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100+ Free Cert Medical Oncology(SA) Paed Practice Questions

Prepare for the CMSA Sub-specialty Certificate in Medical Oncology Cert Medical Oncology(SA) Paed — South Africa exam with instant access — no signup required.

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2026 Statistics

Key Facts: Cert Medical Oncology(SA) Paed Exam

2 components

Written + oral/OSCE

CMSA Regulations

50% each

Subminimum per component

CMSA Regulations

R24 650

Exam Fee

CMSA 2026 Fee Schedule

50% overall

Pass Mark

CMSA Regulations

CMSA

Exam Body

College of Paediatricians

The Cert Medical Oncology(SA) Paed is a two-component sub-specialty exit examination (written short-answer papers plus an oral/OSCE/clinical component, each 50%) assessing expert clinical competency in paediatric haematology-oncology for qualified paediatricians seeking sub-specialist registration in South Africa. This bank provides 100 practice MCQs as a study aid.

Sample Cert Medical Oncology(SA) Paed Practice Questions

Try these sample questions to test your Cert Medical Oncology(SA) Paed exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1A 4-year-old boy presents with pallor, lethargy, fever, and diffuse petechiae. Bone marrow aspirate confirms precursor B-cell acute lymphoblastic leukaemia (B-ALL). Cytogenetic analysis reveals a t(12;21)(p13;q22) translocation. Which gene fusion is formed by this translocation, and what is its prognostic significance?
A.ETV6-RUNX1 (TEL-AML1); favorable prognosis
B.TCF3-PBX1 (E2A-PBX1); unfavorable prognosis
C.KMT2A-AFF1 (MLL-AF4); favorable prognosis
D.BCR-ABL1; unfavorable prognosis
Explanation: The t(12;21)(p13;q22) translocation generates the ETV6-RUNX1 (formerly TEL-AML1) fusion gene. Present in approximately 22-25% of childhood precursor B-ALL cases, it is associated with cryptic translocation detectable by FISH or RT-PCR and portends an excellent (favorable) event-free and overall survival under modern risk-adapted therapy.
2A 13-year-old adolescent boy presents with a 2-week history of worsening shortness of breath, facial puffiness, orthopnoea, and venous distension over the upper chest. Chest radiograph demonstrates a massive anterior mediastinal mass with left pleural effusion. Full blood count reveals WBC 145 x 10^9/L with 85% circulating blasts. What is the most likely diagnosis?
A.Precursor B-cell acute lymphoblastic leukaemia (B-ALL)
B.Chronic myeloid leukaemia (CML)
C.Acute promyelocytic leukaemia (APML)
D.T-cell acute lymphoblastic leukaemia (T-ALL)
Explanation: T-cell acute lymphoblastic leukaemia (T-ALL) characteristically presents in older children/adolescents (predominantly males) with hyperleukocytosis, a large anterior mediastinal mass, pleural/pericardial effusions, and high risk of superior vena cava (SVC) syndrome and acute airway compression.
3Minimal residual disease (MRD) measurement at the end of induction chemotherapy is the most powerful post-treatment prognostic marker in paediatric ALL. What threshold measured by flow cytometry or quantitative PCR is standardly used to define MRD negativity?
A.Less than 0.0001% (< 1 in 1,000,000 cells / 10^-6)
B.Less than 0.01% (< 1 in 10,000 cells / 10^-4)
C.Less than 0.1% (< 1 in 1,000 cells / 10^-3)
D.Less than 1.0% (< 1 in 100 cells / 10^-2)
