Paediatric solid tumours: retinoblastoma and others

• A paediatric solid tumour is any abnormal mass of tissue in a child that is not leukaemia, lymphoma or a brain tumour: retinoblastoma of the eye, rhabdomyosarcoma of soft tissue, hepatoblastoma of the liver, germ cell tumours at midline and gonadal sites, and the tumour-like disorder Langerhans cell histiocytosis (LCH) are the core set on this page.
• Four ideas run through the topic: these cancers are rare but curable when found early; the child's age and the site of the mass point to the diagnosis; every one of these tumours is managed by risk-stratified multimodal therapy agreed by SIOP (International Society of Paediatric Oncology) or COG (Children's Oncology Group) rather than by a single drug; and "cure" includes the late effects of that therapy.
• Retinoblastoma, the commonest intraocular malignancy, declares itself through a white pupil (leukocoria): 60% of children present this way, and an absent fundal red reflex in a baby is a referral trigger in NICE NG12 (last updated 15 April 2026). ^[1]
• Hepatoblastoma is the commonest malignant liver tumour of early childhood and its diagnosis is clinched by a raised alpha-fetoprotein (AFP) with imaging; 5-year survival in standard-risk disease is around 91% or better with surgery and cisplatin-based chemotherapy.
• LCH is not a true malignancy but a clonal proliferation of myeloid-derived Langerhans-type cells; it ranges from a single bone lesion that may heal on its own to high-risk multisystem disease with liver, spleen or marrow involvement.

By the end of this page you should be able to:

1. Recognise retinoblastoma from leukocoria and list the red-flag referral patterns for childhood solid tumours under NICE NG12.
2. Outline the pathophysiology, presentation, investigation and risk-stratified management of retinoblastoma, rhabdomyosarcoma, hepatoblastoma, childhood germ cell tumours and LCH.
3. Explain what each first-line test and tumour marker measures, and how the classifications (IIRC, IRSG, PRETEXT, single-system versus multisystem LCH) change management.
4. List the late effects of platinum-based chemotherapy, radiotherapy and surgery in childhood solid tumour survivors and how they are monitored.
5. Describe the roles of SIOP and COG protocols and the situations that need urgent referral or specialist centre care.

Childhood solid tumours outside the central nervous system make up roughly two fifths of cancers in children. They differ from adult cancers in almost every way: they arise from immature tissues, present as rapidly growing masses rather than as organ dysfunction, and are highly chemosensitive. The five conditions on this page are all seen in the first decade of life, yet they share an important theme - most are curable, but only if the first clinician to see the child (often a GP, paediatrician or ophthalmologist) recognises the mass as possibly malignant and refers urgently. This page therefore gives equal weight to recognition and referral, to investigation, and to treatment.

Because children differ by age and site, the question "what causes a swelling?" is best answered by asking where it is and how old the child is. A baby with a white pupil has retinoblastoma until proven otherwise; a preschool child with a right upper quadrant mass has hepatoblastoma until proven otherwise; a girl with an abdominal mass and a raised AFP has a germ cell tumour until proven otherwise. The flowchart later in this page sets out the common first steps.

A paediatric solid tumour is a tumour of solid (non-haematological, non-lymphoid) tissue arising between birth and late adolescence. They are classified by tissue of origin:

• Neuroblastic / neuroendocrine: neuroblastoma is covered separately but is the commonest extracranial solid tumour in infancy.
• Embryonal tumour of the developing eye: retinoblastoma, arising from immature retinal cells.
• Soft-tissue sarcoma: rhabdomyosarcoma, a tumour with skeletal muscle differentiation.
• Hepatic tumour: hepatoblastoma, recapitulating fetal liver.
• Germ cell tumour (GCT): arising from primordial germ cells; benign teratomas through to malignant yolk sac tumours, germinomas, embryonal carcinomas and choriocarcinomas.
• Myeloid/neoplastic proliferative disorder with a paediatric peak: Langerhans cell histiocytosis (LCH), in which CD1a-positive, CD207-positive dendritic cells proliferate in bone, skin, liver, spleen and other organs.

