.
A) Physical examination
Focused blood pressure assessment (sitting and standing). The clinician measures BP to detect persistent hypertension or dramatic surges that suggest catecholamine excess. Orthostatic vitals also show volume status and aldosterone effects.
Cushing features check. The doctor looks for central obesity, moon face, buffalo hump, purple stretch marks, thin skin, acne, and easy bruising—classic signs of cortisol excess from a functional tumor.
Virilization or feminization exam. In women, excess androgens cause facial/body hair, acne, and clitoromegaly; in men, excess estrogens cause breast enlargement and reduced body hair. These clues point to hormone-secreting ACC.
Abdominal and flank palpation. Gentle–deep palpation may detect a mass, tenderness, or fullness in the upper abdomen or back area where the adrenals sit.
B) Manual/bedside tests
Postural (orthostatic) blood pressure test. Manual BP readings after lying down and standing can reveal volume depletion or aldosterone-driven hypertension patterns.
Neuromuscular strength testing. Simple bedside maneuvers (rising from a chair without hands, hip flexion against resistance) detect proximal muscle weakness common in Cushing syndrome and severe hypokalemia.
Ferriman–Gallwey hair scoring (in women). A standardized visual score for hair growth at specific body sites helps quantify androgen effects from an adrenal tumor.
C) Laboratory and pathological tests
Overnight 1-mg dexamethasone suppression test (DST). You take dexamethasone at night; a morning cortisol is drawn. Failure of cortisol to suppress suggests autonomous cortisol production from an adrenal tumor.
24-hour urinary free cortisol (UFC). Measures cortisol over a day. High values confirm cortisol excess and help judge severity.
Late-night salivary cortisol. Cortisol should be low at bedtime. A high level points to loss of normal rhythm and autonomous secretion.
Plasma aldosterone concentration and plasma renin (aldosterone/renin ratio). A high ratio suggests primary aldosteronism from an aldosterone-producing tumor, especially with low potassium.
Plasma free metanephrines (± urinary fractionated metanephrines). These breakdown products of catecholamines are very sensitive for pheochromocytoma. Markedly high levels need imaging confirmation.
Adrenal androgen panel (DHEA-S, testosterone) and estradiol. Elevated adrenal androgens (or estradiol in men) point to hormone-secreting ACC.
Basic metabolic panel (potassium, sodium, bicarbonate, glucose). Low potassium and metabolic alkalosis suggest aldosterone excess; high glucose suggests cortisol excess.
Pathology of the adrenal mass (when appropriate). If the adrenal is removed, the pathologist applies Weiss criteria, Ki-67 index, and other features to confirm ACC and estimate aggressiveness. Needle biopsy is usually avoided for suspected ACC because it rarely changes management and may risk tumor seeding; it is reserved for cases where metastasis from another cancer is sspected and results would change treatment.
D) Electrodiagnostic / physiologic monitoring
12-lead electrocardiogram (ECG). Looks for hypokalemia-related changes (from aldosterone excess), arrhythmias due to high catecholamines, or strain from severe hypertension.
Ambulatory blood pressure monitoring (24-hour). Captures BP spikes and daily patterns that office readings can miss, helping confirm catecholamine surges or aldosterone-related hypertension.
E) Imaging tests
Adrenal-protocol CT scan. Thin-slice CT measures size, density (Hounsfield units), and contrast washout. ACC often has irregular edges, higher density (>10 HU), and delayed washout, while benign adenomas often show rapid washout and fat content.
MRI with chemical-shift imaging. MRI detects intracellular fat within adenomas and characterizes soft tissue and vascular invasion. ACC usually lacks signal drop on out-of-phase images and may invade nearby vessels.
FDG PET-CT for staging. Cancer cells use more glucose and light up on PET. This test helps detect spread to lymph nodes, liver, lungs, or bone and can distinguish active disease from scar tissue.
