100+ Free ABP Pediatric Hematology-Oncology Practice Questions

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Question 1

Score: 0/0

A 5-year-old with B-cell precursor ALL has blasts showing t(12;21)(p13;q22) ETV6-RUNX1 fusion. Which prognostic category does this cytogenetic finding indicate?

No prognostic significance

Unfavorable/high-risk prognosis

Intermediate prognosis requiring HSCT

Favorable prognosis

to track

2026 Statistics

Key Facts: ABP Pediatric Hematology-Oncology Exam

~200

MCQ Items

ABP subspecialty certifying exam (approximate)

Half-day

Exam Format

Computer-based test at Pearson VUE

$2,242

2026 Standard Fee

Regular registration $2,992 (includes $750 processing fee)

3 years

Required Fellowship

ACGME-accredited Pediatric Hematology-Oncology training

Content Domains

General Oncology, Heme Malignancies, Solid Tumors, HSCT, Scholarly Activities

5 yr

MOC Cycle

Maintenance of Certification enrollment required every 5 years

The ABP Pediatric Hematology-Oncology exam is a half-day computer-based test with approximately 200 single-best-answer multiple-choice items administered at Pearson VUE. The 2026 content outline covers five domains: General Oncology Issues, Hematologic Malignancies, Solid Tumors, Hematopoietic Stem-Cell Transplant, and Core Knowledge in Scholarly Activities — plus a large classical hematology component (sickle cell, hemoglobinopathies, bleeding disorders, ITP, HUS). The 2026 standard registration fee is $2,242 (regular registration $2,992 includes a $750 processing fee). Eligibility: ABP General Pediatrics certification plus 3 years of ACGME-accredited Pediatric Hematology-Oncology fellowship.

Sample ABP Pediatric Hematology-Oncology Practice Questions

Try these sample questions to test your ABP Pediatric Hematology-Oncology exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1A 5-year-old with B-cell precursor ALL has blasts showing t(12;21)(p13;q22) ETV6-RUNX1 fusion. Which prognostic category does this cytogenetic finding indicate?

A.No prognostic significance

B.Unfavorable/high-risk prognosis

C.Intermediate prognosis requiring HSCT

D.Favorable prognosis

Explanation: ETV6-RUNX1 t(12;21) is the most common recurrent translocation in pediatric B-ALL (~25%) and confers a favorable prognosis with event-free survival >90% on standard COG regimens. Along with high-hyperdiploidy (trisomies of chromosomes 4, 10, and 17), it is one of the two classic favorable-risk genetic lesions in childhood B-ALL.

2A 4-year-old with newly diagnosed B-ALL has blasts positive for BCR-ABL1 (Philadelphia chromosome, t(9;22)). What targeted agent should be added to chemotherapy?

A.Venetoclax

B.Rituximab

C.Brentuximab vedotin

D.Dasatinib (tyrosine kinase inhibitor)

Explanation: Philadelphia-chromosome-positive (Ph+) ALL historically had very poor outcomes but adding a BCR-ABL1 tyrosine kinase inhibitor (dasatinib or imatinib) to intensive multiagent chemotherapy markedly improves event-free survival in children. COG AALL1631 and similar trials established TKI + chemo as standard, reducing the historical need for upfront HSCT in first remission.

3A 3-month-old infant presents with hyperleukocytosis and B-ALL with KMT2A (MLL) rearrangement. Which statement is TRUE?

A.Infant KMT2A-rearranged ALL has a poor prognosis and is treated on infant-specific protocols

B.It has an excellent prognosis similar to ETV6-RUNX1

C.It is a T-cell disease

D.It responds best to single-agent methotrexate

Explanation: KMT2A (MLL) rearrangement (most often t(4;11) MLL-AF4) is the dominant genetic lesion in infant ALL (<1 year) and confers a very poor prognosis with event-free survival ~35-50%. Infants are treated on dedicated protocols (Interfant) often incorporating blinatumomab now, and HSCT is considered for high-risk subsets.

4At end-of-induction for pediatric B-ALL, flow cytometric MRD shows 0.05% residual blasts. What does this finding indicate?

