eMedicine Specialties > Pediatrics: General Medicine > Oncology

Pheochromocytoma: Treatment & Medication

Author: Patricia Myriam Vuguin, MD, MSc, Associate Professor of Pediatrics, Department of Pediatric Endocrinology, Albert Einstein College of Medicine; Consulting Staff, Children's Hospital at Montefiore
Contributor Information and Disclosures

Updated: Aug 27, 2009

Treatment

Medical Care

  • Perform initial workup of pheochromocytoma using the history, physical examination, laboratory, and diagnostic test findings. Indications for evaluation include the following:
    • Patients with high blood pressure or recurrent hot flushes that are indicative of blood pressure peaks
    • Patients with an adrenal mass
    • Relatives of patients with MEN 2 or von Hippel-Lindau disease
  • Schedule surgical removal only after successful pharmacotherapy to block the effects of catecholamine excess. Blockade of the alpha-adrenergic receptors in the preoperative phase is widely recommended, with additional beta-receptor blockade to treat cardiac dysrhythmias.
  • Perform procedures in a hospital with the capability for intensive intraoperative and postoperative monitoring and therapy.
  • During a hypertensive crisis, immediately institute alpha-blockade with phentolamine. Nitroprusside also should be used for uncontrolled hypertension.
  • For further blood pressure control, initiate beta-blockade (esmolol-labetalol). A beta-blockade that is initiated without prior alpha-blockade can further exacerbate hypertension. As vasoconstriction is relieved, use vigorous fluid resuscitation to maintain a normal blood pressure.
  • Ventricular tachyarrhythmias can be treated with lidocaine and amiodarone.
  • The results of malignant pheochromocytoma appear to be related to the tumor quantity and the aggressiveness of the therapy. The long-term survival rate in patients with untreated malignant or unresectable tumors is unclear. Because of the rarity of the condition, no randomized clinical trials concerning the treatment of malignant pheochromocytoma have been performed.
  • Chemotherapy and radiotherapy have been of questionable value in patients with unresectable disease. Unresectable disease may be rendered resectable by intensive chemotherapy. Chemotherapy currently has a response rate of approximately 50%. Unless chemotherapy allows surgical removal of the entire tumor, it is not usually curative. However, chemotherapy offers good palliation (for years) in a significant number of patients. On the other hand, if the treatment is fairly aggressive, palliation therapy (pain, catecholamine excess) may be long term (years). 
  • A long-term study reported follow-up of 18 patients with a diagnosis of malignant pheochromocytoma or paraganglioma who were treated with cyclophosphamide at 750 mg/m2, vincristine at 1.4 mg/m2, and dacarbazine at 600 mg/m2 on day 1 and dacarbazine at 600 mg/m2 on day 2, every 21-28 days.19 The treatment was well tolerated, with only grade I and II toxicities. In this 22-year follow-up, no difference in overall survival was observed between patients whose tumors objectively shrank and those with stable or progressive disease. Combination chemotherapy produced a complete response rate of 11% and a partial response rate of 44%. All patients with tumors scored as responding reported improvement in their symptoms related to excessive catecholamine release and had objective improvements in blood pressure. Median survival was 3.8 years for patients whose tumors respondedto therapy and 1.8 years for patients whose tumors did not respond (P = .65).  
  • Sunitinib (Sutent; previously known as SU11248) appears to be an active agent in the treatment of malignant pheochromocytomas based on limited cohort of patients and is currently in phase 2 trials.20,21,22 Sunitinib inhibits cellular signaling by targeting multiple receptor tyrosine kinases, such as platelet-derived growth factor receptors, and vascular endothelial growth factor receptors, which play a role in both tumor angiogenesis and tumor cell proliferation The best established strategy established is 131I-MIBG therapy, which is well tolerated. MIBG is specifically taken up by chromaffin cells. MIBG can induce remission for a limited period in a significant proportion of patients. Similar to MIBG, cytotoxic chemotherapy with cyclophosphamide, vincristine, and dacarbazine, can induce remission for a limited period. Octreotide as a single agent seems to be largely ineffective. The value of radiation therapy in patients with malignant pheochromocytoma is debatable.
  • Patients with germline mutation and no evidence of active illness should have continued follow-up for pheochromocytoma.23

Surgical Care

Surgery to remove pheochromocytomas is a high-risk procedure because of several reasons. Substantial comorbidity must be expected, including catecholamine-induced myocardiopathy. Intraoperative manipulation of the tumor may induce excessive catecholamine excretion, resulting in a life-threatening hypertensive crisis. Hypotensive crisis may occur because of a postoperative drop of catecholamines.