These groupings are descriptive rather than exhaustive; overlaps occur (a sacrococcygeal mass may be a germ cell tumour, and retroperitoneal masses may turn out to be neuroblastoma or rhabdomyosarcoma).

Because these tumours are rare their exact incidence is difficult to quote, but a few well-supported figures help with perspective.

• Retinoblastoma is the most common intraocular malignancy of childhood. Metastasis occurs in roughly 10-15% of retinoblastomas overall, but in high-income settings with prompt care it is reported as under 10% (with 3-5% metastasis-related deaths); the risk is far higher where delay or advanced disease at presentation is common. ^[2]
• Rhabdomyosarcoma accounts for roughly 3 to 4% of all paediatric malignancies in the United States and for nearly half of childhood soft-tissue sarcomas. ^[9]
• Hepatoblastoma is the most prevalent malignant liver tumour in children under 5 years of age and makes up nearly 70% of paediatric liver malignancies. ^[4]
• Germ cell tumours account for approximately 3% of solid tumours in children under 15 years of age. ^[5]
• LCH has an incidence of roughly 2.6 to 8.9 cases per million Western children per year, with a median age at diagnosis in most series of early childhood. ^[7]

Other useful figures: rhabdomyosarcoma incidence is about 4.6 to 4.7 cases per million children and adolescents aged 20 years or younger (NCI 4.6; independent review 4.71), with roughly half of cases (NCI reports 50%; other series more than half) diagnosed before 10 years of age and a modest male predominance. ^[9] The incidence of hepatoblastoma peaks in the first years of life, and prematurity and low birth weight are recognised risk factors. ^[4]

Retinoblastoma is caused by inactivating mutations of the RB1 tumour-suppressor gene on chromosome 13q14. ^[2] Heritable (germline) disease accounts for roughly 30 to 40% of cases; the rest are sporadic. ^[2] In heritable disease every cell carries one faulty copy of RB1; a second "hit" in a retinal cell produces the tumour. Clinically this produces bilateral, multifocal or, rarely, trilateral (with a pineal primitive neuroectodermal tumour) disease and is autosomal dominant with incomplete penetrance. Sporadic disease is usually unilateral. ^[2] There is no known modifiable risk factor, but heritable retinoblastoma families need genetic counselling and surveillance of carriers. ^[2]

Rhabdomyosarcoma appears to be a failure of skeletal muscle precursor cells to differentiate fully. Embryonal tumours account for about 60% (range 57-70%: NCI SEER 57%, literature 60-70%) of paediatric cases, mainly in children under 5 years, and alveolar tumours driven by PAX-FOXO1 fusion oncogenes are more aggressive and more common in older children. ^[9] Up to 7.3% of patients carry pathogenic or likely pathogenic germline variants, notably in TP53, NF1, HRAS, BRCA2 and DICER1, so a family history and Li-Fraumeni-type features matter. ^[9]

Hepatoblastoma is strongly associated with activation of Wnt/beta-catenin signalling, most often through CTNNB1 (beta-catenin) mutations, which disrupt proliferation and differentiation of fetal liver cells. ^[4] Risk factors include prematurity, low birth weight and Beckwith-Wiedemann syndrome. ^[4] In practice many hepatoblastomas arise in otherwise healthy toddlers, so absence of risk factors never excludes the diagnosis.

Germ cell tumours are believed to arise from errors in the migration or development of primordial germ cells, which is why they occur along the body midline and in the gonads. They separate into two developmental types. ^[6]

• Type I (infancy and early childhood): teratomas and yolk sac (endodermal sinus) tumours. The commonest malignant histology in prepubertal children is the pure yolk sac tumour. ^[5][6]
• Type II (puberty onwards): seminoma/germinoma, embryonal carcinoma, choriocarcinoma and mixed non-seminomatous tumours. Teratomas make up a large fraction of prepubertal tumours, and mixed tumours predominate in adolescents. ^[5][6]

LCH is a clonal proliferation of myeloid precursors that become CD1a- and CD207-positive Langerhans-type cells. ^[7] It is not a true malignancy in the conventional sense and is not inherited; the clonal origin explains why it can behave like a cancer in its high-risk multisystem form and can be self-limiting in its single-bone form.

