Recent years have seen major advances in the management of solid malignant tumours in the paediatric population. While fewer than 20 per cent of such patients survived in the 1950s, co-ordinated use of modern surgery, radiotherapy, and combination chemotherapy has produced survival rates of over 60 per cent. The response of different solid tumours in childhood varies. While there has been substantial improvement of patients with Wilms' tumours and lymphomas, such improvement has been moderate in soft tissue sarcomas and insignificant in neuroblastoma.

Much of the progress has been brought about by the co-operative efforts of large national and international study groups such as The National Wilms' Tumour Study, the Children's Cancer Study Group, The Intergroup Rhabdomyosarcoma Study, and The International Society of Pediatric Oncology. The pooling of resources has allowed proper assessment of new treatment protocols and identification of risk factors. Treatment strategies continue to evolve.

Newer potent drugs are being tried in attempts to improve survival of patients with tumours resistant to present treatment regimens. For patients with tumours which respond to established treatment procedures, attempts are made to reduce the intensity of treatment with the aim of minimizing long-term morbidity from chemotherapy without jeopardizing survival. The common solid malignant tumours in children are neuroblastoma, Wilms' tumour, lymphomas, brain tumours, and embryonic sarcomas, Wilms' tumour and neuroblastoma being the two most common abdominal cancers.

Wilms' tumour, or nephroblastoma, is a renal embryonoma that is grossly often large and heterogenous. It is usually confined within a capsule or pseudocapsule but can invade neighbouring tissues, particularly the renal vein. The mode of metastasis is mainly haematogenous.

Microscopically, it contains premature renal parenchymal cells (blastemal cells), stromal cells, and epithelial cells. Primitive to well-differentiated glomerular and tubular structures may be present. The presence of anaplasia or sarcomatous changes constitutes unfavourable histology associated with a poor prognosis. There are two types of sarcomatous change, the clear cell type, which frequently metastasizes to the bone and the rhabdoid type, which spreads to the brain.

The incidence of Wilms' tumour is 7.8 per million population. Eighty per cent of patients present before the age of 5 years; the peak incidence is at 3 years of age. Both sexes are equally affected, but the left side is more commonly involved (left:right—1.3:1). Bilateral disease, simultaneously or successively, occurs in 5.7 per cent of patients.

Conditions commonly associated with Wilms' tumour include congenital aniridia, hemihypertrophy, and genitourinary anomalies (hypospadias, undescended testes, gonadal dysgenesis, duplex renal system). Association with mental retardation, chromosomal abnormalities, and Beckwith-Wiedemann syndrome (exomphalos-macroglossia-gigantism) has also been described.

The most common presentation is an asymptomatic abdominal mass discovered by the parent or physician. Occasionally the child presents with haematuria, but symptoms are often non-specific: abdominal fullness, abdominal pain, gastrointestinal upset, fever, weight loss, malaise, and anaemia. Hypertension is sometimes detectable. Rarely, a left varicocele arises as a result of tumour occlusion of the left renal vein.

Ultrasonography is recommended as the first investigation. This can distinguish a tumour from a multicystic kidney or hydronephrosis and may also detect a tumour in the contralateral kidney, tumour thrombi in the inferior vena cava, and abdominal metastases.

Plain abdominal radiography reveals a soft tissue shadow, usually without calcification. Intravenous urography is usually diagnostic, showing distortion of the caliceal system (Fig. 3) 2204. An inferior vena cavagram to demonstrate tumour thrombi can be performed at the same time if sufficient contrast is injected into a vein of the lower limb. These investigations can be replaced by computed tomography (CT) (Fig. 4) 2205 with contrast.

A chest radiograph should always be performed to detect pulmonary metastasis. The search for metastases in other sites is undertaken when indicated.

Treatment is multimodal and is dependent on staging and histology. Anaplasia or sarcomatous changes (rhabdoid or clear cell) in the histological examinations are unfavourable signs.