  • Preoperative blockade of alpha-1 receptors has been used to reduce the risk of hypertensive episodes. Drugs such as urapidil has shown a significant reduction in hypertensive peaks.24
  • Transabdominal surgery has been the traditional approach; it allows early ligation of the adrenal vein to minimize systemic catecholamine release during manipulation. This approach also facilitates exploration of the sympathetic chain for multifocality.
  • Other options include a subcostal or posterior extraperitoneal approach that offers rapid recovery and avoids the risk of transperitoneal surgery (adhesions, bowel obstruction). Alternatively, a laparoscopic adrenalectomy can be considered; tumors as large as 11 cm have been successfully removed. The contraindications to laparoscopy include evidence of soft-tissue or vascular extra-adrenal extension. Bilateral tumors develop in children with multiple endocrine neoplasia type 2 and pheochromocytoma, and bilateral adrenalectomy has been recommended at presentation.
  • Careful and intensive monitoring of the patient's status throughout the perioperative period is imperative.
  • Hypotension that develops after tumor removal reflects reversal of the volume-contracted state and should respond to judicious replacement of fluids.
  • Some patients may develop pulmonary edema, possibly as a result of impaired myocardial function and the inability to tolerate intravenous fluids.
  • When the tumor is removed, the blood pressure usually falls to approximately 90/60 mm Hg. Lack of a fall in pressure at the time of tumor removal indicates the presence of additional tumor tissue.
  • When bilateral adrenal tumors are found and both adrenals are removed, adrenocortical lifelong steroid replacement is required. Significant morbility is associated with bilateral adrenalectomy. Because of these risks, some clinicians have recommended adrenal-sparing surgery in patients who have bilateral tumors or who are at particular risk for a metachronous contralateral tumor.

Consultations

  • Obtain consultations as needed for comorbid conditions and their definitive treatment (eg, pediatric surgeon, oncologist, cardiologist, ophthalmologist, endocrinologist).

Medication

To provide optimal treatment of patients with pheochromocytomas, an understanding of the pathophysiology produced by excessive catecholamines and an acquaintance with the action of adrenergic antagonists and other drugs used in the treatment of these patients is necessary.

Alpha-adrenergic blocking agents

These agents are used preoperatively in combination with beta-blockers. At low doses, alpha-adrenergic receptor blockers may be used as monotherapy in the treatment of hypertension. At higher doses, the agents may cause sodium and fluid to accumulate. As a result, concurrent diuretic therapy may be required to maintain the hypotensive effects of the alpha-receptor blockers.


Phenoxybenzamine (Dibenzyline)

Alpha1- and alpha2-adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action, reducing hypertension. The agent decreases sympathetic tone on the vasculature, dilates blood vessels, and lowers arterial blood pressure. Long-acting properties produce and maintain a chemical sympathectomy. Lowers supine and upright blood pressures. Does not affect the parasympathetic nervous system.

Adult

10 mg PO bid initially; increase dose by 10-mg increments every other day until an optimal dosage is obtained; usual dosage range is 20-40 mg PO bid/tid

Pediatric

0.2 mg/kg PO initially (not to exceed 5-10 mg bid); gradually increase according to BP to 0.25-1 mg/kg/d PO divided q6-8h

Coadministration with alpha-adrenergic agonists decreases effects of phenoxybenzamine; beta-blockers increase toxicity

Documented hypersensitivity; MI; evidence of CAD; those in whom a fall in blood pressure would be undesirable

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use cautiously during lactation; change position slowly; frequent and small meals are recommended to avoid GI upset; avoid tasks that require visual acuity; monitor heart rate and blood pressure; report unusual swelling of the extremities, difficulty in breathing, dizziness, lightheadedness, or fainting; caution in tachycardia, peptic ulcer, and gastritis; cerebrovascular occlusions and myocardial infarctions can occur following phentolamine administration


Phentolamine

Nonselective alpha-adrenergic blocking agent. Drug action is transient and alpha-adrenergic blockade incomplete. Often used immediately prior to or during adrenalectomy to prevent or control paroxysmal hypertension that results from anesthesia, stress, or operative manipulation of the tumor. Alpha1- and alpha2-adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action, reducing hypertension that results from catecholamine effects on the alpha-receptors. First-line agent to treat hypertensive crisis.

