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Nephroblastoma(WT1)

MedGen UID:
10221
Concept ID:
C0027708
Neoplastic Process
Synonyms: Wilms tumor; Wilms' tumor
Modes of inheritance:
Heterogeneous
MedGen UID:
67020
Concept ID:
C0242960
Organism Attribute
Source: HPO
The production of the same or similar phenotypes (observed biochemical, physiological, and morphological characteristics of a person determined by his/her genotype) by different genetic mechanisms. There are two types: (1) allelic heterogeneity - when different alleles at a locus can produce variable expression of a condition; and (2) locus heterogeneity - the term used to describe disease in which mutations at different loci can produce the same disease phenotype.
Autosomal dominant inheritance
MedGen UID:
141047
Concept ID:
C0443147
Intellectual Product
Sources: OMIM, Orphanet
Autosomal dominant inheritance refers to genetic conditions that occur when a mutation is present in one copy of a given gene (i.e., the person is heterozygous).
Somatic mutation
MedGen UID:
107465
Concept ID:
C0544886
Cell or Molecular Dysfunction
Sources: HPO, OMIM
An alteration in DNA that occurs after conception. Somatic mutations can occur in any of the cells of the body except the germ cells (sperm and egg) and therefore are not passed on to children. These alterations can (but do not always) cause cancer or other diseases.
Autosomal dominant inheritance
MedGen UID:
892334
Concept ID:
CN000007
Functional Concept
Source: HPO
A mode of inheritance that is observed for traits related to a gene encoded on one of the autosomes (i.e., the human chromosomes 1-22) in which a trait manifests in heterozygotes. In the context of medical genetics, an autosomal dominant disorder is caused when a single copy of the mutant allele is present. Males and females are affected equally, and can both transmit the disorder with a risk of 50% for each child of inheriting the mutant allele.
not inherited
MedGen UID:
832438
Concept ID:
CN227390
Intellectual Product
Source: Orphanet
Describes a disorder that is not inherited.
Somatic mutation (HPO, OMIM)
not inherited (Orphanet)
SNOMED CT: [M]Nephroblastoma NOS (31470003); Perlman syndrome (302849000); Wilm's tumor (302849000); Wilms tumor (302849000); Nephroblastoma (25081006); Wilms' tumor (25081006); Embryonal nephroma (25081006); Embryonal adenosarcoma (25081006); Renal adenosarcoma (25081006); Nephroma (25081006); Nephroblastoma (302849000); Nephroma (302849000)
 
OMIM®: 194070; 600185; 607102
HPO: HP:0002667
Orphanet: ORPHA654

Definition

Wilms tumor is a rare type of kidney cancer. It causes a tumor on one or both kidneys. It usually affects children, but can happen in adults. Having certain genetic conditions or birth defects can increase the risk of getting it. Children that are at risk should be screened for Wilms tumor every three months until they turn eight. Symptoms include a lump in the abdomen, blood in the urine, and a fever for no reason. Tests that examine the kidney and blood are used to find the tumor. Doctors usually diagnose and remove the tumor in surgery. Other treatments include chemotherapy and radiation and biologic therapies. Biologic therapy boosts your body's own ability to fight cancer. NIH: National Cancer Institute.  [from MedlinePlus]

Clinical features

Nephroblastoma
MedGen UID:
10221
Concept ID:
C0027708
Neoplastic Process
Wilms tumor is a rare type of kidney cancer. It causes a tumor on one or both kidneys. It usually affects children, but can happen in adults. Having certain genetic conditions or birth defects can increase the risk of getting it. Children that are at risk should be screened for Wilms tumor every three months until they turn eight. Symptoms include a lump in the abdomen, blood in the urine, and a fever for no reason. Tests that examine the kidney and blood are used to find the tumor. Doctors usually diagnose and remove the tumor in surgery. Other treatments include chemotherapy and radiation and biologic therapies. Biologic therapy boosts your body's own ability to fight cancer. NIH: National Cancer Institute.
Nephroblastoma
MedGen UID:
10221
Concept ID:
C0027708
Neoplastic Process
Wilms tumor is a rare type of kidney cancer. It causes a tumor on one or both kidneys. It usually affects children, but can happen in adults. Having certain genetic conditions or birth defects can increase the risk of getting it. Children that are at risk should be screened for Wilms tumor every three months until they turn eight. Symptoms include a lump in the abdomen, blood in the urine, and a fever for no reason. Tests that examine the kidney and blood are used to find the tumor. Doctors usually diagnose and remove the tumor in surgery. Other treatments include chemotherapy and radiation and biologic therapies. Biologic therapy boosts your body's own ability to fight cancer. NIH: National Cancer Institute.