Uncontrolled division of immature retinal cells forms a vascular, calcifying mass in the posterior chamber. The tumour blocks light from reaching the retina and, as it enlarges, the abnormal vessels shine through the pupil as leukocoria. From the eye it spreads along the optic nerve, through the choroid into the orbit and, late, to bone marrow, lymph nodes and the brain. In the heritable form the same RB1 loss predisposes to second primary tumours decades later. ^[2]

Failed terminal muscle differentiation leaves a mass of primitive rhabdomyoblasts. The mass is firm and rapidly enlarging and invades along tissue planes, which is why head-and-neck tumours erode skull base bone and why bladder/prostate tumours obstruct urine. Alveolar tumours express PAX-FOXO1 and are biologically more aggressive than embryonal tumours. ^[3]

A proliferating clone of fetal hepatocyte-like cells forms a mass in one or both liver lobes. Alpha-fetoprotein is secreted by fetal liver tissue, so the tumour produces large amounts of AFP, which makes AFP both a diagnostic handle and a treatment-response marker. Large tumours may rupture and bleed, and vascular invasion makes surgical clearance difficult. ^[4]

The biology follows the germ cell's retained potential. Yolk sac tumours secrete AFP; choriocarcinomas (and some seminomas/germinomas) secrete beta-hCG. Teratomas contain differentiated tissues from multiple germ layers, so a dermoid cyst, cartilage or neural tissue may be found. ^[6]

Clonal Langerhans cells infiltrate tissues and behave as an inflammatory, expanding lesion. In bone they cause lytic lesions that may fracture or produce the characteristic "vertebra plana" in the spine. In the pituitary stalk they produce diabetes insipidus; in liver, spleen and marrow they define risk-organ (RO+) disease, which is what makes LCH life-threatening. ^[7]

• Leukocoria in about 60% of presentations: a white pupillary reflex in photographs or on examination, also called the "cat's eye reflex". ^[2]
• Strabismus with reduced vision in one eye.
• Poor red reflex or absent red reflex, the Bruckner/red reflex test abnormality that NICE NG12 lists as a referral trigger. ^[1]
• Late or extraocular disease: a painful red eye, proptosis, an orbital mass, buphthalmos or hyphaema; in low-resource settings these late presentations are common.

Bilateral disease is heritable until proven otherwise; a very young child with apparently unilateral disease should also raise suspicion of the heritable form. ^[2]

• A rapidly enlarging, firm, often painless mass. ^[3]
• Head and neck: nasal obstruction, epistaxis, dysphagia, otitis media from a mass in the middle ear, cranial nerve palsy, cervical lymphadenopathy.
• Orbit: proptosis, periorbital oedema, ptosis, reduced eye movements.
• Genitourinary: haematuria, urinary retention, a vaginal or scrotal mass (sarcoma botryoides); in infants a "grape-like" protruding vaginal lesion.
• Extremity / trunk: deep mass, painful if large.
• Parameningeal tumours (paranasal sinuses, infratemporal fossa) are high risk because they sit close to the brain.

• Abdominal mass or distension, often right upper quadrant.
• Poor weight gain, anorexia, vomiting, sometimes jaundice.
• Fever or pain if the tumour ruptures or haemorrhages.
• Incidental hepatomegaly found during a routine examination.

• Sacrococcygeal mass in an infant (often noticed at birth; may be external and benign-appearing or internal).
• Testicular or ovarian mass, sometimes painful if it twists.
• Mediastinal mass: cough, dyspnoea, superior vena caval obstruction.
• Retroperitoneal mass: abdominal distension, urinary obstruction.
• Raised AFP or beta-hCG noted on routine neonatal or maternal screening.