Other specialized scans (e.g., MIBG for pheochromocytoma, DOTATATE PET for certain neuroendocrine tumors) may be used in selected cases, but the 20 tests above cover the standard diagnostic pathway for most people.
Non-Pharmacological Treatments
Physiotherapy
Personalized Strength Training
Description: A gentle, progressive program focusing on large muscle groups (legs, hips, back, core) 2–3 days/week, adapted for fatigue and steroid myopathy.
Purpose: Maintain muscle mass and function lost from cortisol excess or chemotherapy.
Mechanism: Repeated resistance creates muscle protein synthesis; counters catabolic effects of cortisol; improves insulin sensitivity.
Benefits: Better mobility, less fatigue, improved balance, and fewer falls; supports bone health.Aerobic Walking Plan
Description: Short daily walks (10–30 minutes), with rest as needed, using a step or heart-rate target approved by the care team.
Purpose: Reduce fatigue, improve mood and cardiovascular health.
Mechanism: Increases mitochondrial efficiency and endorphins; improves blood pressure and glucose control.
Benefits: Higher stamina, better sleep, and quality of life.Balance and Gait Training
Description: Supervised drills (tandem stance, single-leg holds, obstacle navigation).
Purpose: Prevent falls in people with muscle weakness or steroid-related myopathy.
Mechanism: Neuromuscular adaptation improves proprioception and reflexes.
Benefits: Fewer falls, safer independence.Flexibility & Joint Mobility
Description: Daily stretching (hips, hamstrings, shoulders, spine) and gentle yoga poses tailored to energy level.
Purpose: Ease stiffness from inactivity and pain.
Mechanism: Lengthens muscle–tendon units and reduces spasm.
Benefits: Better range of motion, easier daily tasks.Pulmonary Conditioning
Description: Breathing exercises, incentive spirometry, and posture drills.
Purpose: Support lung function around anesthesia, abdominal surgery, or bed rest.
Mechanism: Recruits collapsed alveoli and strengthens respiratory muscles.
Benefits: Fewer post-op lung complications; less shortness of breath.Pelvic and Core Stabilization
Description: Gentle core activation (abdominal bracing, bridges), progressing as tolerated.
Purpose: Protect spine weakened by steroid-induced osteoporosis and improve posture.
Mechanism: Strengthens deep stabilizers and reduces mechanical strain.
Benefits: Less back pain, safer lifting.Lymphedema-Aware Mobility
Description: If lymph nodes removed, use graded exercise, elevation, and compression as advised.
Purpose: Limit limb or abdominal wall swelling.
Mechanism: Muscle pump plus external compression aids lymph return.
Benefits: Comfort, function, and lower infection risk.Neuromuscular Electrical Stimulation (as appropriate)
Description: Low-level muscle stimulation prescribed by a therapist.
Purpose: Preserve muscle in severe deconditioning.
Mechanism: Elicits contractions when voluntary effort is limited.
Benefits: Maintains strength; bridges back to active exercise.Post-operative Early Mobilization
Description: Day-of-surgery sitting/standing (if cleared), walking with assistance.
Purpose: Prevent clots, pneumonia, and ileus.
Mechanism: Restores circulation and gut motility.
Benefits: Faster recovery and shorter hospital stay.Bone Health Program
Description: Weight-bearing steps, mini-squats, and safe impact (if allowed).
Purpose: Combat steroid-induced bone loss.
Mechanism: Mechanical loading stimulates osteoblasts.
Benefits: Stronger bones, fewer fractures.Fatigue Pacing & Energy Conservation
Description: Break tasks into chunks, rest planning, use of tools (grabbers, shower chair).
Purpose: Reduce “boom-and-bust” exhaustion.
Mechanism: Balances energy input/output and autonomic stress.
Benefits: More predictable days and better participation in care.Pain-Modulating Movement
Description: Gentle, frequent movement within pain limits (no bed rest unless necessary).
Purpose: Reduce chronic pain spirals.