A.Immediate HSCT regardless of other risk factors

B.Excellent response; de-escalate therapy

C.Remission by morphology makes MRD irrelevant

D.Poor prognosis and need for treatment intensification

Explanation: End-of-induction flow MRD ≥0.01% (1 in 10,000 cells) is a powerful independent adverse prognostic factor in pediatric ALL. MRD ≥0.01% identifies patients who benefit from intensification, and high MRD (≥1%) often prompts blinatumomab or HSCT. MRD is the single most important on-treatment prognostic factor.

5Tisagenlecleucel is approved for pediatric relapsed/refractory B-ALL. What is its mechanism?

A.Anti-CD22 antibody-drug conjugate

B.Bispecific CD19xCD3 T-cell engager

C.Autologous T cells engineered to express a CD19-directed chimeric antigen receptor

D.Anti-CD20 monoclonal antibody

Explanation: Tisagenlecleucel is an autologous CD19-directed CAR-T cell therapy approved for pediatric/young adult relapsed or refractory B-ALL. Response rates exceed 80% in heavily pretreated patients. Blinatumomab is the CD19xCD3 BiTE; inotuzumab ozogamicin is the anti-CD22 ADC; rituximab is anti-CD20.

6A teenager with T-cell ALL presents with a large anterior mediastinal mass and tumor lysis. Compared with B-ALL, T-ALL in children is characterized by which features?

A.Older age, male predominance, mediastinal mass, higher WBC at presentation

B.Younger age and female predominance

C.Absence of CNS involvement

D.Universally favorable prognosis

Explanation: Pediatric T-ALL is more common in older children and adolescents, has a male predominance, often presents with a large anterior mediastinal mass (thymic origin), high WBC, and greater CNS involvement risk. Outcomes have improved substantially with modern COG regimens (AALL0434 nelarabine) but relapse is more often extramedullary.

7Which intervention is used universally for CNS prophylaxis in pediatric ALL?

A.High-dose intravenous cytarabine only

B.Cranial radiation in all patients

C.Intrathecal methotrexate

D.Oral temozolomide

Explanation: Intrathecal methotrexate (alone or as triple IT with hydrocortisone and cytarabine) given throughout induction, consolidation, and maintenance is the backbone of CNS prophylaxis in pediatric ALL. Systemic high-dose methotrexate provides additional CNS coverage. Routine prophylactic cranial radiation has been largely eliminated except for select high-risk CNS disease because of late neurocognitive and endocrine toxicity.

8Hypodiploidy with <44 chromosomes in pediatric B-ALL indicates what?

A.Low risk of relapse

B.Favorable prognosis equivalent to hyperdiploidy

C.Adverse prognosis; often associated with germline TP53 mutations (Li-Fraumeni)

D.T-cell lineage

Explanation: Hypodiploid B-ALL (<44 chromosomes, especially near-haploid 24-31 and low-hypodiploid 32-39) is a very high-risk subtype with poor response to conventional therapy. Low-hypodiploid cases are strongly associated with germline TP53 mutations (Li-Fraumeni syndrome), so germline testing is indicated. HSCT is often considered.

9Ph-like ALL shares gene expression with Ph+ ALL but lacks BCR-ABL1. Which lesion is commonly found and potentially targetable?

A.Trisomy 21 mosaicism

B.ETV6-RUNX1 fusion

C.KMT2A-AF4

D.CRLF2 rearrangement and JAK2/JAK1 mutations (JAK-STAT pathway)

Explanation: Ph-like ALL (BCR-ABL1-like) has a Ph-like gene expression signature without BCR-ABL1. Common genetic events include CRLF2 overexpression (often with P2RY8-CRLF2 or IGH-CRLF2), JAK-STAT activating mutations (JAK1/2), and ABL-class fusions (e.g., EBF1-PDGFRB). These lesions are therapeutically targetable with TKIs or ruxolitinib and confer high relapse risk.

10Children with Down syndrome and ALL have unique treatment considerations. Which is TRUE?