• Bone: pain and swelling, often skull, spine (vertebra plana), ribs or long bones; may be an isolated, self-limiting lesion.
• Skin: seborrhoeic-dermatitis-like rash with crusted papules in infants, sometimes mistaken for eczema.
• Systemic: fever, failure to thrive, hepatosplenomegaly, anaemia, bleeding tendency.
• Endocrine: polyuria and polydipsia from diabetes insipidus; CNS-risk lesions (temporal bone, orbit, mastoid, sphenoid) flag this risk.
• Lung: cough and hypoxia in older children with pulmonary involvement.

The broad rule is: in a child, any unexplained mass that is enlarging, firm, deep, vascular on imaging, or associated with red-flag symptoms is malignant until proven otherwise, and the definitive diagnosis is a biopsy taken by the team that will treat it.

NICE NG12 (last updated 15 April 2026) gives primary-care triggers that are worth memorising. ^[1]

• Suspected retinoblastoma: refer for ophthalmological assessment using a suspected-cancer pathway in children with an absent fundal red reflex; if a new-onset squint occurs with an absent red reflex, treat it as suspected retinoblastoma. ^[1]
• Neuroblastoma: very urgent referral within 48 hours for a child with a palpable abdominal mass or unexplained enlarged abdominal organ. ^[1]
• Wilms' tumour: very urgent referral within 48 hours for a palpable abdominal mass, an unexplained enlarged abdominal organ, or unexplained visible haematuria. ^[1]
• Bone sarcoma (children): very urgent X-ray for unexplained bone swelling or pain; very urgent referral within 48 hours if the X-ray is suspicious. ^[1]
• Soft tissue sarcoma (children): very urgent direct-access ultrasound for an unexplained lump that is increasing in size; very urgent referral within 48 hours if imaging is suggestive, or if uncertain but clinical concern persists. ^[1]
• NICE also advises taking into account the insight of parents and carers: persistent parental concern about a child's symptoms can itself be a reason to refer, even if the symptoms most likely have a benign cause. ^[1]

• Eye: dilated fundoscopy under general anaesthetic in retinoblastoma; Bruckner/red-reflex test; ocular ultrasound; MRI of the orbit and brain. Biopsy is not taken because it risks tumour spread; histology is on the enucleated eye if enucleation is needed. ^[2]
• Liver: ultrasound first, then CT or MRI of the abdomen; AFP at diagnosis and serially afterwards. ^[4]
• Soft tissue: ultrasound first (solid or cystic, vascular), then MRI for extent, then core biopsy (never fine-needle aspiration alone for suspected sarcoma).
• Germ cell tumours: ultrasound of testis/scrotum, pelvis, abdomen and chest; AFP and beta-hCG before surgery or any therapy, because a rapidly falling marker can be missed. ^[6]
• LCH: skeletal survey (or whole-body MRI/PET-CT depending on local practice), chest imaging, full blood count, liver function tests, coagulation, urine specific gravity or water-deprivation assessment for diabetes insipidus, and a biopsy of the most accessible lesion.

• AFP is produced by fetal liver and yolk sac, so it is raised in hepatoblastoma and in yolk sac tumours (and some mixed germ cell tumours). It also falls with a half-life of several days in responding disease, which is how it is used to monitor treatment. ^[4][6]
• beta-hCG is produced by syncytiotrophoblast and is raised in choriocarcinoma and in some germinomas/seminomas. ^[6]
• LDH is often raised in germ cell tumours and is one of the markers used for risk grouping in adults. ^[6]
• AFP in infants must be interpreted against age-appropriate normal ranges, because normal babies have high AFP; the source papers include age-related tables if a precise cut-off is needed. ^[6]

• Retinoblastoma: RB1 mutation testing of the child and, when indicated, first-degree relatives. ^[2]
• Rhabdomyosarcoma: consider a germline panel (p53, NF1, DICER1 and related genes) when the tumour is embryonal in a young child, when there is a family history suggestive of Li-Fraumeni or neurofibromatosis, or when the child has multiple primaries. ^[3]
• Hepatoblastoma: Beckwith-Wiedemann syndrome warrants clinical assessment and, in many centres, a surveillance programme in infancy. ^[4]