Mechanism: Restores central pain inhibition and joint nutrition.
Benefits: Less stiffness, better mood.Scar & Abdominal Wall Care
Description: After healing, guided scar massage and posture training.
Purpose: Prevent adhesions and posture-related discomfort.
Mechanism: Mobilizes tissues and retrains core.
Benefits: Freer movement, less pulling pain.Safe Return-to-Work/Role Training
Description: Task-specific graded practice and ergonomic tweaks.
Purpose: Reintegration into daily roles without flare-ups.
Mechanism: Gradual exposure and workload titration.
Benefits: Confidence and function.Sleep Optimization Routine
Description: Fixed bed/wake times, light exposure in morning, no screens 1 hour before bed.
Purpose: Counter insomnia from steroids/stress.
Mechanism: Resets circadian rhythm and melatonin release.
Benefits: Better energy, mood, immunity support.
Mind-Body, “Gene” & Educational Therapies
Cognitive Behavioral Therapy (CBT)
Description: Short, structured sessions to reframe thoughts and behaviors.
Purpose: Manage anxiety/depression common in cancer and Cushing’s.
Mechanism: Changes stress pathway activation (HPA axis) and coping patterns.
Benefits: Lower distress, better adherence to care.Mindful Breathing & Meditation
Description: 10–15 minutes/day of guided breathing or mindfulness.
Purpose: Reduce stress hormones and improve pain perception.
Mechanism: Activates parasympathetic tone; dampens cortisol spikes.
Benefits: Calmer mood, better sleep, lower BP.Guided Imagery for Nausea/Pain
Description: Audio scripts that prime relaxation during chemo.
Purpose: Ease anticipatory nausea and procedural anxiety.
Mechanism: Top-down modulation of autonomic and pain circuits.
Benefits: Improved tolerance of treatments.Support Groups / Peer Mentoring
Description: In-person or online communities for ACC.
Purpose: Social connection and shared problem-solving.
Mechanism: Reduces isolation; improves resilience.
Benefits: Practical tips, emotional relief.Nutrition Education by Oncology Dietitian
Description: Tailored meal plans for hormone effects (e.g., high potassium, low sodium).
Purpose: Maintain weight, protect bones, control BP/glucose.
Mechanism: Targets metabolic complications of cortisol/aldosterone.
Benefits: More energy, fewer hospitalizations.Medication Literacy Coaching
Description: Teach timing, interactions (e.g., mitotane and steroids), and side-effect logs.
Purpose: Improve safety and effectiveness of therapy.
Mechanism: Increases adherence and early side-effect reporting.
Benefits: Fewer complications.Steroid Safety Education
Description: Wallet card, sick-day rules, emergency hydrocortisone injection training.
Purpose: Prevent adrenal crisis, especially with mitotane or after surgery.
Mechanism: Rapid stress-dose access and recognition of warning signs.
Benefits: Life-saving preparedness.Financial & Navigation Counseling
Description: Help with insurance, leave from work, transport, lodging.
Purpose: Reduce treatment delays.
Mechanism: Removes logistical barriers.
Benefits: Smoother, faster care.Palliative Care Integration (early)
Description: Symptom-focused team support from diagnosis.
Purpose: Manage pain, fatigue, mood—alongside cancer care.
Mechanism: Multidisciplinary symptom science.
Benefits: Better quality of life; often better survival.Advance Care Planning
Description: Discuss values, goals, and preferences.
Purpose: Aligns care with what matters to you.
Mechanism: Clear directives guide teams and families.
Benefits: More control and peace of mind.
Drug Treatments
Important: Exact drug choices, doses, and schedules are individualized. Do not self-medicate. Many of these interact with each other. Always follow your oncology/endocrinology team.
Mitotane (adrenolytic)
Typical role: Cornerstone drug for ACC; used after surgery (adjuvant) or for advanced disease; also to control cortisol.