Conditions with this feature

Beckwith-Wiedemann syndrome
MedGen UID:
2562
Concept ID:
C0004903
Congenital Abnormality
Beckwith-Wiedemann syndrome (BWS) is a growth disorder variably characterized by neonatal hypoglycemia, macrosomia, macroglossia, hemihyperplasia, omphalocele, embryonal tumors (e.g., Wilms tumor, hepatoblastoma, neuroblastoma, and rhabdomyosarcoma), visceromegaly, adrenocortical cytomegaly, renal abnormalities (e.g., medullary dysplasia, nephrocalcinosis, medullary sponge kidney, and nephromegaly), and ear creases/pits. BWS is considered a clinical spectrum, in which affected individuals may have many of these features or may have only one or two clinical features. Early death may occur from complications of prematurity, hypoglycemia, cardiomyopathy, macroglossia, or tumors. However, the previously reported mortality of 20% is likely an overestimate given better recognition of the disorder along with enhanced treatment options. Macroglossia and macrosomia are generally present at birth but may have postnatal onset. Growth rate slows around age seven to eight years. Hemihyperplasia may affect segmental regions of the body or selected organs and tissues.
Nephroblastoma
MedGen UID:
10221
Concept ID:
C0027708
Neoplastic Process
Wilms tumor is a rare type of kidney cancer. It causes a tumor on one or both kidneys. It usually affects children, but can happen in adults. Having certain genetic conditions or birth defects can increase the risk of getting it. Children that are at risk should be screened for Wilms tumor every three months until they turn eight. Symptoms include a lump in the abdomen, blood in the urine, and a fever for no reason. Tests that examine the kidney and blood are used to find the tumor. Doctors usually diagnose and remove the tumor in surgery. Other treatments include chemotherapy and radiation and biologic therapies. Biologic therapy boosts your body's own ability to fight cancer. NIH: National Cancer Institute.
Russell-Silver syndrome
MedGen UID:
104492
Concept ID:
C0175693
Disease or Syndrome
Russell-Silver syndrome (RSS) is characterized by intrauterine growth retardation accompanied by postnatal growth deficiency. The birth weight of affected infants is typically two or more SD below the mean, and postnatal growth two or more SD below the mean for length or height. Affected individuals typically have proportionately short stature, normal head circumference, fifth-finger clinodactyly, typical facial features with triangular facies characterized by broad forehead and narrow chin, and limb-length asymmetry that may result from hemihypotrophy with diminished growth of the affected side. Growth velocity is normal in children with RSS. The average adult height of males is 151.2 cm and that of females is 139.9 cm. Evidence exists that children with RSS are at significant risk for developmental delay (both motor and cognitive) and learning disabilities.
Sotos syndrome
MedGen UID:
61232
Concept ID:
C0175695
Disease or Syndrome
Sotos syndrome is a disorder characterized by a distinctive facial appearance, overgrowth in childhood, and learning disabilities or delayed development of mental and movement abilities. Characteristic facial features include a long, narrow face; a high forehead; flushed (reddened) cheeks; and a small, pointed chin. In addition, the outside corners of the eyes may point downward (down-slanting palpebral fissures). This facial appearance is most notable in early childhood. Affected infants and children tend to grow quickly; they are significantly taller than their siblings and peers and have an unusually large head. However, adult height is usually in the normal range.People with Sotos syndrome often have intellectual disability, and most also have behavioral problems. Frequent behavioral issues include attention deficit hyperactivity disorder (ADHD), phobias, obsessions and compulsions, tantrums, and impulsive behaviors. Problems with speech and language are also common. Affected individuals often have a stutter, a monotone voice, and problems with sound production. Additionally, weak muscle tone (hypotonia) may delay other aspects of early development, particularly motor skills such as sitting and crawling.Other signs and symptoms of Sotos syndrome can include an abnormal side-to-side curvature of the spine (scoliosis), seizures, heart or kidney defects, hearing loss, and problems with vision. Some infants with this disorder experience yellowing of the skin and whites of the eyes (jaundice) and poor feeding.A small percentage of people with Sotos syndrome have developed cancer, most often in childhood, but no single form of cancer occurs most frequently with this condition. It remains uncertain whether Sotos syndrome increases the risk of specific types of cancer. If people with this disorder have an increased cancer risk, it is only slightly greater than that of the general population.
