Beckwith-Wiedemann Syndrome and Childhood Tumor Risk

Beckwith-Wiedemann syndrome (BWS) is the most common genetic overgrowth condition and the most common imprinting disorder. A baby with the syndrome may be born large, with a big tongue, an opening in the belly wall, low blood sugar in the first days of life, or one side of the body growing faster than the other. Some children show many of these signs; others show only one. The syndrome also raises the chance of certain childhood cancers, mainly Wilms tumor of the kidney and hepatoblastoma of the liver, during the first years of life.

This page explains the small region of chromosome 11 where the syndrome starts, the four main molecular causes and how often each is found, how doctors now score the features and confirm the diagnosis under the 2018 international consensus, the link with conception by assisted reproduction, and what the research reports about tumor risk and tumor screening with ultrasound and blood tests. It goes deeper into the syndrome than the general Wilms Tumor page, which covers the kidney cancer itself.

Table of Contents

  1. What Beckwith-Wiedemann Syndrome Is
  2. The Chromosome 11p15 Changes Behind It
  3. Features Seen in Babies and Children
  4. How the Diagnosis Is Made Under the 2018 Consensus
  5. The Link With Assisted Reproduction
  6. Tumor Risk Depends on the Molecular Cause
  7. Wilms Tumor in Children With the Syndrome
  8. Tumor Screening With Ultrasound and Alpha-Fetoprotein
  9. Growing Up: Outlook Into Adulthood
  10. What Is Not Yet Known
  11. Key Research Papers
  12. Connections
  13. Featured Videos

What Beckwith-Wiedemann Syndrome Is

Most genes come in two working copies, one from each parent. A small group of genes is different: only the copy from one particular parent is switched on, and the other copy is kept silent by chemical tags called methyl groups. This parent-of-origin pattern is called genomic imprinting. Beckwith-Wiedemann syndrome is an imprinting disorder. It arises when the balance of imprinted growth genes on the short arm of chromosome 11, in a band called 11p15.5, is upset, so that growth-promoting signals are turned up and growth-restraining signals are turned down.

The 2018 international consensus statement describes the syndrome as a condition with variable features that might include overgrowth, an enlarged tongue (macroglossia), abdominal wall defects, low blood sugar in the newborn period, overgrowth of one side of the body (lateralized overgrowth) and a predisposition to embryonal tumors, which are cancers that grow from tissue resembling the developing embryo. The same consensus introduced the term Beckwith-Wiedemann spectrum, which covers both the classical syndrome and milder pictures, such as isolated one-sided overgrowth, in which an 11p15.5 molecular change is found.

How common it is

Counts differ with how hard a region looks for mild cases. A study that searched every source in the Piedmont region of north-west Italy for children born from 1997 to 2009 found 46 clear-cut cases, a prevalence of 1 in 10,340 live births, the highest figure reported at the time. A European population study using 34 congenital-anomaly registries in 16 countries, which counted mostly classical cases picked up before birth or in early childhood, estimated a mean prevalence of 3.8 per 100,000 births, or 1 in 26,000. A 2025 review by the scientific committee of the Italian patient association states that the prevalence of the spectrum exceeds 1 in 10,000, making it the most common imprinting disorder.

The Chromosome 11p15 Changes Behind It

The 11p15.5 region holds two neighboring control switches. Imprinting center 1 (IC1) controls a pair of genes: IGF2, which makes insulin-like growth factor 2, a strong growth signal, and H19, which acts as a brake. Imprinting center 2 (IC2) controls genes that include CDKN1C, which makes a protein (cyclin-dependent kinase inhibitor 1C) that slows cell division. Four kinds of change account for most cases with a molecular diagnosis:

How often each cause is found

In an Italian study of 318 patients with a proven molecular defect, 190 had loss of methylation at imprinting center 2, 87 had paternal uniparental disomy, 31 had gain of methylation at imprinting center 1, and 10 had CDKN1C variants. In the Piedmont population study, 41 children underwent molecular tests and 70.7% were positive: loss of methylation at imprinting center 2 was found in 29.3%, paternal uniparental disomy in 24.4%, gain of methylation at imprinting center 1 in 14.6% and a CDKN1C mutation in 2.4%, while 29.3% had negative tests.