Dose/Time: Slowly escalated over weeks to reach target blood level (often 14–20 µg/mL; lab-guided). Long-term use common.
Purpose/Mechanism: Destroys/impairs adrenal cortical cells; induces CYP3A4.
Side effects: Nausea, fatigue, neurologic effects, high lipids; adrenal insufficiency—needs glucocorticoid replacement.EDP-M Regimen (Etoposide, Doxorubicin, Cisplatin + Mitotane)
Class: Combination chemotherapy + adrenolytic.
Dose/Time: Given in cycles (e.g., every 3–4 weeks); specifics vary by protocol.
Purpose/Mechanism: Multi-agent cytotoxic attack on rapidly dividing cells.
Side effects: Low blood counts, nausea, hair loss, kidney/heart toxicity—needs close monitoring.Streptozocin (± Mitotane)
Class: Alkylating/cytotoxic.
Use: Option when EDP-M not suitable; sometimes with mitotane.
Risks: Kidney toxicity, nausea; labs needed.Gemcitabine + Capecitabine
Class: Antimetabolite combo (used in refractory cases).
Mechanism: Interferes with DNA synthesis.
Common effects: Fatigue, low counts, hand-foot syndrome (capecitabine).Platinum Doublets (e.g., Cisplatin + Etoposide without doxorubicin)
Use: Alternative in selected patients.
Key risks: Kidney/nerve injury (cisplatin), marrow suppression.Temozolomide
Class: Alkylating agent (oral).
Role: Salvage settings; activity variable.
Effects: Low counts, fatigue; rare opportunistic infections.Pembrolizumab (PD-1 inhibitor)
Class: Immunotherapy.
Use: For MSI-H/dMMR or high-TMB tumors; sometimes considered off-label in trials.
Risks: Immune-related side effects (colitis, thyroiditis, adrenalitis)—requires prompt management.Nivolumab ± Ipilimumab
Class: PD-1 and CTLA-4 inhibitors.
Use: Clinical trials/selected refractory cases.
Risks: Immune toxicities; endocrinopathies.Metyrapone
Class: Steroidogenesis inhibitor.
Use: Rapidly lowers cortisol in functional ACC.
Mechanism: Blocks 11β-hydroxylase.
Effects: Hypertension, low potassium; needs monitoring.Osilodrostat
Class: 11β-hydroxylase inhibitor.
Use: Control of Cushing’s from ACC when rapid cortisol reduction needed.
Effects: Adrenal insufficiency risk; ECG/QT monitoring sometimes needed.Ketoconazole (off-label for Cushing’s)
Class: Antifungal that inhibits steroid enzymes.
Use: Lowers cortisol; watch liver toxicity and drug interactions.Mifepristone
Class: Glucocorticoid receptor antagonist.
Use: Controls effects of cortisol when levels hard to lower.
Effects: Low potassium, endometrial thickening; requires careful follow-up.Spironolactone / Eplerenone
Class: Mineralocorticoid receptor blockers.
Use: Treats hypertension and low potassium due to aldosterone-producing ACC.
Effects: High potassium risk; spironolactone may cause breast tenderness.Hydrocortisone (or Prednisone) Replacement
Class: Glucocorticoid.
Use: Essential when mitotane or surgery causes adrenal insufficiency; stress-dose during illness.
Risks: Over- or under-replacement if not monitored.Bisphosphonates or Denosumab (supportive)
Class: Anti-resorptives.
Use: Osteoporosis from cortisol excess or bone metastases pain.
Effects: Low calcium, rare jaw osteonecrosis—dental check recommended.
Dietary Molecular Supplements
Always review supplements with your oncology team to avoid drug interactions (especially with mitotane, which alters drug metabolism).
Vitamin D3 – For deficiency; supports bone and muscle; mechanism: improves calcium absorption and bone turnover.
Calcium (if needed) – Bone health; mechanism: mineral supply; avoid excess if hypercalcemia risk.
