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Paediatric Solid Tumours: Classification, Diagnosis, and Management

RACP Paediatrics LO FRACPPAEDS_HAEMONC_019 2,205 words
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Overview

Solid tumours constitute a significant proportion of childhood malignancies, second in frequency only to leukaemia and CNS tumours. The spectrum includes embryonal tumours (neuroblastoma, Wilms tumour, hepatoblastoma), sarcomas (rhabdomyosarcoma, Ewing sarcoma, osteosarcoma), germ cell tumours, and retinoblastoma. Each tumour type has a characteristic age distribution, molecular biology, and therapeutic approach. Management requires integration of clinical recognition, molecular pathology, staging, and multidisciplinary care within the framework of international cooperative groups - the Children's Oncology Group (COG) and the International Society of Paediatric Oncology (SIOP). All major Australian and New Zealand paediatric oncology centres operate within the COG framework.


Epidemiology and Aetiology

Incidence and Age Distribution

Tumour Type Peak Age Relative Frequency
Neuroblastoma Infancy-3 years ~8-10% of childhood cancers
Wilms tumour (nephroblastoma) 3-4 years ~5-6%
Hepatoblastoma <3 years ~1%
Retinoblastoma <5 years ~3%
Rhabdomyosarcoma Bimodal: 2-6 yrs, adolescence ~3-4%
Osteosarcoma Adolescence ~3%
Ewing sarcoma Adolescence ~2%
Germ cell tumours Infancy + adolescence ~3-4%

Neonatal solid tumours account for approximately 2-3% of all paediatric cancers. Neuroblastoma is the most common neonatal solid malignancy; soft-tissue tumours account for ~25% of neonatal tumours (benign in >two-thirds of cases). Rhabdoid tumours and rhabdomyosarcoma are rare neonatal malignancies but carry a poor prognosis.

Genetic Predisposition Syndromes

Syndrome / Gene Associated Tumour
WAGR (WT1 deletion, 11p13) Wilms tumour
Denys-Drash (WT1 mutation) Wilms tumour
Beckwith-Wiedemann (IGF2/CDKN1C, 11p15) Wilms tumour (4-10% risk), hepatoblastoma
Li-Fraumeni (TP53) Osteosarcoma, rhabdomyosarcoma, brain tumours
Neurofibromatosis type 1 (NF1) Optic pathway glioma, GIST, MPNST
Retinoblastoma (RB1 germline) Retinoblastoma; second primaries (osteosarcoma)
Familial adenomatous polyposis (APC) Hepatoblastoma, desmoid tumours
Down syndrome Reduced risk of most solid tumours; increased risk of testicular GCTs (~50× general population)

Recognition of predisposition syndromes is essential for family counselling, cascade testing, and tumour surveillance planning.


Pathophysiology

Paediatric solid tumours arise predominantly from embryonic precursor cells that fail to undergo normal differentiation, reflected histologically as small round blue cells or undifferentiated stroma. Key molecular mechanisms:

Precision oncology enables molecular stratification and identification of targetable driver mutations for risk-adapted therapy.


Clinical Features

General Red Flags


Neuroblastoma

Arises from neural crest cells in the adrenal medulla or sympathetic chain. Most common extracranial solid tumour in children under 5 years.

Clinical features: - Abdominal mass (most common primary site - adrenal gland) - Paravertebral or posterior mediastinal mass - Periorbital bruising ("panda eyes") - metastatic orbital disease - Opsoclonus-myoclonus syndrome (paraneoplastic, 2-3%) - Horner syndrome (cervical/thoracic primary) - Hypertension, secretory diarrhoea (excess VIP), sweating - Stage 4S: Infants <12 months with localised primary + dissemination restricted to skin, liver, and/or bone marrow (excluding cortical bone) - spontaneous regression typically occurs

International Neuroblastoma Staging System (INSS)

Stage Description
1 Localised tumour, complete resection, negative nodes
2A Localised, incomplete resection, ipsilateral nodes negative
2B Localised, ipsilateral nodes positive
3 Unresectable unilateral tumour crossing midline, or bilateral extension
4 Distant metastases (bone, bone marrow, liver, distant nodes)
4S Infant <12 months, localised primary + skin/liver/bone marrow (not cortical bone); spontaneous regression usual

Note: The International Neuroblastoma Risk Group Staging System (INRGSS) - based on image-defined risk factors (IDRFs) rather than surgical findings - is increasingly used in clinical trials alongside the INSS.