• Retinoblastoma - International Intraocular Retinoblastoma Classification (IIRC): groups A to E by tumour size, location and seeding, with group E describing tumours occupying more than 50% of the globe or with obvious extraocular extension. ^[2]
• Retinoblastoma - heritable category (H): H0 for normal RB1 alleles, H1 for bilateral/extraocular/familial/genetically confirmed disease. ^[2]
• Rhabdomyosarcoma: IRSG clinical groups I to IV describe resection status, from complete resection to metastatic disease, and risk grouping (low, intermediate, high) then assigns treatment. ^[3]
• Hepatoblastoma: the PRETEXT system (pre-treatment extent of disease) divides the liver into sectors and notes vascular involvement; POSTTEXT reassesses after chemotherapy. ^[4]
• LCH: single-system (one organ, possibly multifocal) versus multisystem (two or more organs), and within multisystem, risk-organ involvement (liver, spleen or haematopoietic system) marks high-risk disease. ^[7]

The guiding principle for every tumour here is risk-stratified multimodal therapy delivered in centres experienced in paediatric oncology, following SIOP or COG protocols, with surgery by paediatric surgical oncologists/radiation oncologists where safe. ^[3][4]

Treatment goals in order are: save life, then the eye, then vision. ^[2]

• Examination under anaesthesia and imaging define group and stage. ^[2]
• Small tumours (group A, and many B): focal therapy with cryotherapy and transpupillary thermotherapy (810 nm laser) for tumours under 3 mm. ^[2]
• Intra-arterial chemotherapy (IAC) is now the cornerstone for many teams, delivered into the ophthalmic artery to concentrate drug in the eye. ^[2]
• Intravitreal chemotherapy is used for vitreous seeds.
• Intravenous chemotherapy (VEC: carboplatin, etoposide, vincristine) monthly for 6 to 9 cycles, used to shrink the tumour, to treat micrometastases and, crucially, to prevent second cancers. ^[2]
• Enucleation for group E or tumours unsuitable for conservative treatment, with the full thickness of the optic nerve removed.
• External beam radiotherapy is reserved for extraocular extension, orbital recurrence or a positive optic-nerve margin, and causes osseous growth retardation and possible facial deformity. ^[2]
• Genetic counselling, survivorship follow-up (screening for second cancers) and visual rehabilitation are part of standard care.

• Surgery where the tumour can be completely resected without causing severe loss of function; "delayed primary excision" after chemotherapy is common for head-and-neck and genital sites. ^[3]
• Chemotherapy: the North American standard is vincristine, dactinomycin and cyclophosphamide, sometimes with irinotecan (VAC). ^[3]
• Radiotherapy is central, especially for head-and-neck and parameningeal sites and any residual disease, while eye-sparing radiotherapy or brachytherapy may be used in the orbit.
• Autologous transplant/high-dose approaches are reserved for relapsed or very high-risk disease and are outside the scope of this page.
• Because metastatic rhabdomyosarcoma and relapse carry a poor prognosis, these patients are referred to trials. ^[3]

• Neoadjuvant cisplatin-based chemotherapy shrinks the tumour and converts many unresectable tumours into resectable ones. Accepted regimens from SIOPEL/COG protocols include PLADO (cisplatin + doxorubicin), cisplatin monotherapy for standard risk, C5VD, dose-dense cisplatin/carboplatin/doxorubicin and others. ^[4]
• Surgery: complete resection is the aim; extreme (extended) liver resection is sometimes used instead of transplantation. ^[4]
• Liver transplantation is indicated for major vascular involvement, multifocal disease or inadequate future liver remnant. ^[4]
• AFP is followed serially to judge response and detect recurrence. ^[4]
• Applicability of high-risk regimens in resource-limited settings: cisplatin monotherapy remains acceptable for standard-risk disease. ^[4]

(Agents and outcomes as reported in Fan, Na and Shi (ref 4).)