Omega-3 (Fish Oil) – May help triglycerides (mitotane can raise lipids) and inflammation; mechanism: eicosanoid modulation.
Protein/Leucine-Rich Oral Nutrition – Counters catabolism from cortisol and cancer; mechanism: stimulates muscle protein synthesis.
Probiotics (evidence-based strains) – May reduce chemo-related diarrhea; mechanism: gut microbiome support.
Magnesium & Potassium (food-first; supplements if prescribed) – Correct losses from hypercortisolism/aldosteronism; mechanism: electrolyte balance; monitor labs.
Curcumin (caution) – Anti-inflammatory/antioxidant; mixed clinical data; may interact with chemo—medical approval required.
Green Tea Extract/EGCG (caution) – Antioxidant; potential interactions with liver metabolism—use only if cleared.
Soluble Fiber (oats, psyllium) – Helps lipids and glycemic control; mechanism: bile acid binding and delayed glucose absorption.
Multivitamin (no mega-doses) – Covers gaps when appetite is low; mechanism: micronutrient adequacy without high doses.
Immunity Booster / Regenerative / Stem-Cell” Drugs
There are no approved “stem cell drugs” for ACC. However, some supportive biologic medicines help your body tolerate chemotherapy or prevent infections. Use only under medical supervision.
Pegfilgrastim / Filgrastim (G-CSF) – Stimulates neutrophils to prevent or treat chemotherapy-induced neutropenia; lowers infection risk.
Sargramostim (GM-CSF) – Broader white-cell stimulation in selected regimens.
Epoetin alfa / Darbepoetin – Red-cell growth factors for persistent chemo-related anemia when appropriate; require iron status checks and careful risk–benefit discussion.
IV Iron (e.g., ferric carboxymaltose) – Corrects iron-deficiency anemia that limits energy and response to ESAs.
Vaccinations (Influenza, COVID-19, Pneumococcal) – Not “drugs” in the chemo sense, but essential immune protection before/during treatment (timed around cycles).
IVIG (in specific cases) – For severe hypogammaglobulinemia or recurrent infections; not routine in ACC.
(Experimental cell therapies and regenerative approaches should only be taken in regulated clinical trials.)
Surgeries
Open Adrenalectomy (Preferred for Suspected ACC)
Procedure: Open incision to remove the adrenal tumor with a margin; avoids tumor rupture.
Why: Best chance of R0 resection (complete removal) in large or invasive tumors.En-Bloc Resection of Adjacent Structures
Procedure: Remove adrenal plus involved tissues (kidney, spleen, diaphragm, or part of liver) if invaded.
Why: Achieve negative margins and reduce local recurrence.Regional Lymphadenectomy
Procedure: Remove nearby lymph nodes.
Why: Staging and possibly better local control.IVC Thrombectomy
Procedure: If tumor extends into the inferior vena cava, vascular surgery removes the thrombus.
Why: Prevents embolic events and enables complete resection.Metastasectomy / Local Ablation (RFA/Microwave) for Limited Spread
Procedure: Surgical removal or thermal destruction of isolated liver/lung/bone metastases.
Why: Symptom control and, in selected patients, longer survival.
Prevention
Genetic counseling/testing if you or family have Li-Fraumeni, BWS, MEN1, Lynch, or early ACC.
Syndrome-specific surveillance in high-risk families (regular exams and imaging per expert guidelines).
Avoid unnecessary radiation exposure, especially in childhood.
Healthy weight, activity, and diet to support general cancer prevention.
Do not use anabolic steroids or unregulated hormone boosters.
Smoking cessation for overall cancer risk reduction.
Workplace protection from solvents/pesticides where relevant.
Control blood pressure and blood sugar – improves surgical fitness and outcomes.
Keep vaccines current to avoid infections that delay treatment.
Seek care early for persistent abdominal symptoms or new hormone-like changes.
When to See a Doctor (Red Flags)
New abdominal pain/fullness, rapidly growing side mass, or early satiety.