Risk stratification integrates INSS stage, age at diagnosis, Shimada histological classification, ploidy (hyperdiploid = favourable), and MYCN amplification status. High-risk disease (stage 4, age >12 months; or any stage with MYCN amplification) has markedly inferior outcomes.


Wilms Tumour (Nephroblastoma)

Most common renal malignancy in children; peak age 3-4 years.

Clinical features: - Smooth, non-tender unilateral abdominal mass (most common presentation) - Haematuria (gross or microscopic), hypertension - Associated anomalies: aniridia, hemihypertrophy, genitourinary anomalies - Bilateral in 5-10% (higher in predisposition syndromes) - Rhabdoid tumours of the kidney are histologically distinct, treated similarly, but carry considerably worse outcomes

Histology: Triphasic - blastemal, stromal, and epithelial components. Anaplastic histology (diffuse > focal) is the main adverse histological feature.

COG surgical staging (post-nephrectomy):

Stage Description
I Tumour limited to kidney, completely resected
II Extension beyond kidney, completely resected
III Residual non-haematogenous disease confined to abdomen
IV Haematogenous metastases (lung, liver, bone, brain)
V Bilateral renal involvement

Mesoblastic nephroma accounts for ~80% of solid renal masses in neonates. Although generally benign (capable of rare metastasis), it is treated by nephrectomy alone; chemotherapy is considered only for incomplete excision or rupture of the cellular/atypical histological type. Prognosis is excellent (~95% overall survival).

Wilms tumour surveillance: Abdominal ultrasound every 3 months until age 7 years is recommended for children with ≥5% risk - Beckwith-Wiedemann syndrome (4-10% risk), WT1-associated syndromes (WAGR, Denys-Drash), familial Wilms tumour, or offspring of a parent treated for bilateral disease.


Hepatoblastoma

Clinical features: - Large right-sided abdominal mass, typically in children <3 years - Markedly elevated alpha-fetoprotein (AFP) - key diagnostic and response biomarker - Association with Beckwith-Wiedemann syndrome, FAP, extreme prematurity


Rhabdomyosarcoma

Most common soft-tissue sarcoma in children. Histological subtypes: embryonal, alveolar (PAX-FOXO1 fusion, worse prognosis), and botryoid (a variant of embryonal; most common in neonatal period along with embryonal subtype).

Primary Site Clinical Presentation
Head and neck - orbit Proptosis, periorbital swelling
Parameningeal (nasopharynx, middle ear) Cranial nerve palsy, epistaxis, otorrhoea
Genitourinary (bladder, vagina) Haematuria, urinary obstruction, grape-like polyps
Extremity Painless soft-tissue mass
Paratesticular Painless scrotal mass

Infantile Fibrosarcoma

Most common soft-tissue sarcoma in neonates/infants. Although histologically similar to adult fibrosarcoma, it has a much more favourable biology - metastases are rare, and spontaneous maturation can occur. Presents as a soft-tissue mass, most commonly in the head, neck, or extremities. ETV6-NTRK3 fusion is the defining cytogenetic abnormality. Treatment is surgical excision; chemotherapy (vincristine, actinomycin D, cyclophosphamide) is used when excision would be disfiguring or is incomplete. TRK inhibitors (larotrectinib, entrectinib) have excellent activity.


Osteosarcoma


Ewing Sarcoma


Retinoblastoma


Neonatal Brain Tumours

CNS tumours are the most common solid malignancy in childhood but are rare in the neonatal period (0.5-1.5% of all childhood CNS neoplasms; incidence ~4.24 per million live births). Neonatal brain tumours are predominantly supratentorial. Teratomas account for one-third to one-half of all cases, frequently in the pineal or suprasellar region, often very large with calcification visible on CT, and carry high operative mortality. Astrocytomas account for 20-30%, with PNETs/medulloblastoma the next most common.