Mosaicism and negative blood tests

A negative blood test does not rule the syndrome out. The causative change is often present in only a fraction of cells, and blood may carry fewer affected cells than the tongue, skin or an overgrown limb. A United States laboratory study of samples from 1,057 people tested with sensitive multi-method assays confirmed a molecular diagnosis in 27.4%, and 43.4% of those diagnosed had mosaic disease. Testing solid tissue samples from people whose blood test was negative improved the diagnostic yield. The 2025 Italian review lists diagnosis after a negative blood methylation test as a major focus, noting that somatic mosaicism often makes testing of another tissue necessary.

Features Seen in Babies and Children

The signs of the syndrome vary widely from one child to the next. The main ones described in the consensus and in large cohort studies are:

Features differ by molecular cause

In the 318-patient Italian study, each molecular group showed its own growth pattern. Large size at birth was almost constant with gain of methylation at imprinting center 1, overgrowth after birth was typical of loss of methylation at imprinting center 2, and one-sided overgrowth was more common with paternal uniparental disomy. Exomphalos was more common with imprinting center 2 or CDKN1C changes. Kidney defects were typical of uniparental disomy and imprinting center 1 cases. Ear anomalies and nevus flammeus went with imprinting center 2 and CDKN1C changes, and macroglossia was less common in the uniparental disomy group.

What happens around birth

The European registry study, covering 371 cases from 1990 to 2015, found that 39.9% of cases with a known time of diagnosis were suspected before birth and 36.3% at birth. Prematurity was present in 40.6% of boys and 33.9% of girls, and macrosomia was common. Of the live-born babies with survival information, 3.6% died in the first week of life, most of them preterm, and first-year survival was 90.9%. Twin pregnancies were recorded in 5.7% of cases.

A Swedish national cohort of all children born from 1997 to 2016 found the syndrome in 15 of 207 children born with an omphalocele (7.2%).

Low blood sugar from too much insulin

A United States study of 28 children with both the syndrome (or one-sided 11p overgrowth) and congenital hyperinsulinism found mosaic paternal uniparental disomy in 26 of the 28. Most of these children did not respond to diazoxide, the standard first medicine for hyperinsulinism, and half needed removal of most of the pancreas. The authors report that hyperinsulinism linked to paternal uniparental disomy is persistent and severe, while the low blood sugar seen with other causes of the syndrome tends to be transient. Signs that hospitals treat as urgent in a newborn include jitteriness, limpness, poor feeding, breathing pauses and seizures, because untreated low blood sugar can injure the brain.

How the Diagnosis Is Made Under the 2018 Consensus

Before 2018, clinics used several competing lists of major and minor criteria. An international consensus group then agreed on 72 recommendations covering molecular testing, care and treatment from before birth into adulthood. The consensus introduced a points-based clinical score that sorts signs into cardinal features, the more distinctive ones, and suggestive features, which are commoner and less specific. Studies since then have tied the score to the chance that a molecular test is positive, and a person can be placed within the Beckwith-Wiedemann spectrum either on clinical grounds or because an 11p15.5 change is found.

How well the score performs

An Italian study tested the scoring systems in 831 patients. The 2018 consensus score performed best of the systems compared, with a sensitivity of 0.85 and a specificity of 0.43. Blood-based testing found a molecular cause in only about 20% of patients with a score of 2, and the score did not correlate with later cancer. The authors suggest that tissue testing may be considered as a first step in patients scoring below 4 points, and they discourage use of the score as a measure of cancer risk.

A British study of 94 people with lateralized overgrowth found a molecular change in 15 (16%), and the rate of a positive blood test rose with the consensus score. Only 3 of 48 people with isolated one-sided overgrowth had a molecular change. In the United States laboratory series, a single cardinal feature was enough to be associated with a molecular diagnosis in 20% of cases.