Explanation: In pediatric ALL protocols (COG, BFM, NOPHO), end-induction MRD negativity is defined as < 0.01% (< 10^-4, or fewer than 1 leukemic blast per 10,000 nucleated cells). Patients achieving < 0.01% MRD at end-induction have significantly higher event-free survival and lower relapse rates.
4A 6-month-old infant is diagnosed with acute lymphoblastic leukaemia. Immunophenotyping shows CD19+, CD22+, HLA-DR+, but CD10 (CALLA) negative blasts. Which molecular genetic alteration is found in over 70-80% of infant ALL cases and accounts for its dismal prognosis?
A.High hyperdiploidy (>50 chromosomes)
B.NUP98-NSD1 gene fusion
C.ETV6-RUNX1 translocation t(12;21)
D.KMT2A (MLL) gene rearrangement on chromosome 11q23
Explanation: Infant ALL (< 12 months of age) is a biologically distinct entity characterized by high rate of KMT2A (formerly MLL) gene rearrangements located on chromosome 11q23 (most commonly t(4;11) KMT2A-AFF1). It typically presents with high WBC, hepatosplenomegaly, CNS involvement, and a pro-B CD10-negative immunophenotype with poor event-free survival.
5An 8-year-old boy presents with rapid abdominal distension, ascites, and an ileocecal mass causing intussusception. Biopsy reveals medium-sized lymphoid cells with amphophilic cytoplasm, multiple nucleoli, a high mitotic index (>99% Ki-67 positivity), and interspersed tingible body macrophages ('starry-sky' pattern). What is the characteristic chromosomal translocation?
A.t(8;14)(q24;q32) translocating MYC to the IGH heavy chain locus
B.t(14;18)(q32;q21) translocating BCL2 to IGH
C.t(11;14)(q13;q32) translocating CCND1 to IGH
D.t(2;5)(p23;q35) translocating NPM1 to ALK
Explanation: Burkitt lymphoma is a highly aggressive mature B-cell non-Hodgkin lymphoma characterized by t(8;14)(q24;q32) in ~85% of cases (or variant translocations t(2;8) or t(8;22)), leading to constitutive overexpression of the MYC proto-oncogene under the control of immunoglobulin gene enhancers. Histology demonstrates the classic 'starry-sky' appearance.
6A 9-year-old girl is diagnosed with Acute Promyelocytic Leukaemia (APML / AML M3) after presenting with severe epistaxis, ecchymoses, and disseminated intravascular coagulation (DIC). Blood film reveals hypergranular blasts packed with Auer rods (Faggot cells). What targeted therapeutic combination represents first-line standard of care?
A.Imatinib mesylate + Prednisone
B.High-dose Methotrexate + Pegasparaginase
C.All-trans retinoic acid (ATRA) + Arsenic trioxide (ATO)
D.Cytarabine + Daunorubicin (7+3 regimen)
Explanation: Standard first-line therapy for pediatric APML (driven by the t(15;17)(q22;q21) PML-RARA fusion) is the chemo-free targeted combination of All-trans retinoic acid (ATRA) and Arsenic trioxide (ATO). This combination induces differentiation and degradation of the PML-RARA fusion protein, achieving cure rates >95% while dramatically reducing chemotherapy toxicities.
7A 2-week-old newborn with Down syndrome (Trisomy 21) presents with hepatosplenomegaly and a WBC count of 65 x 10^9/L. Peripheral smear reveals circulating megakaryoblasts. Molecular testing identifies a mutation in which gene, and what is the expected clinical course?
A.CEBPA mutation; lifelong indolent myeloproliferative state
B.GATA1 mutation; spontaneous resolution in most cases within 1-3 months
C.JAK2 V617F mutation; rapid progression requiring immediate bone marrow transplantation