Investigations

Initial Assessment (All Solid Tumours)

Investigation Purpose
FBC, film, ESR, CRP Baseline; evidence of marrow infiltration
UEC, LFTs, uric acid, LDH Tumour bulk, hepatic involvement, TLS risk
Coagulation profile Pre-operative; hepatic function
AFP, β-hCG Germ cell tumour, hepatoblastoma
Urinary catecholamines (VMA, HVA) Neuroblastoma
^{123}I-MIBG scintigraphy Neuroblastoma staging and response
Bone marrow aspirate + trephine Neuroblastoma, Ewing, rhabdomyosarcoma staging

Imaging

Modality Application
Ultrasound First-line abdominal mass assessment
CT chest/abdomen/pelvis Staging, lymph nodes, pulmonary metastases
MRI Soft-tissue detail, spinal cord, brain, local extension
PET-CT (FDG) Ewing, osteosarcoma; response assessment
^{123}I-MIBG scintigraphy Neuroblastoma-specific
Plain radiographs Osteosarcoma, Ewing - bone lesion characterisation

Molecular and Genetic Testing


Diagnosis

Diagnosis requires histopathological confirmation in virtually all cases. Core biopsy or excisional biopsy (depending on site and resectability) is standard. Molecular pathology is integral to WHO-based classification.

Tumour Diagnostic Hallmarks
Neuroblastoma Catecholamine excess, MIBG avidity, Homer Wright rosettes
Wilms tumour Triphasic histology (blastemal, stromal, epithelial)
Hepatoblastoma Markedly elevated AFP, fetal/embryonal histology
Retinoblastoma Clinical + imaging (Flexner-Wintersteiner rosettes on biopsy - rarely required)
Rhabdomyosarcoma Myogenic markers (MyoD1, desmin, myogenin); PAX-FOXO1 in alveolar subtype
Osteosarcoma Malignant osteoid production
Ewing sarcoma EWS-ETS gene fusion; CD99 positivity
Infantile fibrosarcoma ETV6-NTRK3 fusion
Germ cell tumour AFP/β-hCG elevation; histological subtype

Management

Principles of Multidisciplinary Care

Management is conducted through an MDT including paediatric oncologists, surgeons, radiation oncologists, pathologists, radiologists, psychosocial support, and allied health. Australian and NZ centres operate within COG or SIOP clinical trial frameworks. Precision therapeutics guided by genomic profiling of driver mutations is now standard approach.

Surgery

Tumour Surgical Approach
Wilms tumour (unilateral) Upfront nephrectomy (COG); pre-operative chemotherapy then surgery (SIOP bilateral or renal-sparing cases)
Wilms tumour (bilateral) Pre-operative chemotherapy first; renal-sparing surgery attempted
Neuroblastoma (low/intermediate risk) Upfront resection
Neuroblastoma (high risk) Induction chemotherapy first, then resection
Hepatoblastoma Resection ± liver transplantation; pre-operative cisplatin-based chemotherapy to downstage
Rhabdomyosarcoma Wide local excision where feasible; organ preservation prioritised
Osteosarcoma/Ewing Limb-salvage surgery standard; amputation reserved for selected cases
Mesoblastic nephroma Nephrectomy alone; chemotherapy only for incomplete excision/rupture of cellular type
Infantile fibrosarcoma Surgical excision; chemotherapy if excision disfiguring or incomplete

Intraoperative tumour spillage in Wilms tumour significantly worsens staging and prognosis.

