A Child With Cancer_paediatric Cancers
Paediatric cancers are a diverse group of malignancies arising in children and adolescents, most commonly leukaemias, brain tumours, and lymphomas, often originating from embryonal or developing tissues rather than from environmental exposures.
A Child with Cancer: Paediatric Cancers
Lecture Map
Paediatric cancers are rare but are the 2nd leading cause of death in children (after accidents). They are fundamentally different from adult cancers in almost every way — type, biology, aetiology, treatment approach, and prognosis. This lecture covers the approach to a child with suspected cancer, the major paediatric malignancies (leukaemia, lymphoma, CNS tumours, neuroblastoma, Wilms tumour, soft tissue sarcomas, bone tumours, retinoblastoma, hepatoblastoma, germ cell tumours), and the principles of management including oncological emergencies and long-term complications of treatment. [1][2]
- Understand the epidemiology and how paediatric cancers differ from adult cancers
- Recognise common presentations of childhood cancers
- Know the major paediatric cancer types, their age distribution, clinical features, investigations, and management principles
- Understand oncological emergencies in paediatrics
- Appreciate the late effects of cancer treatment in survivors [2]
- This is a GC lecture (GC 140) — the examiners directly test from it.
- Past papers frequently ask about: leukaemia presentation/complications, abdominal masses in children (neuroblastoma vs Wilms), late effects of chemotherapy (e.g., anthracycline cardiomyopathy — see Q89 from 2022 MCQ), and oncological emergencies. [7]
- Expect MCQs on distinguishing features of different tumours and SAQs on approach to a child with an abdominal mass.
Paediatric cancers are rare. HK has around 1.1 million children, with approximately 160–190 new children diagnosed every year. However, cancer is the 2nd leading cause of death in children (number 1 is accidents). [2]
Paediatric cancers differ from adult cancers: adult cancers are mostly epithelial/glandular tissue (carcinomas), whereas paediatric carcinomas are rare. [2]
Why Are They Different?
| Feature | Adult Cancers | Paediatric Cancers |
|---|---|---|
| Histology | Carcinomas (epithelial origin) | Embryonal tumours, sarcomas, leukaemias, lymphomas |
| Aetiology | Strong environmental link (smoking, alcohol, sun) | Mostly unknown; some genetic predisposition |
| Screening | Widely used (cervical, breast, colorectal) | No effective screening (too rare, too heterogeneous) |
| Prevention | Modifiable risk factors identifiable | Few modifiable risk factors |
| Response to chemo | Variable, often poor in solid tumours | Often highly chemosensitive |
| Prognosis | Variable | Overall 5-year survival ~80% (UK/HK) |
| Late effects | Less of a concern (shorter remaining lifespan) | Major concern (decades of life ahead) |
First-principles explanation: Adult epithelial tissues undergo decades of accumulated mutations from environmental exposures (the "multi-hit" hypothesis). Children haven't lived long enough for this — instead, paediatric cancers typically arise from embryonal tissue that fails to differentiate properly, or from genetic/developmental abnormalities.