D.FLT3-ITD mutation; high mortality requiring emergency intensive AML chemotherapy
Explanation: Transient Myeloproliferative Disorder (TMD), or transient leukaemia, occurs in ~10% of neonates with Down syndrome. It is caused by acquired somatic mutations in exon 2 of the erythroid/megakaryocytic transcription factor gene GATA1. Most cases undergo spontaneous regression within 1-3 months, though ~20-30% subsequently develop myeloid leukaemia of Down syndrome (ML-DS / AMKL) within 4 years.
8A 15-year-old girl presents with painless, firm cervical lymphadenopathy and low-grade night sweats. Biopsy of a cervical lymph node demonstrates fibrous bands dividing the lymphoid tissue into nodules, containing classic binucleated Reed-Sternberg cells ('owl-eye' nuclei). Immunophenotyping confirms CD15+ and CD30+ expression. What is the most common histological subtype of Hodgkin lymphoma in adolescents?
A.Nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL)
B.Nodular sclerosis classic Hodgkin lymphoma
C.Mixed cellularity classic Hodgkin lymphoma
D.Lymphocyte-depleted classic Hodgkin lymphoma
Explanation: Nodular sclerosis classic Hodgkin lymphoma (NScHL) accounts for approximately 70-80% of Hodgkin lymphoma cases in adolescents and young adults. Histology shows collagen bands encapsulating nodular aggregates of lymphocytes, plasma cells, eosinophils, and lacunar Reed-Sternberg variants expressing CD15 and CD30.
9A 10-year-old boy presents with fever, generalized lymphadenopathy, and cutaneous nodules. Biopsy shows large atypical cells with kidney-shaped (horseshoe) nuclei ('hallmark cells') that strongly express CD30 and Anaplastic Lymphoma Kinase (ALK). Which chromosomal translocation is pathognomonic for ALK-positive Anaplastic Large Cell Lymphoma (ALCL)?
A.t(2;5)(p23;q35) NPM1-ALK fusion
B.t(11;14)(q13;q32) CCND1-IGH fusion
C.t(15;17)(q22;q21) PML-RARA fusion
D.t(8;14)(q24;q32) MYC-IGH fusion
Explanation: ALK-positive Anaplastic Large Cell Lymphoma (ALCL) is characterized in >80% of cases by the t(2;5)(p23;q35) translocation, which fuses the Nucleophosmin (NPM1) gene to the Anaplastic Lymphoma Kinase (ALK) gene, leading to constitutive ALK tyrosine kinase activation.
10A 7-year-old boy with relapsed precursor B-ALL receives Blinatumomab infusion. On day 4 of therapy, he develops a temperature of 39.5°C, tachycardia, hypotension, and tachypnoea. Laboratory studies reveal elevated IL-6, ferritin, and CRP. What is the primary mechanism of action of Blinatumomab, and what acute adverse effect is he experiencing?
A.Antibody-drug conjugate targeting CD22; Hepatic Veno-Occlusive Disease (VOD)
B.Bispecific T-cell engager (BiTE) connecting CD19 on B-blasts to CD3 on T-cells; Cytokine Release Syndrome (CRS)
C.Chimeric Antigen Receptor T-cell therapy; Graft-versus-Host Disease (GvHD)
D.Anti-CD20 monoclonal antibody; Tumor Lysis Syndrome (TLS)
Explanation: Blinatumomab is a bispecific T-cell engager (BiTE) antibody construct that simultaneously binds CD19 on precursor B-lymphoblasts and CD3 on cytotoxic T-cells, triggering T-cell activation and blast lysis. Massive systemic T-cell activation releases proinflammatory cytokines (IL-6, IFN-gamma, TNF-alpha), causing Cytokine Release Syndrome (CRS), treated with Tocilizumab (anti-IL-6 receptor antibody) and supportive care.