Before birth

An omphalocele or a large baby seen on a pregnancy scan can raise the possibility of the syndrome. In the European registry study, the prenatal detection rate was 64.1% (141 of 220), with no significant change over time, and the mean stage of pregnancy at prenatal diagnosis by ultrasound was 19.8 weeks. The 2025 Italian review proposes a prenatal scoring system and supports including pregnancies conceived through assisted reproduction in the diagnostic criteria.

The Link With Assisted Reproduction

Imprinting marks are set in eggs and sperm and maintained in the early embryo, which is the window when in vitro fertilization and related techniques handle eggs and embryos. Several research groups have therefore asked whether these techniques change the risk of imprinting disorders.

In Piedmont, Italy, 379,872 babies were born live from 2005 to 2014, including 7,884 conceived through assisted reproduction. Thirty-eight babies with the syndrome were born in that period, 7 after assisted reproduction and 31 naturally conceived. The birth prevalence was 1 in 1,126 in the assisted-reproduction group and 1 in 12,254 in the naturally conceived group, a relative risk of 10.7 (95% confidence interval 4.7 to 24.2). Put as absolute numbers, the study reports a live-birth risk of 887.9 per million in the assisted-reproduction group against 83.3 per million in the naturally conceived group. Of 8 tested children conceived this way, 4 had loss of methylation at imprinting center 2, 2 had paternal uniparental disomy and 2 had negative results, which the authors read as a sign that the techniques might be implicated in genetic events beyond methylation errors.

A 2018 meta-analysis that pooled 8 studies on the syndrome gave a summary odds ratio of 5.8 (95% confidence interval 3.1 to 11.1) for a history of conception through assisted reproduction, and found positive associations for Angelman, Prader-Willi and Silver-Russell syndromes as well. The European registry study found that 7.2% of affected children (13 of 181) had been conceived by assisted reproduction, three times the rate in the general population of the countries studied. The reasons for the association, including any part played by the underlying infertility rather than the techniques themselves, are still under investigation. Even in the Piedmont study, the syndrome occurred in 1 in 1,126 births after assisted reproduction.

Tumor Risk Depends on the Molecular Cause

The cancers seen in the syndrome are mostly embryonal tumors of early childhood: Wilms tumor of the kidney, hepatoblastoma of the liver, and less often neuroblastoma, adrenocortical carcinoma and rhabdomyosarcoma. The chance of a tumor depends strongly on which 11p15 change a child carries.

The 2016 meta-analysis

A systematic review of studies published from 2000 to 2015 included 1,370 patients, of whom 102 developed tumors (7.4%). Tumor prevalence was 2.5% with loss of methylation at imprinting center 2, 13.8% with paternal uniparental disomy, 22.8% with gain of methylation at imprinting center 1 and 8.6% with CDKN1C mutations. Wilms tumor was strongly associated with gain of methylation at imprinting center 1 (odds ratio 68.3) and with uniparental disomy (odds ratio 13.2). Uniparental disomy was also associated with hepatoblastoma (odds ratio 5.2) and adrenal carcinoma (odds ratio 7.0), and CDKN1C mutations with neuroblastic tumors (odds ratio 7.2). The authors found screening questionable for the imprinting center 2 group, given its low tumor risk.

The Dutch cohort and literature pool

A Dutch study combined 229 of its own patients with published cohorts to reach 1,971 patients. Tumor risk was highest with gain of methylation at imprinting center 1 (28%) and with paternal uniparental disomy (16%), and lower with imprinting center 2 changes (2.6%), CDKN1C changes (6.9%) and in children with no detectable molecular defect (6.7%). Wilms tumors, with a median age at diagnosis of 24 months, were frequent with imprinting center 1 changes (24%) and uniparental disomy (7.9%). Hepatoblastoma occurred mostly with uniparental disomy (3.5%) and imprinting center 2 changes (0.7%), never with imprinting center 1 or CDKN1C changes, and always before 30 months of age. In the CDKN1C group, 2.8% developed neuroblastoma.