A large supraumbilical transverse abdominal incision is made, extended into the thorax if necessary. The renal artery and the renal vein are ligated. If tumour thrombus in the renal vein extends into the inferior vena cava, control of the vena cava above the thrombus should be obtained. The vena cava is opened and the thrombus is removed by suction; the vena cava is then repaired. The kidney bearing the tumour is excised with the adjacent lymph nodes and peritoneal tissues. The para-aortic lymph nodes are examined and all affected nodes are removed. If there is no gross involvement, at least one para-aortic node should be sampled. The rest of the abdominal organs, particularly the contralateral kidney and the liver, should be examined.

Postoperative radiotherapy is an effective adjuvant treatment of Wilms' tumour but long-term follow-up has revealed delayed side-effects, especially on the growth of bones and soft tissues. The effectiveness of combination chemotherapy has obviated the use of radiotherapy for tumours of favourable histology and early stage.

Postoperative chemotherapy is now an essential part of the treatment of Wilms' tumour. Preoperative chemotherapy after diagnosis by percutaneous biopsy has also been tried in some centres in an attempt to facilitate surgery. The main chemotherapeutic agents are vincristine and actinomycin D. In high-risk patients, Adriamycin is added.

Treatment is adapted to each case individually, and usually consists of chemotherapy and combinations of partial, unilateral, or bilateral nephrectomy. Radiography may also be used, but care must be taken to avoid irradiation of the remaining kidney tissue. If bilateral nephrectomy is performed the child is placed on haemodialysis, with the expectation of a renal transplant after 2 years if there is no evidence of recurrence.

Indicators of a poor prognosis include unfavourable histology, advanced stage, and age over 2 years. Overall survival rates now approach 90 per cent. With favourable histology, 4-year survival rates are Stage I, 97 per cent; Stage II, 95 per cent; Stage III, 91 per cent; Stage IV, 87 per cent. With unfavourable histology, 4-year survival rates are: I–III 68 per cent, IV 58 per cent. Patients with bilateral tumours have a survival rate similar to that of Stage II disease.

This renal tumour was previously considered as a type of Wilms' tumour, but is now regarded as a separate condition. Unlike Wilms' tumour it presents in the neonatal period, its prognosis is excellent (survival approach 100 per cent), and its treatment consists of complete excision only. Chemotherapy and radiotherapy are not required.

Neuroblastoma is a tumour of neural crest origin which may occur in the adrenal medulla or anywhere along the sympathetic ganglion chain, namely in the neck, thorax, abdomen, and pelvis. Seventy-five per cent of tumours occur in the abdomen (adrenal medulla 50 per cent, paraspinal ganglia 25 per cent), 20 per cent occur in the thorax, and 5 per cent occur in the neck and the pelvis.

Macroscopically, the tumour appears as a very vascular, nodular, friable, solid mass which grows rapidly and invades the adjacent tissues. Areas of haemorrhage, necrosis, and cystic degeneration are not uncommon (Fig. 5) 2206.

Microscopically, a neuroblastoma is composed of small, round cells with little cytoplasm. The cells are arranged in rosettes which have fine nerve fibres in the centres ( Figs 6 2207,2208 and 7). Electron microscopy reveals the presence of neurofibrils and neurosecretory granules. The degree of differentiation varies widely among different neural crest tumours: the most mature form is the benign ganglioneuroma. Spontaneous maturation of neuroblastoma to ganglioneuroma is a rare but well-described phenomenon.

The incidence of neuroblastoma is 9.6 per million population. Of all patients, 50 per cent are younger than 2 years and 90 per cent are younger than 8 years; the peak incidence occurs at 18 months of age. Boys are affected slightly more often than girls. Familial occurrence has been reported.

Neuroblastoma has been reported in patients with Beckworth– Wiedemann syndrome (exomphalos-macroglossia-gigantism syndrome), Hirschsprung's disease (congenital intestinal aganglionosis), Klippel-Feil syndrome (short, immobile neck due to cervical vertebral fusion), and other neuropathies.