A.Methotrexate clearance is enhanced, so doses must be increased

B.They never develop ALL

C.They universally have favorable cytogenetics

D.Higher risk of methotrexate toxicity and infection, but excellent MRD response; dose modifications often needed

Explanation: Children with Down syndrome have ~20-fold increased risk of ALL (and AML, especially acute megakaryoblastic leukemia preceded by transient abnormal myelopoiesis). DS-ALL has increased treatment-related toxicity (methotrexate mucositis, infection, hyperglycemia with steroids) and often requires dose modifications. Cytogenetics in DS-ALL frequently include CRLF2 rearrangements; outcomes are inferior to non-DS patients.

About the ABP Pediatric Hematology-Oncology Exam

The ABP Pediatric Hematology-Oncology subspecialty certification validates expert-level knowledge across pediatric leukemias (ALL, AML, APL), lymphomas (Hodgkin, Burkitt, lymphoblastic, ALCL), CNS tumors (medulloblastoma, gliomas, AT/RT, ependymoma), solid tumors (neuroblastoma, Wilms, rhabdomyosarcoma, Ewing, osteosarcoma, retinoblastoma, germ cell), histiocytic disorders (LCH, HLH), sickle cell disease and hemoglobinopathies, bleeding disorders (hemophilia, vWD), immune thrombocytopenia, HUS/TTP, transfusion medicine, hematopoietic stem cell transplantation, and pediatric oncology supportive care (febrile neutropenia, tumor lysis syndrome, late effects, palliative care). Requires ABP General Pediatrics certification plus 3 years of ACGME-accredited Pediatric Hematology-Oncology fellowship.

Questions

200 scored questions

Time Limit

Half-day CBT at Pearson VUE (~200 MCQs)

Passing Score

Criterion-referenced scaled score (modified Angoff)

Exam Fee

$2,242 standard registration (regular $2,992 with $750 processing fee) (American Board of Pediatrics (ABP) / Pearson VUE)

ABP Pediatric Hematology-Oncology Exam Content Outline

~15%

Acute Lymphoblastic Leukemia (ALL)

B-ALL vs T-ALL, Ph+ t(9;22) BCR-ABL1 (TKI + chemo), ETV6-RUNX1 t(12;21) favorable, KMT2A/MLL 11q23 infant ALL (poor), hyperdiploid >50 favorable vs hypodiploid <44 poor, Ph-like, MRD-guided therapy, CNS prophylaxis, blinatumomab/inotuzumab/CD19 CAR-T (tisagenlecleucel).

~7%

AML & APL

WHO 2022 pediatric AML (KMT2A, RUNX1-RUNX1T1 t(8;21), CBFB-MYH11 inv(16), NUP98, FLT3-ITD), Down syndrome AML (GATA1). APL t(15;17) PML-RARA — DIC emergency, induce with ATRA + arsenic trioxide. HSCT in high-risk.

~7%

Hodgkin & Non-Hodgkin Lymphoma

Classical Hodgkin (Reed-Sternberg CD15+/CD30+, nodular sclerosing, Lugano staging, ABVE-PC + brentuximab). NHL: Burkitt (MYC, TLS risk), lymphoblastic lymphoma (T-cell mediastinal mass), DLBCL, ALCL (ALK+, CD30+), PTLD (EBV).

~8%

CNS Tumors

Medulloblastoma WHO 2021 molecular groups (WNT best, SHH, Gp3 MYC worst, Gp4), H3 K27-altered DMG, H3 G34-mutant, AT/RT (SMARCB1 loss), ependymoma (PFA posterior fossa, ZFTA supratentorial), pilocytic astrocytoma (KIAA1549-BRAF), craniopharyngioma.

~5%

Neuroblastoma

INRG stratification (L1/L2/M/MS), age ≥18 mo adverse, MYCN amplification poor prognosis, 11q aberration, DNA ploidy, INPC/Shimada histology. Stage MS special infants. Multimodal therapy + GD2 immunotherapy (dinutuximab) in high-risk.