Wilms tumor, aniridia, genitourinary anomalies, and mental retardation syndrome
MedGen UID:
64512
Concept ID:
C0206115
Disease or Syndrome
Aniridia is characterized by complete or partial iris hypoplasia usually (but not always) with associated foveal hypoplasia resulting in reduced visual acuity and nystagmus presenting in early infancy. Frequently associated ocular abnormalities (often of later onset) include cataract, glaucoma, and corneal opacification and vascularization. Aniridia may occur either as an isolated ocular abnormality without systemic involvement, caused by mutation of PAX6 or deletion of a regulatory region controlling its expression, or as part of the Wilms tumor-aniridia-genital anomalies-retardation (WAGR) syndrome, with a deletion of 11p13 involving the PAX6 (aniridia) locus and the adjacent WT1 (Wilms tumor) locus. Individuals with deletion of PAX6 and WT1 are at up to a 50% risk of developing Wilms tumor.
Diffuse mesangial sclerosis
MedGen UID:
78698
Concept ID:
C0268747
Disease or Syndrome
Nephrotic syndrome, a malfunction of the glomerular filter, leads to proteinuria, edema, and, in steroid-resistant nephrotic syndrome, end-stage renal disease (ESRD). Renal histopathology in NPHS4 due to WT1 mutations most often shows diffuse mesangial sclerosis (DMS), but can also show focal segmental glomerulosclerosis (FSGS). Both of these terms refer to pathologic findings and may be associated with the same clinical phenotype, namely nephrotic syndrome (review by Schumacher et al., 1998). For a general phenotypic description and a discussion of genetic heterogeneity of nephrotic syndrome, see NPHS1 (256300).
Mulibrey nanism syndrome
MedGen UID:
99347
Concept ID:
C0524582
Disease or Syndrome
Mulibrey nanism is a rare autosomal recessive growth disorder with prenatal onset, including occasional progressive cardiomyopathy, characteristic facial features, failure of sexual maturation, insulin resistance with type 2 diabetes, and an increased risk for Wilms tumor (summary by Hamalainen et al., 2006).
Wilms tumor 2
MedGen UID:
151968
Concept ID:
C0694899
Gene or Genome
This gene is putatively involved in the negative regulation of cell growth.
Renal hamartomas nephroblastomatosis and fetal gigantism
MedGen UID:
162909
Concept ID:
C0796113
Disease or Syndrome
Perlman syndrome is an autosomal recessive congenital overgrowth syndrome with similarities to Beckwith-Wiedemann syndrome (BWS; 130650). Affected children are large at birth, are hypotonic, and show organomegaly, characteristic facial dysmorphisms (inverted V-shaped upper lip, prominent forehead, deep-set eyes, broad and flat nasal bridge, and low-set ears), renal anomalies (nephromegaly and hydronephrosis), frequent neurodevelopmental delay, and high neonatal mortality. Perlman syndrome is associated with a high risk of Wilms tumor, with a 64% incidence in infants surviving beyond the neonatal period. The tumor is diagnosed at an earlier age in these individuals compared with sporadic cases (less than 2 years and 3-4 years of age, respectively), and there is a high frequency of bilateral tumors (55%). Histologic examination of the kidneys in children with Perlman syndrome shows frequent nephroblastomatosis, which is a precursor lesion for Wilms tumor (summary by Astuti et al., 2012).
Simpson-Golabi-Behmel syndrome
MedGen UID:
162917
Concept ID:
C0796154
Disease or Syndrome