Unexplained weight loss, severe fatigue, night sweats.
Signs of Cushing’s (easy bruising, purple stretch marks, muscle weakness) or virilization/feminization changes.
High blood pressure that is hard to control or low potassium symptoms (cramps, palpitations).
Very high or low blood sugar, new fractures, or sudden mood changes.
After adrenal surgery or on mitotane, symptoms of adrenal crisis: severe weakness, vomiting, belly pain, low BP—emergency.
Any new chest pain, shortness of breath, severe headache, or neurologic changes—urgent evaluation.
What to Eat and What to Avoid
What to eat
Protein at every meal (eggs, fish, poultry, legumes, dairy) to fight muscle loss.
Potassium-rich foods (bananas, oranges, tomatoes, leafy greens) if your potassium is low—confirm with labs.
High-calcium/vitamin D foods (dairy, fortified plant milks, small bony fish) for bone health.
Whole grains, beans, vegetables, and fruit for fiber and steady blood sugar.
Healthy fats (olive oil, nuts, avocados) to meet energy needs when appetite is poor.
Plenty of fluids unless restricted; small, frequent meals if nauseated.
What to avoid
High-sodium foods (canned soups, processed meats) if aldosterone excess or hypertension.
Sugary drinks and refined sweets if cortisol-related diabetes risk.
Alcohol excess (worsens liver and sleep; interacts with meds).
Herbal products without oncology approval (e.g., St John’s wort, high-dose green tea extract, unlisted “hormone boosters”)—drug interactions with mitotane and chemo.
Grapefruit/grapefruit juice and other strong CYP inhibitors/inducers unless cleared by your team (they can alter drug levels).
Raw/unsafe foods when neutropenic (food safety rules).
Frequently Asked Questions (FAQ)
Is adrenal gland cancer curable?
Yes—some people are cured, especially with early-stage tumors completely removed by surgery. Advanced disease is harder to cure but often treatable.How rare is ACC?
Very rare—only a few cases per million people each year.Why do some ACCs cause hormone symptoms?
The tumor cells keep making steroid hormones (cortisol, aldosterone, androgens/estrogens), leading to visible body changes.Do all adrenal tumors need surgery?
No. Many adrenal incidentalomas are benign. Functional tumors or lesions with cancer features usually need removal.Is laparoscopic surgery okay for ACC?
Open surgery is preferred when ACC is suspected to reduce rupture risk and to achieve complete margins.Will I need medicines after adrenal surgery?
Often yes. You may need glucocorticoid replacement temporarily or long-term. If on mitotane, steroid replacement is common.What is mitotane and why is it special?
It is an adrenolytic drug that targets adrenal cortex cells and changes how the liver handles many medicines; it requires blood-level monitoring.Can immunotherapy help ACC?
It can help selected patients (e.g., MSI-H/high-TMB) and in clinical trials, but it is not a universal solution yet.What if my tumor spreads?
Treatment may use chemotherapy (e.g., EDP-M), targeted hormone control, local therapies for metastases, and clinical trials.How are hormones controlled during treatment?
Drugs like metyrapone, osilodrostat, ketoconazole, mifepristone, and mineralocorticoid blockers manage symptoms while anti-cancer therapy works.Can lifestyle changes shrink the tumor?
No. Lifestyle measures support your body and quality of life but do not replace surgery or medical therapy.Is biopsy always needed?
Not always. If imaging and hormones strongly suggest ACC and surgery is planned, many teams avoid biopsy to prevent spread and proceed to definitive surgery.How often will I be followed after treatment?
Regular imaging (CT/MRI/PET as indicated) and hormone tests, typically every 3–6 months at first, then less often.Can I get pregnant after ACC?
Discuss with your team. Some treatments affect fertility; planning and timing are important.Should I consider a clinical trial?
Yes. Because ACC is rare, clinical trials can offer access to newer therapies and help improve future care.
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 08, 2025.