5-year survival in paediatric cancers is approximately 75–80%. [3]
The relative frequencies of paediatric cancers: Leukaemia ~30%, Brain tumours ~25%, Lymphoma ~15%, Neuroblastoma ~8%, Wilms tumour (nephroblastoma) ~6%, Soft tissue sarcomas ~7%, Bone tumours ~5%, Retinoblastoma ~3%, Hepatoblastoma ~1%, Germ cell tumours ~3%. [1][4]
High Yield — Age-Specific Tumour Distribution
Age of onset varies with disease:
- Leukaemia: All ages, peak 2–5 years (ALL)
- Neuroblastoma, Wilms tumour: Typically < 6 years
- Hodgkin lymphoma, bone tumours: Adolescents
- Retinoblastoma, hepatoblastoma: Infants/toddlers (< 2–3 years)
Aetiology
Aetiology is complex and multifactorial. [3]
Environmental factors (including viral infections):
- EBV → Burkitt lymphoma, Hodgkin lymphoma, NPC
- HBV → HCC
- HIV, HHV8 → Kaposi sarcoma
Genetic factors:
- Retinoblastoma (RB1 gene)
- Leukaemia in Down syndrome (trisomy 21)
- Glioma in Neurofibromatosis (NF1)
- Wilms tumour in WAGR syndrome, Beckwith-Wiedemann syndrome, Denys-Drash syndrome
- Hepatoblastoma in FAP, Beckwith-Wiedemann, Li-Fraumeni [3][5][6]
Clinical presentations include: localised mass/effect (e.g., airway compression), systemic features (e.g., disseminated disease), functional disturbance, paraneoplastic syndromes, and oncological emergencies. [3]
Red Flag Symptoms and Signs in Children
| Presentation | Think About |
|---|---|
| Persistent unexplained fever, weight loss, night sweats | Lymphoma, leukaemia |
| Pallor, fatigue, bruising, petechiae | Bone marrow failure (leukaemia) |
| Painless abdominal mass | Wilms, neuroblastoma, hepatoblastoma |
| Lymphadenopathy (> 2 cm, persistent, non-tender) | Lymphoma, leukaemia |
| Bone pain (especially waking at night) | Leukaemia, bone tumours |
| Headache, vomiting (especially morning), new neurological deficit | CNS tumour |
| Leukocoria (white pupillary reflex) | Retinoblastoma |
| Proptosis, periorbital ecchymosis ("raccoon eyes") | Neuroblastoma metastasis |
| Precocious puberty (male) | Hepatoblastoma (hCG secretion), HCG-secreting GCT |
4. Major Paediatric Cancers — Slide-by-Slide High-Yield Content
ALL is the most common childhood malignancy, accounting for ~30% of all childhood cancers. ALL accounts for ~80% of childhood leukaemia. Peak incidence is 2–5 years. Males > Females. [8]
Why does ALL present the way it does? The malignant lymphoblasts crowd out the normal bone marrow → pancytopenia:
- ↓ RBC → anaemia → pallor, fatigue
- ↓ Platelets → thrombocytopenia → bruising, petechiae, bleeding
- ↓ Normal WBC → infections despite high total WBC count (blasts are non-functional)
- Infiltration: bone pain (marrow expansion), hepatosplenomegaly, lymphadenopathy, CNS (cranial nerve palsies, headache), testes
Investigations:
- CBC + blood film: anaemia, thrombocytopenia, ↑/↓ WCC with blasts
- Bone marrow aspirate: ≥ 25% blasts = ALL (< 25% → lymphoblastic lymphoma)
- Immunophenotyping (Pre-B 75%, T-cell 20%, B-cell 5%)
- Cytogenetics: t(9;22) Philadelphia chromosome = poor prognosis; hyperdiploidy = good prognosis
- Lumbar puncture: CNS involvement staging
- CXR: mediastinal mass (T-cell ALL) [8][3]
Management principles:
- Induction → Consolidation → Maintenance (total ~2–3 years)
- CNS-directed therapy (intrathecal methotrexate)
- Risk stratification guides intensity
Childhood ALL is the first disseminated cancer shown to be curable. [8]
Exam Trap — Late Effects of Leukaemia Treatment
A past paper (2022 MCQ Q89) presents a 10-year-old girl treated for leukaemia at age 2, now presenting with SOB, ankle oedema, displaced apex, hepatomegaly. The answer is cardiomyopathy — this is anthracycline cardiotoxicity, a classic late effect. Do NOT confuse with VSD or mitral regurgitation.
Primary malignant CNS tumours are the 2nd most common childhood malignancy after leukaemia. They are the most common paediatric solid organ tumour, carry the highest mortality from childhood cancer (surpassing ALL), and the highest morbidity (neurological deficits). [9][10]
Four most common CNS tumours in children in HK: [9][10]
- Astrocytoma / Other gliomas
- Primitive neuroectodermal tumours (PNETs) including medulloblastoma
- Germ cell tumours (GCTs) — note: Asians:Caucasians = 6:1
- Ependymoma
Site distribution:
- Infratentorial (posterior fossa) tumours predominate in ages 1–10 years → medulloblastoma, juvenile pilocytic astrocytoma (JPA) [9][10]
- Supratentorial tumours predominate in < 1 year and > 10 years
- This is opposite to adults where ~80% are supratentorial [11]
Why does location matter?