Adult

Prevention or control of hypertension in pheochromocytomas: 5 mg IV/IM 1-2 h before surgery; repeat prn; administer 5 mg IV during surgery as indicated to control paroxysms of hypertension, tachycardia, respiratory depression, or seizures

Pediatric

Preoperative reduction of elevated BP: 1 mg IV/IM 1-2 h (0.05-0.1 mg/kg/dose, not to exceed 5 mg/dose) before surgery; repeat prn; administer 1 mg IV during surgery as indicated to control paroxysms of hypertension, tachycardia, respiratory depression, and convulsions

Decreases vasoconstrictor and hypertensive effects of epinephrine and ephedrine

Documented hypersensitivity; evidence of CAD; renal impairment

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May produce weakness, dizziness, and nausea; acute and prolonged hypotensive episodes; tachycardia; and arrhythmias


Prazosin (Minipress)

Postsynaptic alpha1-antagonist; decreases blood pressure with minimal risk of reflex tachycardia.

Adult

1 mg PO bid/tid initially; increase prn; not to exceed 20 mg/d PO divided bid/tid

Pediatric

Initial: 5 mcg/kg PO test dose
Maintenance: 25-150 mcg/kg/d divided q6h; not to exceed 15 mg/d

Severity and duration of hypotension following first dose of prazosin may be increased in patients receiving beta-adrenergic blocking drugs (eg, propranolol) or verapamil; indomethacin may decrease antihypertensive activity of prazosin; prazosin may decrease antihypertensive effects of clonidine

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Marked orthostatic hypotension, syncope, and loss of consciousness may occur with first dose; rash, pruritus, alopecia, diaphoresis, lupus erythematosus, dizziness, headache, drowsiness, lack of energy, nausea, palpitations, and weakness can occur; decrease dose in severe renal insufficiency

Beta-adrenergic blocking agents

These agents are used as adjunctive therapy for cardiac effects. The agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation.


Propranolol (Inderal)

Nonselective beta-adrenergic receptor blocker. After primary treatment with an alpha-receptor blocker, propranolol may be used as adjunctive therapy if control of tachycardia becomes necessary before or during surgery. May be used to treat excessive beta-receptor stimulation in patients with inoperable metastatic pheochromocytoma. Has membrane-stabilizing activity and decreases automaticity of contractions. Decreases effects of the sympathetic nervous system on the heart and juxtaglomerular apparatus, release of renin, and blood pressure. Acts in the CNS to reduce sympathetic outflow and vasoconstrictor tone. Not suitable for emergency treatment of hypertension. Do not administer IV in hypertensive emergencies.

Adult

Hypertension: 40 mg/dose PO bid; may increase 10-20 mg/dose q3-5d; not to exceed 640 mg/d
Pheochromocytoma preoperatively: 60 mg/d PO for 3 d in divided doses; inoperable tumor, 30 mg/d PO in divided doses

Pediatric

0.5-1 mg/kg/d PO divided q6-12h initially; may increase dose q3-5d prn; not to exceed 8 mg/kg/d

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol

Documented hypersensitivity; sinus bradycardia; second- or third-degree heart block; cardiogenic shock; CHF; asthma; COPD

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Can cause dizziness, fatigue, gastric pain, flatulence, constipation, diarrhea, nausea, vomiting, bradycardia, cardiac arrhythmias, AV nodal block, bronchospasm, impotence, decrease in exercise tolerance, hyperglycemia, or hypoglycemia; may decrease signs of acute hypoglycemia and hyperthyroidism; use cautiously in hypoglycemia and diabetes, thyrotoxicosis, hepatic dysfunction


Labetalol (Trandate)

Blocks beta1-, alpha-, and beta2-adrenergic receptor sites, thus decreasing blood pressure.