~4%

Wilms & Renal Tumors

Wilms triphasic (blastemal/epithelial/stromal), favorable vs anaplastic histology, WT1 11p13, ILNR/PLNR rests. Syndromes: WAGR, Denys-Drash, Beckwith-Wiedemann. Clear cell sarcoma kidney (BCOR ITD), malignant rhabdoid (SMARCB1), mesoblastic nephroma (ETV6-NTRK3).

~8%

Sarcomas (Soft Tissue & Bone)

Rhabdomyosarcoma — embryonal (11p15 LOH, better) vs alveolar (PAX3/7-FOXO1, worse). Ewing (EWSR1-FLI1 t(11;22) 85%, CD99). Osteosarcoma (TP53/RB1, MAP chemo). Infantile fibrosarcoma (ETV6-NTRK3 — NTRK inhibitor).

~3%

Retinoblastoma & Germ Cell Tumors

Retinoblastoma RB1 two-hit, unilateral sporadic vs bilateral/trilateral hereditary, leukocoria, Flexner-Wintersteiner rosettes, osteosarcoma risk. Germ cell: yolk sac (AFP), dysgerminoma, immature teratoma, sacrococcygeal teratoma.

~4%

Histiocytic & Rare Disorders

LCH (BRAF V600E ~50%, CD1a/S100/langerin+, Birbeck granules; risk organs BM/liver/spleen). HLH (PRF1/UNC13D/STX11/STXBP2, fever, splenomegaly, cytopenias, ferritin >500, low NK, sCD25 high; HLH-94/2004 with etoposide).

~10%

Sickle Cell Disease & Hemoglobinopathies

HbSS, HbSC, HbS/β-thal. Pain crisis, acute chest syndrome (transfuse, cef+macrolide), splenic sequestration, aplastic crisis (parvovirus B19), stroke (TCD >200 → chronic transfusion). Hydroxyurea, L-glutamine, voxelotor, crizanlizumab, HSCT. Thalassemias (α, β — chelation, betibeglogene).

~5%

Other Anemias & Bone Marrow Failure

IDA, G6PD (bite/Heinz cells), hereditary spherocytosis (ankyrin/spectrin, EMA, splenectomy), AIHA (warm IgG vs cold IgM). Inherited BMF: Diamond-Blackfan (RPS19), Fanconi (chromosomal breakage, AML risk), SCN (ELANE), Shwachman-Diamond (SBDS). Acquired aplastic anemia.

~7%

Bleeding Disorders & Coagulation

Hemophilia A (FVIII) and B (FIX) — severity by factor level, factor replacement, emicizumab, gene therapy. Inhibitors (bypassing agents, ITI). vWD types 1/2A/2B/2M/2N/3 (DDAVP, VWF concentrate). Vitamin K deficiency of newborn.

~5%

Platelet Disorders & TMA

ITP (postviral, self-limited in kids, IVIG/anti-D/steroids; eltrombopag/romiplostim chronic). STEC-HUS (supportive), atypical HUS (eculizumab/ravulizumab). TTP (ADAMTS13 <10% — PLEX, caplacizumab). Bernard-Soulier, Glanzmann, WAS, MYH9.

~3%

Transfusion Medicine

PRBC/platelets/FFP/cryoprecipitate indications. Irradiation (prevent TA-GVHD), CMV-seronegative/leukoreduced. Reactions: acute hemolytic (ABO), FNHTR, TRALI, TACO, anaphylactic (IgA deficient). Massive transfusion 1:1:1. Exchange transfusion.

~4%

Hematopoietic Stem Cell Transplantation

Allo (MSD, MUD, haplo, cord) vs auto indications. Conditioning (myeloablative vs RIC, TBI). Acute GVHD (skin/GI/liver — tacro+MTX, steroids, ruxolitinib refractory). Chronic GVHD (scleroderma, BOS). VOD/SOS (defibrotide), viral reactivation, PTLD.

~3%

Supportive Care (FN, TLS, Infection)

Febrile neutropenia (ANC <500, T ≥38.3) — empiric cefepime or pip-tazo within 60 min, vanco if MRSA risk. Tumor lysis syndrome (Burkitt, T-ALL, high-WBC ALL) — hydration, allopurinol vs rasburicase (avoid in G6PD). Typhlitis, mucositis, PJP prophylaxis.