Abdominal neuroblastoma commonly presents as an abdominal mass. There may be weight loss, failure to thrive, fever, anaemia, abdominal fullness, abdominal pain, anorexia, nausea, and vomiting. Rarely, the child presents with intractable diarrhoea due to production of vasoactive intestinal polypeptide by the tumour. Occasionally, hypertension and flushing may be caused by excessive catecholamine production. Thoracic neuroblastoma may give rise to respiratory symptoms. Cervical neuroblastoma presents as a neck mass and sometimes as Horners' syndrome. Pelvic neuroblastoma can cause disturbances of urinary function and defecation. Dumb-bell neuroblastomas are paraspinal tumours that extend into the spinal canal causing neurological symptoms. Rarely, the child may develop a form of encephalopathy characterized by opsomyoclonus (the ‘dancing eye’) and cerebellar ataxia.

Neuroblastoma sometimes presents with symptoms such as bone pain, subcutaneous nodules, and jaundice caused by metastatic lesions.

Ultrasonography distinguishes neuroblastoma (solid, extrarenal) from cystic lesions and renal tumours. The radiographic detection of calcification in the tumour is suggestive of neuroblastoma. In children with an abdominal neuroblastoma, intravenous urography shows displacement rather than distortion of the pelvicaliceal system. A skeletal survey and chest radiograph are mandatory to detect possible metastases. CT gives good anatomical data about the tumour. Recent studies suggest that magnetic resonance imaging (MRI) is useful both to delineate the primary tumour and to evaluate bone marrow metastasis, vessel involvement, and extension into spinal cord.

A new and useful imaging technique is the [¹³¹I] m-iodobenzylguanidine (MIBG) scan; MIBG has a molecular structure similar to that of adrenaline and is specifically taken up by neuroectodermal tumours. It is therefore useful in the location ofthe primary tumour as well as in the detection of residual, recurrent, or metastatic disease. Monoclonal antibodies to neuroblastomas are now available and can also be radiolabelled for similar purposes. Bone marrow aspiration is always required to detect skeletal metastasis. More than 90 per cent of neuroblastomas produce high levels of catecholamines or their byproducts, such as vanilmandelic acid and homovanillic acid. Although a vanilmandelic acid spot test may be used as a screening technique, most centres prefer to quantify catecholamines and their metabolites by analysis of a 24-h urine collection. This investigation also has some prognostic value: the higher the ratio of vanilmandelic acid to homovanillic acid, the better the prognosis.

Raised serum levels of neurone-specific enolase have been found at diagnosis in all stages of neuroblastoma. The values are directly proportional to the staging of the disease: stage IV neuroblastomas are associated with the highest serum levels of neurone-specific enolase.

Treatment is dependent on the stage of the tumour. The staging system described by Evans et al. (Children's Cancer Study Group) is widely used. The present recommended treatment regimen is shown in. The standard chemotherapeutic agents used in the treatment of neuroblastoma are cyclophosphamide and vincristine. Various drugs, including Adriamycin, ditriazoimidazole carboximide, cisplatin, VM–26, and melphalan have been included in more recent treatment regimens.

In contrast to the excellent response of Wilms' tumour to adjuvant therapy, results of chemotherapy and radiotherapy for neuroblastoma have remained disappointing. The prognosis of patients with Stage III and Stage IV neuroblastoma has not altered in the past two decades. Of the new approaches which are being tried high-dose chemotherapy, total body irradiation, and allogeneic or autologous bone marrow transplantation appear particularly promising for neuroblastoma patients with a poor prognosis. Before reinfusion, autologous bone marrow may be ‘cleaned’ of tumour cells by treatment with cytotoxic agents coupled to monoclonal antibodies directed against neuroblastoma cells. Tumour cells may also be physically extracted from the marrow by magnetic separation after the application of magnetic beads coupled to monoclonal antibodies or by the counterflow centrifugal elutriation technique. Another approach (‘intracellular’ radiotherapy) relies on the affinity of radioactive [¹³¹I] MIGB to tumour tissues.

The overall 3-year survival rate for all stages of neuroblastoma is 30 to 50 per cent. The most important prognostic factors are the age and the stage of disease: patients younger than 2 years have a 2-year survival rate of 77 per cent whereas only 38 per cent of older children survive this long. Survival is inversely proportional to the stage of disease, except for Stage IV cases: Stage I (100 per cent), Stage II (82 per cent), Stage III (42 per cent), Stage IV (30 per cent), and Stage IV (100 per cent). Other poor prognostic factors include unfavourable histology, primary abdominal lesion, high serum neurone-specific enolase level, high serum ferritin level and low ratio of urinary vanilomandelic acid to homovanillic acid, multiple copies of the N- myc oncogene (genomic amplification), and specific chromosomal abnormalities (marker chromosome 1, double minutes or homogenously staining regions).