• Mature teratoma: surgery alone is usually curative. ^[5]
• Malignant tumours (yolk sac, embryonal carcinoma, choriocarcinoma, mixed): platinum-based chemotherapy plus surgery, with AFP and beta-hCG monitored before, during and after treatment every few months for 5 years. ^[5][6]
• Germinoma/seminoma/dysgerminoma are exquisitely chemosensitive and radiosensitive; most are cured. ^[6]
• Infantile choriocarcinoma is aggressive but curable if recognised: the mother or infant may present with bleeding and very high beta-hCG. ^[6]

• Single bone lesion: observation, curettage, or local treatment can suffice; many small lesions resolve. ^[7]
• Multifocal bone or low-risk multisystem disease: vinblastine with corticosteroids in combination regimens per the Histiocyte Society LCH protocols, given for about 12 months in many regimens; exact regimens should follow the LCH protocol in use.
• Risk-organ (RO+) multisystem disease: intensified multi-agent chemotherapy, sometimes with targeted inhibition of MAPK signalling in refractory or relapsed disease (this is evolving and should only be used in trial/protocol settings). ^[7]
• CNS-risk bone lesions and diabetes insipidus need endocrine and neurological monitoring.

• Retinoblastoma: metastatic spread along the optic nerve, orbital recurrence, and extraocular disease; second primary tumours in heritable disease, especially peaking in the fourth decade of life, particularly after radiotherapy. ^[2]
• Rhabdomyosarcoma: local recurrence, especially parameningeal tumours; metastatic disease has a poor prognosis. ^[3]
• Hepatoblastoma: tumour rupture, metastases at diagnosis and relapse, particularly in high-risk patients. ^[4]
• Germ cell tumours: surgical morbidity (sacrococcygeal resection, fertility), recurrence in mixed/malignant types. ^[5]
• LCH: reactivation of disease, diabetes insipidus, organ failure in RO+ disease, growth and endocrine problems. ^[7]

• Retinoblastoma: 5-year survival is as high as 98% with timely detection and proper treatment; untreated disease is usually fatal within 1 to 2 years. ^[2]
• Rhabdomyosarcoma: children with localised disease achieve good survival with multimodal therapy; outcomes remain poor in metastatic or relapsed disease. ^[3]
• Hepatoblastoma: long-term survival is 91 to 95% in standard- and middle-risk groups, and remains lower in high-risk metastatic disease. ^[4]
• Germ cell tumours: in one large childhood series the estimated 5-year overall survival for extracranial germ cell tumours treated completely was 83%, with gonadal tumours doing better (87.6%) than extragonadal tumours (75.6%); mature teratomas and dysgerminomas had the best outcomes. ^[5]
• LCH: single-system and low-risk multisystem disease usually have excellent long-term survival; RO+ multisystem LCH still carries a significant risk of death and reactivation, though 5-year overall survival now exceeds 80% in many series. ^[7]

Childhood cancer therapy is delivered while tissues are still growing, so the same drugs that cure often cause delayed harm.

• Platinum ototoxicity: cisplatin causes hearing loss in more than 60% of treated children, carboplatin in about 20%, and combination platinum therapy in up to 90%; radiotherapy directed at the head, neck or brain adds to this risk. ^[8]
• Renal and neurological: cisplatin nephrotoxicity, peripheral neuropathy and hypomagnesaemia are well described; vincristine adds neuropathy. ^[8]
• Second primary tumours after heritable retinoblastoma, particularly in radiotherapy fields and in the fourth decade of life. ^[2]
• Facial growth arrest after external beam radiotherapy to the orbit. ^[2]
• Cardiac toxicity from anthracyclines (doxorubicin in hepatoblastoma and some germ cell regimens) is a lifelong concern and is monitored with echocardiography in survivorship clinics.
• Endocrine and fertility effects follow surgery, radiotherapy and alkylating agents; adolescents and young adults need fertility counselling before gonadotoxic therapy where it is safe.
• Surveillance: long-term follow-up includes audiometry after platinum agents, renal function, echocardiography, growth and puberty tracking, and counselling about future cancer screening after heritable retinoblastoma.

Where a risk is mentioned here without a precise citation, no number is asserted beyond the sources listed; those items are standard practice points rather than dose claims.