~2%

Late Effects, Survivorship & Palliative Care

Cardiotoxicity (anthracyclines, dexrazoxane), pulmonary (bleomycin/busulfan/CSI), endocrine (GH, thyroid, gonadal), fertility preservation, secondary malignancies (alkylators, topo-II), neurocognitive. Early palliative care, symptom management, advance care planning.

~3%

Core Knowledge — Scholarly Activities

Biostatistics (sensitivity/specificity, HR, Kaplan-Meier, NNT), study design (RCT, cohort, case-control), bias, pediatric research ethics (45 CFR 46 Subpart D), informed consent/assent, EBM hierarchy, QI, clinical ethics.

How to Pass the ABP Pediatric Hematology-Oncology Exam

What You Need to Know

Passing score: Criterion-referenced scaled score (modified Angoff)
Exam length: 200 questions
Time limit: Half-day CBT at Pearson VUE (~200 MCQs)
Exam fee: $2,242 standard registration (regular $2,992 with $750 processing fee)

Keys to Passing

Complete 500+ practice questions
Score 80%+ consistently before scheduling
Focus on highest-weighted sections
Use our AI tutor for tough concepts

ABP Pediatric Hematology-Oncology Study Tips from Top Performers

1Sickle cell stroke prevention rule: TCD (transcranial Doppler) screening annually in HbSS children age 2-16 years. Time-averaged mean velocity ≥200 cm/s in MCA/ICA is ABNORMAL → start chronic transfusion therapy (STOP trial). Conditional 170-199 cm/s → repeat. Hydroxyurea can replace chronic transfusion after ≥1 year of transfusions per TWiTCH trial.

2APL (AML-M3) emergency rule: t(15;17) PML-RARA with coagulopathy/DIC is a hematologic emergency. Start ATRA (all-trans retinoic acid) + arsenic trioxide on clinical suspicion BEFORE cytogenetic confirmation — delay kills from intracranial/pulmonary hemorrhage. Differentiation syndrome (fever, dyspnea, hypoxia, weight gain) is treated with dexamethasone without stopping ATRA.

3Tumor lysis syndrome mnemonic: High-risk = Burkitt, T-ALL, high-WBC ALL (>100k). Labs: ↑K, ↑PO4, ↓Ca, ↑uric acid, ↑LDH → AKI. Prophylaxis: hydration + allopurinol (low/int risk) or rasburicase (high risk; CONTRAINDICATED in G6PD deficiency — causes methemoglobinemia/hemolysis). Treatment: aggressive hydration, rasburicase, dialysis if needed.

4Neuroblastoma INRG high-risk rule: MYCN amplification (>10 copies) is an independent adverse factor regardless of stage or age. Age ≥18 months, stage M disease, unfavorable INPC (Shimada) histology, 11q aberration, and diploid DNA all worsen risk. Stage MS (infants <18 mo with skin/liver/<10% BM involvement) can regress spontaneously without MYCN amplification.

5Hemophilia inhibitor pearl: High-responder inhibitors (Bethesda titer ≥5 BU) → bypassing agents (rFVIIa or activated prothrombin complex concentrate aPCC/FEIBA) for bleeding; immune tolerance induction (ITI) for eradication. Emicizumab (bispecific Ab bridging FIXa to FX) works regardless of inhibitor status and is transforming prophylaxis in severe hemophilia A.

6Febrile neutropenia timer rule: ANC <500 + T ≥38.3°C (or ≥38.0°C sustained 1 hour) = medical emergency. Blood cultures + empiric broad-spectrum antipseudomonal beta-lactam (cefepime, pip-tazo, or meropenem) within 60 MINUTES. Add vancomycin if hemodynamic instability, mucositis, catheter infection, MRSA history, or skin/soft-tissue source. Antifungals after 4-7 days persistent fever.

Frequently Asked Questions

What is the ABP Pediatric Hematology-Oncology subspecialty certification?