Newer findings

Wilms Tumor in Children With the Syndrome

Wilms tumor (nephroblastoma) is the main cancer concern in the syndrome. The growth-signal imbalance at 11p15 is thought to let pockets of embryonic kidney tissue, called nephrogenic rests, persist after birth and occasionally turn into tumors.

A pooled analysis of published and unpublished cases compared the age at Wilms tumor diagnosis in children with the Beckwith-Wiedemann spectrum with the National Institutes of Health Surveillance, Epidemiology, and End Results cancer registry. Children with the syndrome had a significantly higher incidence of diagnosis between 12 and 84 months of age. Children whose tumor was found through screening had significantly lower stages at diagnosis than children who were not screened, and the authors conclude that screening until age 7 detects close to 95% of all Wilms tumors in this group.

An older report from the National Wilms Tumor Study Group reviewed 4,669 children treated on two trial protocols between 1980 and 1995; 53 of them were reported to have the syndrome. These children were more likely to present at a lower stage, with 27 of the 53 at stage I. Overall survival at 4 years was 89% for the children with the syndrome and 90% for those without it. Twenty-one percent of the children with the syndrome had tumors in both kidneys, either at diagnosis (9 of 53) or as a later tumor in the other kidney (2 of 53). Because of that risk to both kidneys, the authors raised the idea of ultrasound screening followed by kidney-sparing surgery.

Tumor Screening With Ultrasound and Alpha-Fetoprotein

Tumor screening in the syndrome aims to find a Wilms tumor or hepatoblastoma while it is small, so that treatment can be lighter and more of the kidney or liver can be kept. Two tools are used: ultrasound of the kidneys or whole abdomen, which needs no radiation, and a blood test for alpha-fetoprotein (AFP), a protein made by the fetal liver that hepatoblastoma also produces.

North America and Europe take different routes

In 2017, a North American expert panel set out uniform screening recommendations for North America for syndromes with at least a 1% tumor risk. For Wilms tumor, the panel recommended kidney ultrasound every 3 months from birth (or from diagnosis) through the seventh birthday. For hepatoblastoma, it recommended full abdominal ultrasound and serum alpha-fetoprotein every 3 months from birth (or from diagnosis) through the fourth birthday. These recommendations were not tailored to the molecular cause, which the panel described as a difference in practice environment between the United States and Europe.

The 2018 international consensus instead recommends a tumor surveillance program targeted by molecular subgroup, while noting that surveillance might differ by health-care system, for example in the United States, and that the results of targeted and universal surveillance need to be evaluated prospectively. The 2016 meta-analysis authors had proposed kidney ultrasound for children with imprinting center 1 gain of methylation or uniparental disomy, alpha-fetoprotein monitoring for children with uniparental disomy, and urine markers plus ultrasound for neuroblastoma in children with CDKN1C mutations.

The 2024 update

In 2024, members of the American Association for Cancer Research Pediatric Cancer Working Group met again to update the 2017 guidelines with a review of newer evidence and risk estimates. Their update covers revised diagnostic criteria and aims to harmonize surveillance recommendations for children with overgrowth syndromes and other syndromes that predispose to Wilms tumor across North America and Australia. The 2025 Italian review, which builds on the 2018 consensus with evidence up to 2024, describes universal alpha-fetoprotein screening for hepatoblastoma up to 3 years of age together with genotype-based protocols for Wilms tumor, and separate neuroblastoma surveillance for CDKN1C-related cases.

Reading alpha-fetoprotein in a young child

Alpha-fetoprotein is naturally very high in newborns and falls over the first year, so a single value is hard to interpret. A United States study collected 1,372 measurements from 147 patients with the Beckwith-Wiedemann spectrum and built age-based reference ranges. The predicted values fell into the normal range for age (below 10 ng/mL) by 14 months. Sex and the testing laboratory did not affect the values, but premature and full-term babies differed, so separate reference values were set for each. More detail on the test itself is on the AFP Test page.