Simpson-Golabi-Behmel syndrome type 1 (SGBS1) is characterized by pre- and postnatal macrosomia; distinctive craniofacies (including macrocephaly, coarse facial features, macrostomia, macroglossia, palatal abnormalities); and commonly, mild to severe intellectual disability with or without structural brain anomalies. Other variable findings include supernumerary nipples, diastasis recti/umbilical hernia, congenital heart defects, diaphragmatic hernia, genitourinary defects, and GI anomalies. Skeletal anomalies can include vertebral fusion, scoliosis, rib anomalies, and congenital hip dislocation. Hand anomalies can include large hands and postaxial polydactyly. Affected individuals are at increased risk for embryonal tumors, including Wilms tumor, hepatoblastoma, adrenal neuroblastoma, gonadoblastoma, and hepatocellular carcinoma.
Drash syndrome
MedGen UID:
181980
Concept ID:
C0950121
Disease or Syndrome
Denys-Drash syndrome is a condition that affects the kidneys and genitalia.Denys-Drash syndrome is characterized by kidney disease that begins within the first few months of life. Affected individuals have a condition called diffuse glomerulosclerosis, in which scar tissue forms throughout glomeruli, which are the tiny blood vessels in the kidneys that filter waste from blood. In people with Denys-Drash syndrome, this condition often leads to kidney failure in childhood. People with Denys-Drash syndrome have an estimated 90 percent chance of developing a rare form of kidney cancer known as Wilms tumor. Affected individuals may develop multiple tumors in one or both kidneys.Although males with Denys-Drash syndrome have the typical male chromosome pattern (46,XY), they have gonadal dysgenesis, in which external genitalia do not look clearly male or clearly female (ambiguous genitalia) or the genitalia appear completely female. The testes of affected males are undescended, which means they are abnormally located in the pelvis, abdomen, or groin. As a result, males with Denys-Drash are typically unable to have biological children (infertile).Affected females usually have normal genitalia and have only the kidney features of the condition. Because they do not have all the features of the condition, females are usually given the diagnosis of isolated nephrotic syndrome.
Hyperparathyroidism 2
MedGen UID:
310065
Concept ID:
C1704981
Neoplastic Process
The spectrum of CDC73-related disorders includes the following phenotypes: Hyperparathyroidism-jaw tumor syndrome (HPT-JT). Parathyroid carcinoma. Familial isolated hyperparathyroidism (FIHP). Primary hyperparathyroidism, the main finding of HPT-JT syndrome, occurs in more than 70% of affected individuals; onset is typically in late adolescence or early adulthood. HPT-JT-associated primary hyperparathyroidism is usually caused by a single parathyroid adenoma. In approximately 10%-15% of cases, primary hyperparathyroidism is caused by parathyroid carcinoma. Ossifying fibromas of the mandible or maxilla, also known as cementifying fibromas and cemento-ossifying fibromas, occur in 30%-40% of individuals with HPT-JT syndrome. Although benign, these tumors can be locally aggressive and may continue to enlarge if not treated. Approximately 20% of individuals with HPT-JT syndrome have kidney lesions, most commonly cysts; renal hamartomas and (more rarely) Wilms tumor have also been reported. Benign and malignant uterine tumors appear to be common in women with HPT-JT syndrome.
Wilms tumor and radial bilateral aplasia
MedGen UID:
316905
Concept ID:
C1832099
Neoplastic Process
Wilms tumor 4
MedGen UID:
318623
Concept ID:
C1832426
Neoplastic Process
Li-Fraumeni syndrome 1
MedGen UID:
322656
Concept ID:
C1835398
Disease or Syndrome
Li-Fraumeni syndrome (LFS) is a cancer predisposition syndrome associated with the development of the following classic tumors: soft tissue sarcoma, osteosarcoma, pre-menopausal breast cancer, brain tumors, adrenocortical carcinoma (ACC), and leukemias. In addition, a variety of other neoplasms may occur. LFS-related cancers often occur in childhood or young adulthood and survivors have an increased risk for multiple primary cancers. Age-specific cancer risks have been calculated.
Fanconi anemia, complementation group N
MedGen UID:
372133
Concept ID:
C1835817
Disease or Syndrome