Mass screening for neuroblastoma at 6 months of age by analysis of urinary catecholamines was introduced in Japan and has increased the detection rate of early tumours with favourable histological features. However mass screening has not affected mortality rate. Trials are being conducted in North America and the United Kingdom. At present, mass screening for neuroblastoma cannot be recommended.

Rhabdomyosarcoma can occur in any part of the body except the brain and bone. In children, rhabdomyosarcoma usually occurs in embryonic tissue that is capable of muscular differentiation. Cross striations and positive staining with the periodic acid–Schiff technique are characteristic histological features. Electron microscopy reveals intracytoplasmic filaments and Z-band materials. Antibodies against myosin and myoglobin are now available for diagnostic immunohistochemistry.

The Intergroup Rhabdomyosarcoma Study divides tumours into embryonal (57 per cent), alveolar (19 per cent), botryoid (6 per cent), undifferentiated (17 per cent), and pleomorphic (1 per cent) types. Embryonal tumours have a favourable prognosis; alveolar tumours have an unfavourable prognosis. The botryoid variant is an embryonal tumour that extends into a hollow viscus or space, such as the bladder, nasopharynx, vagina, or biliary tract. When there are ‘mixed’ components in the tumour, such as embryonal and alveolar, the predominant tissue type is used to determine the category. The tissue type directs therapy and influences the prognosis.

Rhabdomyosarcoma is the most common soft tissue tumour in childhood. It accounts for 8 per cent of all cancers in children under 15 years of age, representing the fifth most common paediatric malignancy (after leukaemia, central nervous system tumours, Wilms' tumour, and neuroblastoma). There are two ages at which incidence peaks: 1 to 7 years and adolescence. Distal genitourinary tract and head and neck tumours occur mostly in the younger age group. Trunk and paratesticular tumours occur mostly in adolescence. Young patients are more frequently affected by embryonal tumours.

Families containing members affected by carcinoma of the breast have an increased risk of rhabdomyosarcomas. Association with other soft tissue sarcomas and with central nervous system neoplasms has also been reported.

Symptoms and signs relate to the primary site of the tumour. Distal genitourinary tract tumours may present with an abdominal mass, urinary symptoms due to obstruction and bleeding, or vaginal discharge. Head and neck rhabdomyosarcomas may be parameningeal or non-parameningeal. Patients with parameningeal tumours of the nasopharynx and paranasal sinus, apart from having local symptoms, are at risk of developing intracranial problems. The extremities and trunk, paratesticular tissues, perineum, retroperitoneum, abdominal viscera (liver, biliary tract, pelvis), and thorax are all known primary sites of rhabdomyosarcomas.

Biopsy (open, percutaneous, or endoscopic) is required for diagnosis and histological typing, which directs therapy. The extent of the tumour is defined by imaging techniques such as ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI).

Treatment is determined on an individual basis, according to the site, stage, and histological type of the tumour. The Intergroup Rhabdomyosarcoma Study staging system is shown in Table 5 575.

Treatment of rhabdomyosarcoma should be multimodal, consisting of chemotherapy, surgery, and radiotherapy. The sequence and extent of the procedures are less well agreed. After the diagnosis of rhabdomyosarcoma is confirmed by biopsy, the primary tumour, together with any affected adjacent lymph nodes, are excised. Re-excision is undertaken if the initial resection has been inadequate (gross or microscopic). In determining the extent of surgical excision, the resultant functional and cosmetic impairment should be taken into account. Preoperative chemotherapy may reduce the extent of surgery required and should be considered. Postoperative chemotherapy is helpful in eradicating residual disease and micrometastases. Chemotherapy is the primary treatment for patients with metastatic disease at presentation. The commonly used drugs are a combination of cyclophosphamide, vincristine, actinomycin D, and Adriamycin. Doxorubicin, DTIC (ditriazoimidazole carboximide), cisplatin, and ifosfamide have also been known to be effective agents.