Because blood draws every three months are a burden for young children, an Italian group developed an alpha-fetoprotein test on dried blood spots from a finger or heel prick. In 259 paired plasma and dried-spot measurements from 171 children, including 39 with the spectrum, the two methods overlapped across the full range of values, with occasional differences falling within standard laboratory error.

Costs and families

A 2001 cost model built on two hypothetical groups of 1,000 infants with the syndrome estimated that ultrasound screening from birth to 4 years cost $9,642 per life-year saved and screening to 7 years cost $14,740 per life-year saved, under the model's assumptions of a one-stage shift at diagnosis and high test accuracy. The authors called for a real screening trial to settle how often, and until when, screening is worthwhile.

Growing Up: Outlook Into Adulthood

The features of the syndrome usually soften with age, and most of its tumors appear in early childhood. Data on adults remain limited.

An Italian study followed 34 adults with the syndrome, aged 18 to 58 years. Final tall stature was present in 44%, and 85% had needed surgery for features of the syndrome. Four had developed Wilms tumor in childhood (at ages 2, 3, 5 and 10 years). In early adulthood, one developed hepatoblastoma at 22, one acute lymphoblastic leukemia at 21, and one an adrenal adenoma and a testicular Sertoli cell tumor at 22 and 24; three benign tumors were also recorded. The authors note that this cumulatively raised the tumor rate in their cohort to 20% over the observation period, a figure from a small group. Lasting problems included speech and swallowing difficulties from macroglossia in 9, painful scoliosis linked to one-sided overgrowth in 4, recurrent kidney stones in 4 and absent sperm in 4, likely linked to undescended testes. Four of the adults had healthy children.

The syndrome is not usually associated with intellectual disability. In a study of 29 children and teenagers aged 5 to 18, most performed adequately on cognitive tests, with more difficulty in language than in visual-spatial tasks, slower reading and mental arithmetic, and a pattern of increased anxiety, low self-esteem and social withdrawal. The 2025 Italian review notes that the move to adult care remains underexplored and points to residual childhood complications, fertility and possible long-term risks.

Children who develop Wilms tumor in the setting of the syndrome have done about as well with modern treatment as other children with Wilms tumor in the trial data described above. The rarer tumors of the syndrome are covered on the Neuroblastoma and Adrenocortical Carcinoma pages.

What Is Not Yet Known

Decisions about testing, screening schedules and treatment belong with a clinical genetics and pediatric oncology team.