- Posterior fossa tumours → obstruct 4th ventricle → obstructive hydrocephalus → ↑ICP → morning headache, vomiting, papilloedema
- Supratentorial tumours → focal neurological deficits, seizures
- Brainstem tumours → cranial nerve palsies, long tract signs
Presentation clues by tumour type:
| Tumour | Key Features |
|---|---|
| Medulloblastoma | Posterior fossa, rapid growth, CSF dissemination ("drop mets"), cerebellar signs (ataxia) |
| Juvenile pilocytic astrocytoma | Posterior fossa, slow-growing, good prognosis, cystic with mural nodule on MRI |
| Craniopharyngioma | Suprasellar, calcification on imaging (50%), growth failure, diabetes insipidus, bitemporal hemianopia [12] |
| Ependymoma | 4th ventricle, hydrocephalus, arises from ependymal lining |
| Intracranial GCT | Pineal/suprasellar region, ↑AFP/βhCG, commoner in Asian boys |
Hodgkin Lymphoma (HL):
- Bimodal age distribution (adolescents and older adults)
- Painless cervical lymphadenopathy, mediastinal mass
- Reed-Sternberg cells on biopsy
- B-symptoms: fever, night sweats, weight loss > 10%
- Excellent prognosis with chemoradiation (~90% cure)
Non-Hodgkin Lymphoma (NHL):
- More common in younger children than HL
- Often extranodal, disseminated at presentation
- Major subtypes: Burkitt lymphoma (EBV-associated, jaw mass in African form, abdominal mass in sporadic form, t(8;14)), lymphoblastic lymphoma (mediastinal mass, T-cell), DLBCL
- More aggressive than HL but chemosensitive
Neuroblastoma is the most common extracranial solid tumour in childhood and the most common malignancy in children < 18 months. [4]
Origin: Neural crest cells → arises anywhere along the sympathetic chain
- Most commonly: adrenal medulla (40%), abdominal paraspinal ganglia
- Also: thorax, pelvis, neck
Key feature: Neuroblastoma crosses the midline (unlike Wilms tumour). [4]
Presentation depends on location:
- Abdominal mass (most common): large, irregular, crosses midline, often calcified on imaging
- Thoracic: SVCO, Horner syndrome (miosis, ptosis, anhidrosis)
- Metastatic disease: periorbital ecchymosis ("raccoon eyes") — orbital metastasis; bone pain; skin nodules ("blueberry muffin" in infants)
- Paraneoplastic: opsoclonus-myoclonus syndrome ("dancing eyes–dancing feet"), secretory diarrhoea (VIP)
Investigations:
- Urine VMA/HVA (vanillylmandelic acid / homovanillic acid) — catecholamine metabolites [3]
- MIBG scan (meta-iodobenzylguanidine — taken up by sympathetic tissue)
- CT/MRI, bone marrow biopsy
- Histology: small round blue cell tumour, Homer-Wright rosettes
Unique biology:
- Infants (< 18 months) may undergo spontaneous regression (Stage 4S)
- MYCN amplification = poor prognosis
- Older age at diagnosis = worse prognosis
Prognosis of neuroblastoma is often poor because it is frequently detected late. [4]
Management: neoadjuvant chemotherapy before surgery. [4]
Wilms tumour is the most common primary renal malignancy in children < 15 years, accounting for 95% of renal tumours and ~6% of all childhood malignancy. [5][6]
Key facts:
- Peak incidence at age 3 years (majority diagnosed 1–5 years)
- 5% bilateral involvement
- 10% multifocal within single kidney
- Does NOT cross the midline (unlike neuroblastoma)
| Syndrome | Genetics | Features |
|---|---|---|
| WAGR | WT1 deletion at 11p13 | Wilms + Aniridia + Genitourinary anomalies + Retardation; 50% risk of Wilms |