The ABP Pediatric Hematology-Oncology subspecialty certification is awarded by the American Board of Pediatrics to pediatricians who demonstrate expert-level knowledge in pediatric leukemias and lymphomas, pediatric solid tumors (neuroblastoma, Wilms, rhabdomyosarcoma, Ewing, osteosarcoma, retinoblastoma, germ cell), CNS tumors, classical hematology (sickle cell disease, hemoglobinopathies, hemophilia, von Willebrand disease, ITP, HUS/TTP), transfusion medicine, hematopoietic stem cell transplantation, and pediatric oncology supportive care. It qualifies pediatricians to practice pediatric hematology-oncology at children's hospitals and academic centers.

Who is eligible to take the ABP Pediatric Hematology-Oncology exam?

Candidates must hold ABP General Pediatrics certification in good standing and have completed three (3) years of full-time training in an ACGME-accredited Pediatric Hematology-Oncology fellowship (or RCPSC-accredited program in Canada). A valid unrestricted medical license is required. Applicants must also satisfy the ABP scholarly activity requirement and apply within 7 years of completing fellowship.

What is the format of the ABP Pediatric Hematology-Oncology exam?

The exam is a half-day computer-based examination administered at Pearson VUE Professional Testing Centers. It consists of approximately 200 single-best-answer multiple-choice questions. All questions are clinical vignette-based and cover the five ABP content outline domains: General Oncology Issues, Hematologic Malignancies, Solid Tumors, Hematopoietic Stem-Cell Transplant, and Core Knowledge in Scholarly Activities, plus classical hematology.

How much does the 2026 ABP Pediatric Hematology-Oncology exam cost?

The 2026 standard registration fee is $2,242. The regular (late) registration fee is $2,992, which includes a $750 processing fee. Cancellation and refund policies follow ABP published deadlines; full forfeiture applies near the exam date. Retakes within the 7-year qualification window require re-registration and full fee payment.

How is the exam scored?

The ABP uses criterion-referenced scoring with a cut-score set in advance by subject-matter experts using the modified Angoff method. A candidate's result depends on performance relative to the fixed standard, not on how other candidates perform. Scores are reported on a scaled basis (not percentages of questions correct). Results are typically posted approximately 2-3 months after the exam administration.

What are the highest-yield topics on this exam?

High-yield domains include: sickle cell disease management (TCD screening, hydroxyurea, acute chest syndrome, stroke prevention), pediatric ALL cytogenetics (Ph+, ETV6-RUNX1, KMT2A, hyperdiploid/hypodiploid) and MRD-guided therapy, APL recognition and emergent ATRA/arsenic trioxide induction, neuroblastoma INRG + MYCN, rhabdomyosarcoma embryonal vs alveolar (PAX-FOXO1), Ewing sarcoma (EWSR1-FLI1), hemophilia A/B management including emicizumab and inhibitor handling, ITP vs HUS vs TTP differentiation, febrile neutropenia empiric therapy, tumor lysis syndrome prophylaxis/management, HSCT GVHD and VOD, and LCH (BRAF V600E) and HLH diagnosis.

How should I study for this exam?

Use a structured 6-12 month plan during or after fellowship. Start with leukemias and lymphomas (highest weighting combined), then pediatric solid tumors with molecular genetics, then classical hematology (sickle cell — highest single-topic weight, hemophilia, ITP, HUS/TTP, bone marrow failure). Finish with HSCT, supportive care, and scholarly activities. Take 2-3 timed full-length practice exams. Integrate the ABP content outline, WHO 2022 Hematolymphoid Classification, WHO 2021 CNS Tumors Classification, Lanzkowsky's Manual of Pediatric Hematology and Oncology, Nathan and Oski's Hematology and Oncology of Infancy and Childhood, and ASH/ASPHO guidelines.

How long is my certification valid?

ABP subspecialty certifications issued since 1988 are time-limited. To remain board-certified, diplomates must enroll in and complete Maintenance of Certification (MOC) every 5 years, including licensure verification, lifelong learning and self-assessment activities (Part 2), an assessment of knowledge (Part 3 — MOCA-Peds or traditional exam), and improvement in medical practice (Part 4).