Chemotherapy

Tumour Common Agents
Neuroblastoma (high-risk induction) Cyclophosphamide, cisplatin, etoposide, doxorubicin, topotecan → ASCT consolidation
Wilms tumour Vincristine, actinomycin D ± doxorubicin (stage-dependent)
Hepatoblastoma Cisplatin ± doxorubicin
Rhabdomyosarcoma Vincristine, actinomycin D, cyclophosphamide (VAC)
Osteosarcoma Cisplatin, doxorubicin, high-dose methotrexate (with leucovorin rescue)
Ewing sarcoma Vincristine, doxorubicin, cyclophosphamide (VDC) alternating with ifosfamide + etoposide (IE)
Retinoblastoma Carboplatin, vincristine, etoposide ± intravitreal/intraarterial chemotherapy
Infantile fibrosarcoma Vincristine, actinomycin D, cyclophosphamide

Dosing is weight-based (mg/kg) in children <12 kg and BSA-based (mg/m²) in larger children. Dose modification required for neonates, infants, and organ dysfunction.

Radiation Therapy

Targeted and Biological Therapies

Agent Indication
Dinutuximab (anti-GD2 monoclonal antibody) Maintenance in high-risk neuroblastoma post-ASCT; significantly improves event-free survival
Isotretinoin (13-cis retinoic acid) Differentiation therapy in neuroblastoma maintenance post-ASCT
ALK inhibitors (crizotinib, lorlatinib) ALK-mutant neuroblastoma (emerging)
Larotrectinib / entrectinib (TRK inhibitors) ETV6-NTRK3-positive infantile fibrosarcoma and other NTRK-fusion tumours
Intraarterial ophthalmic artery chemotherapy Retinoblastoma - eye preservation

Haematopoietic Stem Cell Transplantation


Complications

Acute Treatment Toxicities

Toxicity Associated Agents / Context
Tumour lysis syndrome High-burden tumours at diagnosis
Nephrotoxicity Cisplatin, ifosfamide (Fanconi syndrome)
Cardiotoxicity Anthracyclines (doxorubicin) - cumulative dose-dependent
Ototoxicity Cisplatin - high-frequency sensorineural hearing loss
Peripheral neuropathy Vincristine
Hepatic veno-occlusive disease SCT conditioning regimens
Neutropenic sepsis All cytotoxic regimens

Late Effects of Treatment

Domain Complication
Cardiac Cardiomyopathy (anthracyclines), pericarditis (XRT)
Renal CKD (nephrectomy + nephrotoxic agents)
Endocrine GH deficiency, hypothyroidism, gonadal failure, early/late puberty
Musculoskeletal Scoliosis, limb length discrepancy, avascular necrosis
Neurocognitive Learning difficulties - cranial XRT, high-dose methotrexate
Second malignancies Secondary leukaemia, solid tumours (post-XRT); RB1 germline: very high risk of osteosarcoma
Hearing Sensorineural hearing loss (cisplatin) - impacts schooling
Fertility Gonadotoxicity from alkylating agents; fertility preservation counselling in adolescents pre-treatment

Long-term follow-up uses the COG Long-Term Follow-Up Guidelines (survivorshipguidelines.org). In Australia/NZ, this framework is accessed through COG membership. UK centres utilise the National Cancer Survivorship Initiative (NCSI) care pathways.


Prognosis

Survival by Tumour Type

Tumour 5-Year Survival (Approximate)
Wilms tumour (overall) >85-90%
Mesoblastic nephroma ~95%
Neuroblastoma - low/intermediate risk >90%
Neuroblastoma - high risk 40-50% with modern therapy
Hepatoblastoma (resectable) ~70-80%
Retinoblastoma (non-metastatic) >95%
Rhabdomyosarcoma (localised) ~70-80%
Osteosarcoma (localised) ~65-70%
Ewing sarcoma (localised) ~60-70%
Ewing/osteosarcoma (metastatic) <30%
Rhabdoid tumour Poor - usually fatal regardless of treatment

Poor prognostic features in neuroblastoma: MYCN amplification, age >18 months, INSS stage 4, unfavourable Shimada histology, segmental chromosomal aberrations (1p, 11q loss), diploid tumour.


When to Refer / Admit

Urgent Referral to Paediatric Oncology

Oncological Emergencies Requiring Admission

| Emergency | Key Features |

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