| Beckwith-Wiedemann | 11p15.5 | Macroglossia, visceromegaly, omphalocele, hyperinsulinaemic hypoglycaemia |
| Denys-Drash | WT1 missense mutation | Male pseudohermaphroditism, nephropathy, Wilms |
Presentation:
- Abdominal mass — typically smooth, non-tender, does not cross midline, often discovered incidentally by parent
- Haematuria (20%), hypertension, abdominal pain
- Metastasis: haematogenous to lung (most common), liver, bone, brain [5]
Investigations:
- USS abdomen → intrarenal mass (distinguishes from neuroblastoma which is extrarenal)
- CT/MRI for staging
- Chest CT (lung metastases)
- Do NOT biopsy — risk of tumour rupture and upstaging
Management:
Surgery (nephrectomy) + chemotherapy ± radiotherapy. Good prognosis if early stage. [4]
- SIOP (European) approach: neoadjuvant chemotherapy → surgery
- COG (North American) approach: upfront nephrectomy → adjuvant chemotherapy
- Favourable histology (most cases) → excellent prognosis (~90% survival)
- Unfavourable histology (anaplastic, clear cell sarcoma, rhabdoid) → worse prognosis
| Feature | Neuroblastoma | Wilms Tumour |
|---|---|---|
| Origin | Neural crest (sympathetic chain) | Renal embryonal tissue (metanephric blastema) |
| Age | < 2 years, MC malignancy < 18 months | 1–5 years, peak at 3 |
| Crosses midline | Yes | No |
| Mass character | Irregular, hard, fixed | Smooth, non-tender |
| Calcification | Common | Uncommon |
| Urine catecholamines | ↑ VMA/HVA | Normal |
| Hypertension | Sometimes (catecholamines) | Yes (renin secretion) |
| Haematuria | Rare | Yes |
| Prognosis | Often poor (late detection) | Good if early stage |
Exam Discriminator
If an MCQ or SAQ gives you an abdominal mass in a child, check: Does it cross the midline? → If yes, think neuroblastoma. If no, think Wilms. Then look for urine catecholamines (neuroblastoma) vs haematuria/hypertension (Wilms).
Rhabdomyosarcoma (RMS):
- Most common soft tissue sarcoma in children
- Arises from skeletal muscle precursors
- Common sites: head and neck (orbit, nasopharynx), genitourinary tract, extremities
- Two main subtypes: embryonal (younger children, better prognosis) and alveolar (older children/adolescents, worse)
- Treatment: multimodal — surgery + chemotherapy + radiotherapy
Osteosarcoma:
- Most common primary bone malignancy in children/adolescents
- Peak incidence during pubertal growth spurt (10–20 years)
- Typically around the knee (distal femur, proximal tibia)
- Presentation: pain, swelling, pathological fracture
- X-ray: "sunburst" periosteal reaction, Codman triangle
- Metastases: lung (pulmonary nodules)
- Treatment: neoadjuvant chemotherapy → limb-sparing surgery → adjuvant chemotherapy
Ewing Sarcoma:
- Second most common bone tumour in children
- Younger age than osteosarcoma (5–15 years)
- Diaphysis of long bones, pelvis, ribs
- X-ray: "onion-skin" periosteal reaction
- t(11;22) translocation — EWS-FLI1 fusion
- Highly chemosensitive; treatment: chemo + surgery/RT
Retinoblastoma is the commonest intraocular tumour of childhood. 40% are heritable (related to RB1 gene on chromosome 13q14). The commonest presenting finding is leukocoria (white pupillary reflex). [13]
Genetics — Knudson's Two-Hit Hypothesis:
- Heritable (40%): First hit is germline (inherited or de novo); second hit is somatic. Often bilateral, earlier onset, risk of second primary cancers (e.g., osteosarcoma)
- Sporadic (60%): Both hits are somatic. Always unilateral.