Adult

Incremental doses starting at 20-40 mg IV; a response should be obtained within 5 min and a maximum effect at 10 min; IV dose can be doubled q30-60min until target BP is achieved; not to exceed 300 mg total dose

Pediatric

Limited data available for pediatric hypertensive emergencies; initial doses of 0.2-0.5 mg/kg/dose IV as intermittent bolus; not to exceed 20 mg/dose; alternatively, a continuous IV infusion of 0.4-1 mg/kg/h IV; may increase as warranted; not to exceed 3 mg/kg/h

Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia, resulting from nitroglycerin use, without interfering with hypotensive effects; cimetidine may increase labetalol blood levels; glutethimide may decrease labetalol effects by inducing microsomal enzymes

Documented hypersensitivity; cardiogenic shock; pulmonary edema; bradycardia; atrioventricular block; uncompensated congestive heart failure; reactive airway disease; severe bradycardia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in impaired hepatic function; discontinue therapy upon signs of liver dysfunction; a lower response rate and higher incidence of toxicity may be observed in elderly patients


Esmolol (Brevibloc)

Excellent drug for use in patients at risk for experiencing complications from beta-blockade, particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.

Adult

Loading dose: 500 mcg/kg IV over 1 min, followed by 50 mcg/kg/min for 4 min; if an adequate BP is not achieved within 5 min, repeat loading dose and increase infusion to 100 mcg/kg/min; repeat loading dose and titrate infusion rate upwards at 50 mcg/kg/min every 5 min prn; stop further loading doses once therapeutic blood pressure is reached

Pediatric

Infants and children: Limited information is available; suggested dose is 100-500 mcg/kg IV administered over 1 min initially, followed by 200 mcg/kg/min IV; titrate upward by 50-100 mcg/kg/min q5-10min until heart rate or BP decrease by >10%, typical dose 550 mcg/kg/min (range = 300-1000 mcg/kg/min)

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of esmolol, possibly resulting in decreased pharmacologic effect; cardiotoxicity of esmolol may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of esmolol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication is abruptly withdrawn; withdraw drug slowly and monitor patient closely

Nitrates

These agents provide peripheral and coronary vasodilation.


Sodium nitroprusside (Nitropress)

Acts directly on vascular smooth muscle to cause vasodilatation, reduce BP, and increased inotropic effect.

Adult

0.3-0.5 mcg/kg/min IV continuous IV infusion initially, titrate upward by 0.5 mcg/kg/min increments to effect; usual dose is 3-4 mcg/kg/min; infusion rates >10 mcg/kg/min may lead to cyanide toxicity

Pediatric

Administer as in adults

Additive effects when administered with other antihypertensive agents

Documented hypersensitivity; subaortic stenosis; idiopathic hypertrophic, atrial fibrillation or flutter; decreased cerebral perfusion; situations of compensatory hypertension

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, nitroprusside levels may increase and can cause cyanide toxicity; sodium nitroprusside can lower blood pressure and, thus, should be used only in patients with mean arterial pressures >70 mm Hg

Antiarrhythmic agents

These agents alter the electrophysiologic mechanisms responsible for arrhythmia.


Amiodarone (Cordarone)

May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Before administration, control the ventricular rate and CHF (if present) with digoxin or calcium channel blockers.

Adult

Rapid loading: 5 mg/kg IV; not to exceed 450 mg; mixed in D5W infused over 10-30 min; not to exceed 50 mg/kg

Pediatric

Loading dose: 10-15 mg/kg/d or 600-800 mg/1.73 m2/d PO for 4-14 d or until adequate control of arrhythmia is attained, reduce to 5 mg/kg/d or 200-400 mg/1.73 m2/d for several weeks
Limited data available for IV loading dose
Maintenance dose: 2.5 mg/kg/d PO or lowest effective dose following loading

Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels

Documented hypersensitivity; complete AV block; intraventricular conduction defects; protease inhibitors (eg, indinavir, ritonavir, amprenavir, nelfinavir) inhibit amiodarone metabolism, resulting in increased serum levels, and may prolong QT interval; coadministration may increase myopathy and rhabdomyolysis risk associated with HMG-CoA reductase inhibitors (eg, simvastatin); other drugs that prolong the QT interval (eg, fluoroquinolones, erythromycin, dofetilide, tricyclic antidepressants, thioridazine) may increase life-threatening arrhythmia risk

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in breastfeeding women, thyroid or liver disease, may cause proarrhythmic effect, optic neuritis, CNS toxicity, hypothyroidism, hepatotoxicity, interstitial pneumonitis or pulmonary fibrosis; CNS and GI toxicity may occur and typically dissipate with dose reduction


Lidocaine (Xylocaine)

Class IB antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue.