Local radiotherapy is given to patients with residual disease and lymph node involvement.

The overall 2-year survival rate has increased from 20 per cent to 65 per cent in the past two decades. Five-year survival rates are: Group I, 90 per cent; Group II, 90 per cent; Group III, 64 per cent, Group IV, 30 per cent.

Unfavourable histology, including alveolar monomorphous round cell or anaplastic tumours, is associated with a bad prognosis. Rhabdomyosarcomas of the distal genitourinary tract and the orbit have the best prognosis, while tumours of the extremities and trunk and the mucosal sites (perineum, retroperitoneum, abdominal viscera) have the worst prognosis.

These tumours are rare. Retroperitoneal lymph nodes are affected in 20 to 40 per cent of patients, but more proximal dissemination is uncommon. The standard treatment is radical orchidectomy via a groin incision and ipsilateral retroperitoneal node dissection. Radiotherapy to abdominal nodes is given. If the tumour has been biopsied or locally excised through a transcrotal approach initially, an en-bloc hemiscrotectomy, radical orchidectomy, and node dissection is performed. If the scrotum is involved or if the margins are positive, the contralateral testis is transferred to the thigh and total scrotal irradiation is given. This management policy results in an overall survival rate of 85 per cent.

These include fibrosarcoma, extraosseous Ewing's sarcoma, synovial sarcoma, small cell soft tissue sarcomas, neurofibrosarcoma, liposarcoma, and ileomyosarcoma. The principle of management of these tumours is similar to that of rhabdomyosarcoma.

Germ cell tumours may occur in any part of the reproductive system or in ectopic sites as a result of aberrant migration of primitive germ cells.

The incidence of benign teratoma peaks at birth; yolk sac tumour is most common between the ages of 1 and 5 years, while dysgerminoma and malignant teratoma commonly present in adolescence.

Patients often present with a mass or pain. Hormone-secreting tumours such as dysgerminomas cause precocious development of secondary sexual characteristics or masculinization. Preoperative evaluation should include measurements of &agr;-fetoprotein (yolk sac origin) and &bgr; human chorionic gonadotrophin (trophoblastic origin). Imaging studies are often helpful.

Surgical excision is undertaken for resectable tumours. Ovarian tumours are treated by unilateral salpingo-oophorectomy. Testicular tumours require radical orchidectomy (after high ligation of the spermatic cord via groin incision) and retroperitoneal lymph node dissection. Chemotherapy is effective for germ cell tumours. The most commonly used drug combination is vincristine, actinomycin, and cyclophosphamide. Adriamycin, bleomycin, cisplatin, and VP–16 have also been known to be useful. Trophoblastic tumours respond to methotrexate. The success obtained from the combination of surgery and chemotherapy has obviated the need for radiotherapy in the management of most of these tumours.

Sacrococcygeal teratoma (Fig. 11) 2213 can occur at any age but is most commonly noted in the neonatal period: in fact it represents the most common neoplasm of the newborn, with an incidence of 1:40000. It is more common in females (75 per cent) than in males. The tumours are usually classified according to their location. The external component is predominant in over 80 per cent of cases.

Most (82 per cent) sacrococcygeal teratomas are benign, but there is a malignant potential regardless of location or size if the tumour is not completely excised. The incidence of malignancy increases with the age of presentation, being 7 per cent at birth, 37 per cent at 1 year, and 50 per cent at 2 years.

Excision of the tumour with the coccyx is performed as soon as possible after diagnosis: the risk of malignant transformation is increased with delay in surgery and retention of the coccyx. Long-term follow-up is advisable. Rectal examination is important for detection of presacral recurrence. A high serum &agr;-fetoprotein level is a good indicator of malignancy. Serial postoperative measurements of serum &agr;-fetoprotein are used to detect malignant recurrence.

Malignant sacrococcygeal teratoma requires aggressive multimodal initial therapy, including surgery, irradiation, and chemotherapy. The multiple drug protocol should consist of vincristine, actinomycin D, and cyclophosphamide. Adriamycin, bleomycin, and carmustine may be added if a response is not obtained.