Presentation:
- Leukocoria — white reflex instead of red reflex on fundoscopy/photos
- Strabismus, nystagmus, red eye
- Late: proptosis, orbital cellulitis-like picture (advanced disease)
Management goals (in priority order): [14]
- Life-saving: eradicate disease
- Organ-saving: preserve normal appearance of eye
- Vision-saving: preserve vision
Treatment modalities: [14]
- Focal: cryotherapy, laser photocoagulation (small tumours)
- Regional: ophthalmic artery chemosurgery (OAC), intravitreal chemotherapy, episcleral plaque brachytherapy
- Systemic: systemic chemotherapy
- Enucleation: for advanced unilateral disease (Group E)
- External beam RT: rarely used now due to risk of second cancers
Hepatoblastoma is the most common primary liver malignancy in children. Male:Female = 2:1. Median age of onset ~2 years (rarely > 5 years). Usually unifocal, involving the right lobe. Highly aggressive. [5][6]
Associated conditions: FAP, Beckwith-Wiedemann, Trisomy 18 (Edwards), Trisomy 21 (Down), Li-Fraumeni, GSD Ia [5][6]
Presentation:
- Abdominal mass, pain, distension
- Constitutional symptoms (weight loss, fever, night sweats)
- Paraneoplastic: precocious puberty in males (hCG secretion) [5]
Investigations:
- Serum AFP elevated in ~90% — this is the key tumour marker [3][5]
- CBC: anaemia, thrombocytosis
- LFT: usually normal
- Imaging: USS → CT/PET
- Liver biopsy for histological confirmation
Staging: [5]
- PRETEXT/SIOPEL (Europe): Pre-surgical staging based on number of liver sectors involved (I–IV)
- COG (North America): Post-surgical staging (I–IV based on resection completeness and metastasis)
Management: [5]
- Complete resection is the primary goal — major determinant of survival
- Neoadjuvant chemotherapy to reduce tumour size before surgery
- Liver transplantation for unresectable tumours
- Arise from primordial germ cells
- Can occur in gonadal (testis, ovary) or extragonadal sites (sacrococcygeal, mediastinum, retroperitoneum, intracranial — especially pineal/suprasellar in Asian children)
- Tumour markers: AFP (yolk sac tumour), βhCG (choriocarcinoma), LDH [3]
- Sacrococcygeal teratoma is the most common GCT in neonates
- Treatment: surgery ± chemotherapy (platinum-based)
Investigations include: Radiological (XR, CT, MRI, nuclear imaging), Biochemistry (VMA/HVA for neuroblastoma, AFP for GCT/HCC/hepatoblastoma), Pathological (immunohistochemistry, molecular genetics). [3]
| Investigation | Purpose |
|---|---|
| CBC, blood film | Leukaemia (blasts, cytopenias) |
| Bone marrow aspirate/biopsy | Leukaemia, lymphoma staging, neuroblastoma staging |
| Urine VMA/HVA | Neuroblastoma (catecholamine metabolites) |
| Serum AFP | Hepatoblastoma, HCC, yolk sac tumour |
| Serum βhCG | Choriocarcinoma, some GCTs, hepatoblastoma |
| Serum LDH | Non-specific tumour marker (lymphoma, neuroblastoma) |
| CXR | Mediastinal mass (lymphoma, T-ALL), lung metastases |
| CT/MRI | Staging, surgical planning |
| MIBG scan | Neuroblastoma (sympathetic tissue uptake) |
| PET scan | Lymphoma staging, selected solid tumours |
| Lumbar puncture | CNS leukaemia, CNS tumour staging |
6. Principles of Management
Paediatric oncology uses multimodal therapy (surgery, chemotherapy, radiotherapy) more aggressively than adult oncology because:
- Many paediatric tumours are highly chemosensitive
- Children tolerate chemotherapy better than adults
- The goal is cure, not palliation (in most cases)
- Induction: Rapid tumour kill
- Consolidation/Intensification: Eliminate residual disease
- Maintenance: Prevent relapse (e.g., ALL maintenance for 2–3 years)
- CNS-directed therapy: Intrathecal methotrexate (blood-brain barrier prevents systemic chemo from reaching CNS)
- Primary resection for localised tumours (Wilms, hepatoblastoma)
- Delayed primary surgery after neoadjuvant chemo (neuroblastoma, hepatoblastoma)
- Biopsy for unresectable tumours