Adult

0.7-1.4 mg/kg IV push, repeat in 5 min; not to exceed 300 mg/h; follow with an infusion of 2-4 mg/kg/min

Pediatric

Loading dose: 1 mg/kg IV; repeat in 10-15 min for 2 doses
Continuous infusion: 20-50 mcg/kg/min IV

Coadministration with cimetidine or beta-blockers increases toxicity of lidocaine; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine

Documented hypersensitivity to amide-type local anesthetics; avoid in Adams-Stokes syndrome and Wolf-Parkinson-White syndrome; avoid in severe sinoatrial, AV, or intraventricular block if artificial pacemaker not in place

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Use a solution without preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression, and bradycardia; may increase risk of CNS and cardiac adverse effects in elderly patients; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities

More on Pheochromocytoma

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Differential Diagnoses & Workup: Pheochromocytoma
Treatment & Medication: Pheochromocytoma
Follow-up: Pheochromocytoma
Multimedia: Pheochromocytoma
References
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Further Reading

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Keywords

tumor, catecholamine, catecholamine-secreting tumor, chromaffin cells, vanillylmandelic acid, VMA, homovanillic acid, HVA, paraganglioma, extra-adrenal tumor of the paraganglion system, nonfunctional tumor of the paraganglion system, functional tumor, extra-adrenal pheochromocytoma, paroxysmal attacks, diaphoresis, autosomal dominant trait, mitochondrial complex II, pheochromocytoma-paraganglioma syndrome, neurofibromatosis, von Hippel-Lindau disease, von Hippel-Lindau's disease, tuberous sclerosis

Sturge-Weber syndrome, Sturge-Weber's syndrome, multiple endocrine neoplasia syndromes, MEN, MEN 2A, MEN 2B. neuroendocrine, tyrosine hydroxylase, tachycardia, hypermetabolism, norepinephrine, epinephrine, hypertension, hypotension, syncope, alpha-adrenergic receptor, beta-adrenergic receptor, metastatic disease, alpha-receptor–mediated peripheral vasoconstriction, hyperthermia, cachexia, hypermetabolism, diabetes mellitus, glucose intolerance, hypercalcemia, hyperparathyroidism, cardiomyopathy, neuroblastic cells, neuroblastomas, ganglioneuromas, hypermetabolism, hyperparathyroidism, hypercalcemia, Zellballen, metaiodobenzylguanidine, MIBG, treatment, diagnosis

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Contributor Information and Disclosures

Author

Patricia Myriam Vuguin, MD, MSc, Associate Professor of Pediatrics, Department of Pediatric Endocrinology, Albert Einstein College of Medicine; Consulting Staff, Children's Hospital at Montefiore
Patricia Myriam Vuguin, MD, MSc is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Stephan A Grupp, MD, PhD, Director, Stem Cell Biology Program, Department of Pediatrics, Division of Oncology, Children's Hospital of Philadelphia; Associate Professor of Pediatrics, University of Pennsylvania
Stephan A Grupp, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Society for Blood and Marrow Transplantation, American Society of Hematology, American Society of Pediatric Hematology/Oncology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Steven K Bergstrom, MD, Assistant to the Chairman, Department of Pediatrics, Division of Hematology-Oncology, Kaiser Permanente Medical Center of Oakland
Steven K Bergstrom, MD is a member of the following medical societies: Alpha Omega Alpha, American Society of Clinical Oncology, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Children's Oncology Group, and International Society for Experimental Hematology
Disclosure: Nothing to disclose.

CME Editor

Helen SL Chan, MBBS, FRCP(C), FAAP, Senior Scientist, Research Institute; Professor, Division of Hematology/Oncology, Department of Pediatrics, The Hospital for Sick Children, University of Toronto, Canada
Helen SL Chan, MBBS, FRCP(C), FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association for Cancer Research, American Society of Hematology, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Chief Editor

Max J Coppes, MD, PhD, MBA, Senior Vice President, Children's National Medical Center (Center for Cancer and Blood Disorders); Director, Center for Cancer and Immunology Research, Children's Research Institute, Children's National Medical Center; Professor of Medicine, Oncology, and Pediatrics, Georgetown University
Max J Coppes, MD, PhD, MBA is a member of the following medical societies: American Association for Cancer Research, American Society of Pediatric Hematology/Oncology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
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