Fanconi anemia (FA) is characterized by physical abnormalities, bone marrow failure, and increased risk for malignancy. Physical abnormalities, present in approximately 75% of affected individuals, include one or more of the following: short stature, abnormal skin pigmentation, skeletal malformations of the upper and lower limbs, microcephaly, and ophthalmic and genitourinary tract anomalies. Progressive bone marrow failure with pancytopenia typically presents in the first decade, often initially with thrombocytopenia or leukopenia. The incidence of acute myeloid leukemia is 13% by age 50 years. Solid tumors –particularly of the head and neck, skin, gastrointestinal tract, and genitourinary tract – are more common in individuals with FA.
Brachydactyly-Mental Retardation syndrome
MedGen UID:
373895
Concept ID:
C1838126
Disease or Syndrome
2q37 microdeletion syndrome is characterized by mild-moderate developmental delay/intellectual disability, brachymetaphalangy of digits 3-5 (often digit 4 alone) (>50%), short stature, obesity, hypotonia, characteristic facial appearance, autism or autism spectrum disorder (30%), joint hypermobility/dislocation, and scoliosis. Other findings include seizures (20%-35%), congenital heart disease, CNS abnormalities (hydrocephalus, dilated ventricles), umbilical/inguinal hernia, tracheomalacia, situs abnormalities, gastrointestinal abnormalities, and renal malformations. Wilms tumor has been reported in two individuals.
Mosaic variegated aneuploidy syndrome
MedGen UID:
338026
Concept ID:
C1850343
Disease or Syndrome
Mosaic variegated aneuploidy is an autosomal recessive disorder characterized by mosaic aneuploidies, predominantly trisomies and monosomies, involving multiple different chromosomes and tissues (Hanks et al., 2004). The proportion of aneuploid cells varies but is usually more than 25% and is substantially greater than in normal individuals. Affected individuals typically present with severe intrauterine growth retardation and microcephaly. Eye anomalies, mild dysmorphism, variable developmental delay, and a broad spectrum of additional congenital abnormalities and medical conditions may also occur. The risk of malignancy is high, with rhabdomyosarcoma, Wilms tumor, and leukemia reported in several cases. See also MVA2 (614114), caused by mutation in the CEP57 gene (607951) on chromosome 11q21.
Isolated hemihyperplasia
MedGen UID:
383853
Concept ID:
C1856184
Disease or Syndrome
Isolated hemihyperplasia is an abnormality of cell proliferation leading to asymmetric overgrowth of one or more regions of the body. The term 'hemihyperplasia' has replaced the term 'hemihypertrophy' to describe accurately the increase in cell number found in these patients. The incidence of isolated hemihyperplasia is estimated to be 1 in 86,000. Idiopathic hemihypertrophy is associated with increased risk of embryonal cancers in childhood, particularly Wilms tumor (194070) (Shuman et al., 2006). Hoyme et al. (1998) provided an anatomic classification of hemihyperplasia: complex hemihyperplasia is involvement of half of the body, including at least 1 arm and 1 leg; affected parts may be contralateral or ipsilateral. Simple hemihyperplasia is involvement of a single limb. See also facial hemihyperplasia (133900). Although isolated hemihyperplasia is a distinct clinical entity, it can also occur as a feature of overgrowth syndromes, including Beckwith-Wiedemann syndrome (BWS; 130650), neurofibromatosis (NF1; 162200), Proteus syndrome (176920), and Klippel-Trenaunay-Weber syndrome (149000) (Shuman et al., 2006).
Wilms tumor 3
MedGen UID:
349770
Concept ID:
C1860265
Disease or Syndrome
Megalencephaly cutis marmorata telangiectatica congenita
MedGen UID:
355421
Concept ID:
C1865285
Congenital Abnormality
Megalencephaly-capillary malformation-polymicrogyria syndrome (MCAP) is characterized by a spectrum of anomalies including primary megalencephaly, prenatal overgrowth, brain and body asymmetry, cutaneous vascular malformations, digital anomalies consisting of syndactyly with or without postaxial polydactyly, connective tissue dysplasia involving the skin, subcutaneous tissue, and joints, and cortical brain malformations, most distinctively polymicrogyria (summary by Mirzaa et al., 2012). This disorder is also known as the macrocephaly-capillary malformation (MCM) syndrome (Conway et al., 2007). Mirzaa et al. (2012) suggested use of the term MCAP rather than MCM to reflect the very large brain size, rather than simply large head size, that characterizes this syndrome, and the importance and high frequency of perisylvian polymicrogyria.