- Used in selected settings (Hodgkin lymphoma, Ewing sarcoma, CNS tumours)
- Avoided when possible in young children due to growth and development effects
- High-risk ALL, relapsed leukaemia, high-risk neuroblastoma
- Autologous (patient's own stem cells) or allogeneic (donor)
Oncological emergencies are a key presentation mode of paediatric cancers and must be recognised promptly. [3]
| Emergency | Mechanism | Key Features | Management |
|---|---|---|---|
| Tumour lysis syndrome (TLS) | Rapid cell death → release of intracellular contents | ↑K+, ↑PO4, ↑urate, ↓Ca2+, AKI | IV hydration, rasburicase (urate oxidase), correct electrolytes |
| Febrile neutropenia | Chemo-induced neutropenia + infection | Fever + ANC < 500 | Urgent IV broad-spectrum antibiotics (do NOT wait for cultures) [15] |
| SVC obstruction | Mediastinal mass (T-ALL, NHL) | Facial/upper body oedema, dyspnoea, distended neck veins | Steroids, urgent oncology consult, consider RT/chemo [16] |
| Spinal cord compression | Extradural tumour (neuroblastoma, Ewing) | Back pain, leg weakness, bladder/bowel dysfunction | Emergency MRI, dexamethasone, urgent RT/surgery |
| Raised ICP | Brain tumour + hydrocephalus | Morning headache/vomiting, papilloedema, ↓consciousness | Dexamethasone, neurosurgical referral (VP shunt/EVD) |
| Hyperleukocytosis | WCC > 100 × 10⁹/L → leukostasis | Respiratory distress, CNS symptoms | Hydration, leukapheresis, avoid RBC transfusion (↑viscosity) |
Exam Trap — Febrile Neutropenia
2024 MCQ Q71: A testicular cancer patient 7 days post-chemo with fever 39°C, tachycardia, hypotension. The answer is IV antibiotics after septic workup, then admit — you MUST give antibiotics urgently. Do not discharge, do not wait for results. [15]
This is increasingly examined because survival rates are high and children live for decades after treatment.
| Treatment | Late Effect |
|---|---|
| Anthracyclines (doxorubicin, daunorubicin) | Dilated cardiomyopathy (dose-dependent, may present years later) |
| Cyclophosphamide/Ifosfamide | Haemorrhagic cystitis, gonadal toxicity, secondary malignancy |
| Cisplatin | Ototoxicity, nephrotoxicity |
| Bleomycin | Pulmonary fibrosis |
| Vincristine | Peripheral neuropathy |
| Methotrexate (intrathecal) | Leukoencephalopathy, cognitive effects |
| Cranial RT | Growth hormone deficiency, neurocognitive impairment, secondary CNS tumours |
| Any alkylating agent | Secondary leukaemia (AML), infertility |
| Any RT | Growth retardation (if involving growth plates/spine), secondary malignancy |
Past paper 2022 MCQ Q89: Girl treated for ALL at age 2, now age 10 with displaced apex, hepatomegaly, ankle oedema → anthracycline cardiomyopathy. [7]
- Multidisciplinary team: Paediatric oncologist, surgeon, radiation oncologist, pathologist, radiologist, clinical psychologist, medical social worker, play therapist, palliative care, school liaison
- Family-centred care: Parents are often more distressed than the child; clear communication about diagnosis, prognosis, and treatment plan
- Fertility preservation: Should be discussed before chemotherapy in adolescents (sperm banking, oocyte/embryo cryopreservation)
- Long-term follow-up: Dedicated survivorship clinics monitoring for late effects
- Palliative care: When cure is not possible, early integration of palliative care improves quality of life
Past-Paper Style Stems and Markscheme Points
1. MCQ-style: A 3-year-old child presents with a large, smooth, non-tender abdominal mass that does NOT cross the midline. Urine catecholamines are normal. What is the most likely diagnosis?
- Answer: Wilms tumour. Key discriminators: does not cross midline, normal catecholamines, smooth mass, age 1–5 years.
2. SAQ-style: A 4-year-old presents with pallor, bruising, hepatosplenomegaly, and bone pain. CBC shows Hb 7 g/dL, platelets 20 × 10⁹/L, WCC 45 × 10⁹/L with blasts. Outline your approach to diagnosis and initial management.