The prognosis of benign sacrococcygeal teratoma after complete excision is excellent. Faecal or urinary incontinence may occasionally follow surgical excision. Prognosis of malignant sacrococcygeal teratoma is poor, with an overall mortality rate of 80 per cent.

Lymphoma is the third most common cancer in children, following leukaemia and brain tumours. Hodgkin's disease and non-Hodgkin's lymphoma represent 5 per cent and 10 per cent of all childhood malignancies, respectively. Lymphomas in children have a male preponderance.

Hodgkin's disease in children has a peak incidence at 11 to 15 years of age. The predominant histologic type is nodular sclerosis. The majority of patients do not have systemic symptoms: most present with enlarged lymph nodes. The sites of involvement are, in order of frequency, cervical, supraclavicular, mediastinal abdominal, axillary, and inguinal nodes. Non-Hodgkin's lymphoma in children is most often diffuse and disseminated. The most common primary sites are the abdomen, mediastinum, peripheral nodes, and head and neck, in that order.

Staging laparotomy for Hodgkin's disease is performed routinely for children over 5 years of age in some centres and selectively or not at all in others. The rationale of staging laparotomy is to direct therapy, and particularly to avoid unnecessary irradiation and intensive chemotherapy. A change in staging as a result of laparotomy will be seen in around 35 per cent of patients. Staging laparotomy should include liver biopsy, splenectomy, sampling of iliac, mesenteric, para-aortic, periportal, splenic hilar, and coeliac nodes, marrow biopsy, and ovary transposition in girls if lower abdominal/pelvic irradiation is anticipated.

With the development of highly effective chemotherapy and radiotherapy regimens, there is a limited role for surgery in the management of lymphomas. Biopsy examination is necessary for diagnosis and histological typing. Splenectomy in children carries the risk of overwhelming sepsis, most often due to encapsulated cocci (Streptococcus pneumoniae, Haemophilus influenzae). Patients with Hodgkin's disease have a higher risk of such sepsis than children in whom splenectomy is performed for other reasons. Long-term prophylactic antibiotics and pneumococcal vaccination should be given to these patients.

Non-Hodgkin's lymphoma sometimes presents with acute or subacute abdominal disease such as true or simulated appendicitis, intestinal obstruction, or perforations. Intussusception occurring in children above the age of 2 years should raise the suspicion of a primary pathology, such as Meckel's diverticulum or lymphoma. If the diagnosis of lymphoma is made at operation, the segment of bowel bearing the tumour, together with the adjacent mesentery, is resected and intra-abdominal lymph nodes are sampled.

The prognosis of lymphomas in children following treatment with intensive chemotherapy with or without radiotherapy, is excellent. The overall 10-year survival rates for children with Hodgkin's disease and non-Hodgkin's lymphomas are 90 per cent and 70 to 85 per cent respectively.

Malignant liver tumours are comparatively rare, constituting 2 per cent of malignant tumours in childhood. There are two distinct histological types: hepatoblastoma and hepatocellular carcinoma.

Hepatoblastoma is most common in infancy and early childhood. Varying degrees of differentiation are possible: the well differentiated tumour consists mainly of fetal-type cells and is associated with a good prognosis. The incidence of hepatocellular carcinoma peaks at 4 years and at 12 to 15 years. The histology is similar to that of hepatocellular carcinoma in adults. Liver cirrhosis due to underlying liver disease such as galactosaemia or glycogen storage disease is present in 25 to 50 per cent of paediatric hepatocellular carcinomas.

The presentation is usually an abdominal mass or hepatomegaly. Constitutional symptoms may be present. Diagnosis is suggested by imaging studies, including ultrasonography and CT. An elevated serum &agr;-fetoprotein level is a characteristic finding, and some hepatoblastomas also produce human chorionic gonadotrophin.

Hepatic resection is the main form of treatment. Children have an excellent capacity for hepatic regeneration and can tolerate resection of up to 80 per cent of the liver. Adjuvant chemotherapy is useful. The main chemotherapeutic agent is Adriamycin. Vincristine, cyclophosphamide, and 5-fluorouracil are also included in some regimens. Radiotherapy may also be used selectively. Patients who have tumours completely resected have a survival rate of 80 per cent at 2 years.

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