Recent clinical studies

Etiology

Montalvão-de-Azevedo R, Vasconcelos GM, Vargas FR, Thuler LC, Pombo-de-Oliveira MS, de Camargo B; Brazilian Embryonic Tumor Group.
Genet Test Mol Biomarkers 2015 Feb;19(2):75-81. Epub 2014 Dec 23 doi: 10.1089/gtmb.2014.0177. PMID: 25536437Free PMC Article
Furtwängler R, Schmolze M, Gräber S, Leuschner I, Amann G, Schenk JP, Niggli F, Kager L, von Schweinitz D, Graf N
Klin Padiatr 2014 May;226(3):175-81. Epub 2014 May 12 doi: 10.1055/s-0034-1371840. PMID: 24819388
van Waas M, Wijnen M, Hartman A, de Vries AC, Pieters R, Neggers SJ, van den Heuvel-Eibrink MM
J Pediatr Hematol Oncol 2013 Jul;35(5):361-5. doi: 10.1097/MPH.0b013e31827e8fb9. PMID: 23389502
van Waas M, Neggers SJ, van Eck JP, van Noesel MM, van der Lely AJ, de Jong FH, Pieters R, van den Heuvel-Eibrink MM
Eur J Cancer 2012 May;48(8):1159-66. Epub 2012 Apr 16 doi: 10.1016/j.ejca.2012.02.046. PMID: 22513228
Berrebi D, Leclerc J, Schleiermacher G, Zaccaria I, Boccon-Gibod L, Fabre M, Jaubert F, El Ghoneimi A, Jeanpierre C, Peuchmaur M
PLoS One 2008 May 21;3(5):e2216. doi: 10.1371/journal.pone.0002216. PMID: 18493303Free PMC Article

Diagnosis

Kanyamuhunga A, Tuyisenge L, Stefan DC
Pan Afr Med J 2015 Aug 31;21:326. doi: 10.11604/pamj.2015.21.326.5912. PMID: 26600901Free PMC Article
Littooij AS, Humphries PD, Olsen ØE
Pediatr Radiol 2015 Oct;45(11):1651-60. Epub 2015 May 8 doi: 10.1007/s00247-015-3354-4. PMID: 25951925Free PMC Article
Ludwig N, Nourkami-Tutdibi N, Backes C, Lenhof HP, Graf N, Keller A, Meese E
Pediatr Blood Cancer 2015 Aug;62(8):1360-7. Epub 2015 Mar 18 doi: 10.1002/pbc.25481. PMID: 25787821
Visser YT, Uys R, van Zyl A, Stefan DC
J Med Life 2014 Sep 15;7(3):445-9. Epub 2014 Sep 25 PMID: 25408773Free PMC Article
Furtwängler R, Schmolze M, Gräber S, Leuschner I, Amann G, Schenk JP, Niggli F, Kager L, von Schweinitz D, Graf N
Klin Padiatr 2014 May;226(3):175-81. Epub 2014 May 12 doi: 10.1055/s-0034-1371840. PMID: 24819388

Therapy

Ludwig N, Nourkami-Tutdibi N, Backes C, Lenhof HP, Graf N, Keller A, Meese E
Pediatr Blood Cancer 2015 Aug;62(8):1360-7. Epub 2015 Mar 18 doi: 10.1002/pbc.25481. PMID: 25787821
Visser YT, Uys R, van Zyl A, Stefan DC
J Med Life 2014 Sep 15;7(3):445-9. Epub 2014 Sep 25 PMID: 25408773Free PMC Article
Furtwängler R, Schmolze M, Gräber S, Leuschner I, Amann G, Schenk JP, Niggli F, Kager L, von Schweinitz D, Graf N
Klin Padiatr 2014 May;226(3):175-81. Epub 2014 May 12 doi: 10.1055/s-0034-1371840. PMID: 24819388
Pietras W
Adv Clin Exp Med 2012 Nov-Dec;21(6):809-820. PMID: 23457141
van Waas M, Neggers SJ, Raat H, van Rij CM, Pieters R, van den Heuvel-Eibrink MM
PLoS One 2012;7(12):e52237. Epub 2012 Dec 14 doi: 10.1371/journal.pone.0052237. PMID: 23251703Free PMC Article