• Any child with an emergency (obstructed airway, bleeding tumour, ruptured hepatoblastoma, acute vision loss) needs same-day paediatric oncology contact.
• Suspected retinoblastoma: same or next-day ophthalmology through a suspected-cancer pathway. ^[1]
• Abdominal or soft tissue masses: urgent ultrasound and referral, not watchful waiting; fast access to oncology.
• High-risk/pre-teen masses with systemic features: admission for work-up rather than outpatient investigation.
• Metastatic or relapsed rhabdomyosarcoma and poor-prognosis hepatoblastoma should be considered for clinical trials and national databases.

• Recognition at birth: the red-reflex examination and, in many programmes, universal neonatal screening look for leukocoria; health workers should treat a white pupil as cancer until proven otherwise. ^[1]
• Genetic families: RB1 carrier testing and early eye examinations for children of carriers; Beckwith-Wiedemann syndrome surveillance with liver imaging and AFP in infancy. ^[2][4]
• Environmental risk reduction is not evidence-based for these rare tumours; prevention lies in timely recognition and in avoidance of late presentation.
• Antenatal findings: sacrococcygeal and cystic teratomas may be detected on prenatal ultrasound, which allows delivery planning and neonatal surgical care.

• Red-reflex examination with a direct ophthalmoscope is the single cheapest life-saving test in the first year of life; train community health workers to perform it and to refer an absent reflex. ^[2]
• Where MRI is unavailable, ultrasound plus careful clinical judgement can guide triage for abdominal masses; AFP is a cheap and informative test where the laboratory exists.
• Cisplatin monotherapy remains an acceptable backbone for standard-risk hepatoblastoma when resources are limited. ^[4]
• Radiotherapy and transplantation may not be locally available; early referral to a centre that can deliver them is safer than delayed treatment.
• Ototoxicity monitoring can be done with simple audiometry even where advanced equipment is absent. ^[8]
• Shared care with a regional centre and commitment to completing chemotherapy on schedule improve outcomes more than choice of the newest agent.

• Infants: congenital hepatoblastoma, infantile choriocarcinoma and neonatal sacrococcygeal teratomas; aggressive disease but often curable with prompt treatment.
• Adolescents: adult-type germ cell tumour patterns, fertility preservation and transition to adult oncology services.
• Families: heritable RB1 disease is autosomal dominant; carrier testing and early eye examinations for children of carriers belong to genetics services. ^[2]
• Immunocompromised children: LCH can mimic infection; biopsy is essential.

• Paediatric solid tumours are rare but highly curable; delay in recognising a mass, not lack of drugs, is the main threat to survival.
• Leukocoria is the hallmark of retinoblastoma and an absent fundal red reflex is a NICE NG12 referral trigger.
• Retinoblastoma is a RB1 tumour-suppressor disease: heritable in 30 to 40% of cases, often bilateral, and associated with second cancers later in life.
• Rhabdomyosarcoma is the commonest childhood soft-tissue sarcoma and is the 3-4% group of paediatric malignancies; treatment combines surgery, VAC chemotherapy and radiotherapy.
• Hepatoblastoma is the commonest childhood liver cancer, is AFP-driven and is treated with cisplatin-based neoadjuvant chemotherapy then surgery or transplantation.
• Germ cell tumours present wherever primordial germ cells migrate; yolk sac tumours make AFP, choriocarcinomas make beta-hCG, and teratomas are cured by surgery alone.
• LCH is a clonal Langerhans-cell disorder ranging from self-limiting bone disease to life-threatening risk-organ involvement.
• SIOP and COG protocols are the reference standards; deviations should be discussed with a paediatric oncology centre.
• Childhood treatment cures but also harms: cisplatin causes hearing loss in more than 60% of children, and radiotherapy harms growing bone and soft tissue.
• Every child with a suspected solid tumour needs urgent, specialist, multidisciplinary assessment rather than observation.

Retinoblastoma management in detail; neuroblastoma; Wilms' tumour (nephroblastoma); childhood leukaemia and lymphoma (separate, non-solid); paediatric liver masses; bone and soft tissue sarcomas; survivorship and late effects of childhood cancer; childhood screening and red reflex.