About the Cert Medical Oncology(SA) Paed Exam

The Sub-specialty Certificate in Medical Oncology (Paediatric Oncology) [Cert Medical Oncology(SA) Paed] is the benchmark sub-specialist qualification in South Africa. Administered by the College of Paediatricians of the CMSA, it certifies advanced expertise in the diagnosis, risk stratification, multi-agent chemotherapy, targeted biological therapy, supportive management, and long-term survivorship care for infants, children, and adolescents with cancer.

Assessment

Two components each contributing 50%: a written component (short-answer written papers) and an oral/OSCE/OSPE/clinical component. Content spans 5 blueprint topics: Paediatric Leukaemias & Lymphomas (30%), Paediatric Solid Tumours (25%), Central Nervous System Tumours in Children (20%), Paediatric Chemotherapy, Supportive Care & Toxicity (15%), and Cancer Genetics, Late Effects & Palliative Care (10%).

Time Limit

Written short-answer papers plus an OSCE and viva component.

Passing Score

Overall pass mark 50% with a 50% subminimum in each of the two components (written and oral/OSCE/OSPE/clinical).

Exam Fee

R24 650 (Colleges of Medicine of South Africa (CMSA), College of Paediatricians)

Cert Medical Oncology(SA) Paed Exam Content Outline

30%

Paediatric Leukaemias & Lymphomas

Acute lymphoblastic leukaemia (ALL), acute myeloid leukaemia (AML), chronic myeloid leukaemia, Hodgkin lymphoma, non-Hodgkin lymphomas (Burkitt, DLBCL, ALCL), cytogenetics, risk stratification, and minimal residual disease (MRD).

25%

Paediatric Solid Tumours (Neuroblastoma, Wilms, Sarcomas)

Neuroblastoma, Wilms tumour (nephroblastoma), rhabdomyosarcoma, Ewing sarcoma, osteosarcoma, hepatoblastoma, retinoblastoma, germ cell tumours, and staging protocols (INRGSS, NWTSG/SIOP).

20%

Central Nervous System Tumours in Children

Medulloblastoma molecular subtyping, pilocytic astrocytoma, high-grade gliomas, ependymoma, craniopharyngioma, atypical teratoid/rhabdoid tumour (ATRT), germ cell tumours, and neuro-oncology supportive management.

15%

Paediatric Chemotherapy, Supportive Care & Toxicity

Dosing metrics, febrile neutropenia empirical management, tumor lysis syndrome (TLS), mucositis, anthracycline cardiotoxicity, vincristine neurotoxicity, platinum ototoxicity/nephrotoxicity, stem cell transplant, and antiemetic regimens.

10%

Cancer Genetics, Late Effects & Palliative Care

Cancer predisposition syndromes (Li-Fraumeni, NF1, DICER1, BWS, Gorlin), late organ toxicities, secondary malignancies, fertility preservation, growth and endocrine sequelae, and paediatric palliative symptom control.

How to Pass the Cert Medical Oncology(SA) Paed Exam

What You Need to Know

  • Passing score: Overall pass mark 50% with a 50% subminimum in each of the two components (written and oral/OSCE/OSPE/clinical).
  • Assessment: Two components each contributing 50%: a written component (short-answer written papers) and an oral/OSCE/OSPE/clinical component. Content spans 5 blueprint topics: Paediatric Leukaemias & Lymphomas (30%), Paediatric Solid Tumours (25%), Central Nervous System Tumours in Children (20%), Paediatric Chemotherapy, Supportive Care & Toxicity (15%), and Cancer Genetics, Late Effects & Palliative Care (10%).
  • Time limit: Written short-answer papers plus an OSCE and viva component.
  • Exam fee: R24 650

Keys to Passing

  • Work through all 100 available questions
  • Review every answer and explanation
  • Track weak areas and revisit them
  • Use our AI tutor for tough concepts

Cert Medical Oncology(SA) Paed Study Tips from Top Performers

1Understand the molecular risk stratification in B-ALL (ETV6-RUNX1 vs KMT2A-rearranged vs hyperdiploidy) and MRD cut-offs.
2Know the staging and management differences between SIOP (preoperative chemo) and COG/NWTSG (upfront nephrectomy) for Wilms tumour.
3Master WHO 2021 CNS classification for medulloblastoma (WNT, SHH TP53 wild-type/mutant, Group 3, Group 4) and targeted treatments.

Frequently Asked Questions

What is the structure of the CMSA Cert Medical Oncology(SA) Paed examination?

The exit examination has two components, each contributing 50%: a written component (short-answer written papers) and an oral/OSCE/OSPE/clinical component. Candidates must achieve an overall 50% with a 50% subminimum in each component. This free question bank provides 100 practice MCQs as a study aid and does not replicate the official format.

Who is eligible to take the Cert Medical Oncology(SA) Paed exam?

Medical practitioners registered with HPCSA as Specialist Paediatricians who have completed or are completing 2 years of accredited sub-specialty training in paediatric oncology.

What is the fee for the examination?

The CMSA fee for the Sub-specialty Certificate examination is R24 650.