Prognosis

Ueda M, Iguchi T, Komatsu H, Kidogami S, Hu Q, Sato K, Ogawa Y, Nambara S, Saito T, Sakimura S, Hirata H, Uchi R, Shinden Y, Eguchi H, Ito S, Masuda T, Yamamoto H, Doki Y, Mori M, Mimori K
Anticancer Res 2015 Dec;35(12):6591-7. PMID: 26637874
Littooij AS, Humphries PD, Olsen ØE
Pediatr Radiol 2015 Oct;45(11):1651-60. Epub 2015 May 8 doi: 10.1007/s00247-015-3354-4. PMID: 25951925Free PMC Article
Furtwängler R, Schmolze M, Gräber S, Leuschner I, Amann G, Schenk JP, Niggli F, Kager L, von Schweinitz D, Graf N
Klin Padiatr 2014 May;226(3):175-81. Epub 2014 May 12 doi: 10.1055/s-0034-1371840. PMID: 24819388
Dokmak S, Cabral C, Couvelard A, Aussilhou B, Belghiti J, Sauvanet A
JOP 2009 Jul 6;10(4):396-9. PMID: 19581742
Berrebi D, Leclerc J, Schleiermacher G, Zaccaria I, Boccon-Gibod L, Fabre M, Jaubert F, El Ghoneimi A, Jeanpierre C, Peuchmaur M
PLoS One 2008 May 21;3(5):e2216. doi: 10.1371/journal.pone.0002216. PMID: 18493303Free PMC Article

Clinical prediction guides

Littooij AS, Humphries PD, Olsen ØE
Pediatr Radiol 2015 Oct;45(11):1651-60. Epub 2015 May 8 doi: 10.1007/s00247-015-3354-4. PMID: 25951925Free PMC Article
Tajima S, Waki M
Int J Clin Exp Pathol 2015 Jan 1;8(1):989-94. PMID: 25755807Free PMC Article
van Waas M, Wijnen M, Hartman A, de Vries AC, Pieters R, Neggers SJ, van den Heuvel-Eibrink MM
J Pediatr Hematol Oncol 2013 Jul;35(5):361-5. doi: 10.1097/MPH.0b013e31827e8fb9. PMID: 23389502
van Waas M, Neggers SJ, van Eck JP, van Noesel MM, van der Lely AJ, de Jong FH, Pieters R, van den Heuvel-Eibrink MM
Eur J Cancer 2012 May;48(8):1159-66. Epub 2012 Apr 16 doi: 10.1016/j.ejca.2012.02.046. PMID: 22513228
Taran K, Sitkiewicz A, Kobos J
Pol J Pathol 2010;61(4):234-9. PMID: 21290348

Recent systematic reviews

Ueda M, Iguchi T, Komatsu H, Kidogami S, Hu Q, Sato K, Ogawa Y, Nambara S, Saito T, Sakimura S, Hirata H, Uchi R, Shinden Y, Eguchi H, Ito S, Masuda T, Yamamoto H, Doki Y, Mori M, Mimori K
Anticancer Res 2015 Dec;35(12):6591-7. PMID: 26637874
Brisbin AG, Asmann YW, Song H, Tsai YY, Aakre JA, Yang P, Jenkins RB, Pharoah P, Schumacher F, Conti DV, Duggan DJ, Jenkins M, Hopper J, Gallinger S, Newcomb P, Casey G, Sellers TA, Fridley BL
BMC Med Genet 2011 Dec 5;12:156. doi: 10.1186/1471-2350-12-156. PMID: 22142333Free PMC Article
Vujanić GM, Sandstedt B
J Clin Pathol 2010 Feb;63(2):102-9. Epub 2009 Aug 16 doi: 10.1136/jcp.2009.064600. PMID: 19687012
Vujanić GM, Sandstedt B, Kelsey A, Sebire NJ
Cancer 2009 May 1;115(9):1977-83. doi: 10.1002/cncr.24214. PMID: 19241454
Furtwaengler R, Reinhard H, Leuschner I, Schenk JP, Goebel U, Claviez A, Kulozik A, Zoubek A, von Schweinitz D, Graf N; Gesellschaft fur Pädiatrische Onkologie und Hämatologie (GPOH) Nephroblastoma Study Group.
Cancer 2006 May 15;106(10):2275-83. doi: 10.1002/cncr.21836. PMID: 16596620

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