- Markscheme: Blood film (blasts), bone marrow aspirate (≥25% blasts → ALL), immunophenotyping, cytogenetics, LP for CNS staging. Initial: IV access, blood products, tumour lysis prevention (hydration, rasburicase), infection screening, refer paediatric oncology, discuss with family.
3. MCQ-style: Which paediatric tumour is associated with elevated urinary VMA/HVA?
- Answer: Neuroblastoma.
4. SAQ-style: A child previously treated with anthracyclines for leukaemia presents years later with progressive exercise intolerance, ankle oedema, and displaced cardiac apex. What is the diagnosis and why?
- Answer: Anthracycline-induced dilated cardiomyopathy. Anthracyclines cause dose-dependent cardiotoxicity via free radical damage to cardiomyocytes; may manifest years after treatment. [7]
5. MCQ-style: A newborn with leukocoria. The most important diagnosis to exclude is:
- Answer: Retinoblastoma.
6. SAQ-style: Compare and contrast neuroblastoma and Wilms tumour. (Table format expected — see Section 4.6 above.)
High Yield Summary
Paediatric cancers are rare but are the 2nd cause of death in children. Key differences from adults: embryonal/mesenchymal histology, mostly unknown aetiology, highly chemo-sensitive, excellent prognosis (5-year survival ~80%), but significant late effects.
The Big Five solid tumours to know:
- CNS tumours — 2nd most common, highest mortality, infratentorial in 1–10 year olds
- Neuroblastoma — most common extracranial solid tumour, crosses midline, urine VMA/HVA, poor prognosis
- Wilms tumour — renal, does NOT cross midline, peak age 3, WAGR/BWS associations, good prognosis
- Retinoblastoma — leukocoria, RB1 gene, Knudson's two-hit
- Hepatoblastoma — most common liver malignancy in children, AFP elevated, FAP/BWS associations
Leukaemia (ALL) is the most common overall childhood malignancy (30%). Peak 2–5 years. Presents with marrow failure features. Curable.
Always watch for oncological emergencies: TLS, febrile neutropenia, SVC obstruction, cord compression, raised ICP.
Late effects are increasingly examined — especially anthracycline cardiomyopathy.
Active Recall - Lecture Notes
[1] Lecture slides: GC 140. A child with cancer_paediatric cancers.pdf (overview slide, frequency distribution) [2] Paediatrics lecture: Block C - A child with cancer_ paediatric cancers.pdf (Part 1: learning objectives, statistics) [3] Senior notes: Adrian Lui Pediatrics Notes.pdf (p.415 — Oncology chapter: epidemiology, aetiology, clinical presentation, investigations) [4] Senior notes: Maksim Surgery Notes.pdf (p.343 — Paediatric oncology: neuroblastoma, Wilms, hepatoblastoma) [5] Senior notes: Adrian Lui Pediatrics Notes.pdf (p.437 — Hepatoblastoma: associations, AFP, staging, management) [6] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p.1075–1080 — Hepatoblastoma and Wilms tumour) [7] Past papers: 2022 Fourth Summative MCQ.pdf (Q89 — anthracycline cardiomyopathy) [8] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p.741 — ALL epidemiology, classification) [9] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p.521 — Brain tumours in children) [10] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p.1249 — CNS tumours) [11] Senior notes: Ryan Ho Neurology.pdf (p.161 — Intracranial tumours, adult vs child site distribution) [12] Senior notes: Block A - I keep on bumping into people on my side_ pituitary tumours; hypopituitarism.pdf (p.6 — Craniopharyngioma) [13] Senior notes: Ryan Ho Opthalmology.pdf (p.118 — Leukocoria and retinoblastoma) [14] Senior notes: Ryan Ho Opthalmology.pdf (p.121 — Retinoblastoma management) [15] Past papers: 2024 Fourth Summative MCQ.pdf (Q71 — febrile neutropenia management) [16] Senior notes: Maksim Medicine Notes.pdf (p.45 — SVC obstruction management)
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