Key Research Papers

  1. Brioude F, Kalish JM, Mussa A, Foster AC, Bliek J, Ferrero GB, et al. Expert consensus document: Clinical and molecular diagnosis, screening and management of Beckwith-Wiedemann syndrome: an international consensus statement. Nat Rev Endocrinol. 2018;14(4):229-249. PubMed PMID: 29377879
  2. Kalish JM, Becktell KD, Bougeard G, Brodeur GM, Diller LR, Doria AS, et al. Update on Surveillance for Wilms Tumor and Hepatoblastoma in Beckwith-Wiedemann Syndrome and Other Predisposition Syndromes. Clin Cancer Res. 2024;30(23):5260-5269. PubMed PMID: 39320341
  3. Kalish JM, Doros L, Helman LJ, Hennekam RC, Kuiper RP, Maas SM, et al. Surveillance Recommendations for Children with Overgrowth Syndromes and Predisposition to Wilms Tumors and Hepatoblastoma. Clin Cancer Res. 2017;23(13):e115-e122. PubMed PMID: 28674120
  4. Mussa A, Duffy KA, Carli D, Griff JR, Fagiano R, Kupa J, et al. The effectiveness of Wilms tumor screening in Beckwith-Wiedemann spectrum. J Cancer Res Clin Oncol. 2019;145(12):3115-3123. PubMed PMID: 31583434
  5. Mussa A, Molinatto C, Baldassarre G, Riberi E, Russo S, Larizza L, et al. Cancer Risk in Beckwith-Wiedemann Syndrome: A Systematic Review and Meta-Analysis Outlining a Novel (Epi)Genotype Specific Histotype Targeted Screening Protocol. J Pediatr. 2016;176:142-149.e1. PubMed PMID: 27372391
  6. Maas SM, Vansenne F, Kadouch DJ, Ibrahim A, Bliek J, Hopman S, et al. Phenotype, cancer risk, and surveillance in Beckwith-Wiedemann syndrome depending on molecular genetic subgroups. Am J Med Genet A. 2016;170(9):2248-60. PubMed PMID: 27419809
  7. Mussa A, Russo S, De Crescenzo A, Freschi A, Calzari L, Maitz S, et al. (Epi)genotype-phenotype correlations in Beckwith-Wiedemann syndrome. Eur J Hum Genet. 2016;24(2):183-90. PubMed PMID: 25898929
  8. Mussa A, Russo S, De Crescenzo A, Chiesa N, Molinatto C, Selicorni A, et al. Prevalence of Beckwith-Wiedemann syndrome in North West of Italy. Am J Med Genet A. 2013;161A(10):2481-6. PubMed PMID: 23918458
  9. Barisic I, Boban L, Akhmedzhanova D, Bergman JEH, Cavero-Carbonell C, Grinfelde I, et al. Beckwith Wiedemann syndrome: A population-based study on prevalence, prenatal diagnosis, associated anomalies and survival in Europe. Eur J Med Genet. 2018;61(9):499-507. PubMed PMID: 29753922
  10. Mussa A, Molinatto C, Cerrato F, Palumbo O, Carella M, Baldassarre G, et al. Assisted Reproductive Techniques and Risk of Beckwith-Wiedemann Syndrome. Pediatrics. 2017;140(1):e20164311. PubMed PMID: 28634246
  11. Cortessis VK, Azadian M, Buxbaum J, Sanogo F, Song AY, Sriprasert I, et al. Comprehensive meta-analysis reveals association between multiple imprinting disorders and conception by assisted reproductive technology. J Assist Reprod Genet. 2018;35(6):943-952. PubMed PMID: 29696471
  12. Luca M, Carli D, Cardaropoli S, Milani D, Cocchi G, Leoni C, et al. Performance Metrics of the Scoring System for the Diagnosis of the Beckwith-Wiedemann Spectrum (BWSp) and Its Correlation with Cancer Development. Cancers (Basel). 2023;15(3):773. PubMed PMID: 36765732
  13. Baker SW, Duffy KA, Richards-Yutz J, Deardorff MA, Kalish JM, Ganguly A. Improved molecular detection of mosaicism in Beckwith-Wiedemann Syndrome. J Med Genet. 2021;58(3):178-184. PubMed PMID: 32430359
  14. Radley JA, Connolly M, Sabir A, Kanani F, Carley H, Jones RL, et al. Isolated- and Beckwith-Wiedemann syndrome related- lateralised overgrowth (hemihypertrophy): Clinical and molecular correlations in 94 individuals. Clin Genet. 2021;100(3):292-297. PubMed PMID: 33993487
  15. Kalish JM, Boodhansingh KE, Bhatti TR, Ganguly A, Conlin LK, Becker SA, et al. Congenital hyperinsulinism in children with paternal 11p uniparental isodisomy and Beckwith-Wiedemann syndrome. J Med Genet. 2016;53(1):53-61. PubMed PMID: 26545876
  16. George AM, Viswanathan A, Best LG, Monahan C, Limmina M, Ganguly A, et al. Expanded phenotype and cancer risk in patients with Beckwith-Wiedemann spectrum caused by CDKN1C variants. Am J Med Genet A. 2024;194(10):e63777. PubMed PMID: 38822599
  17. Fogelström A, Caldeman C, Wester T, Löf Granström A, Mesas Burgos C. Prevalence of Beckwith Wiedemann Syndrome and Risk of Embryonal Tumors in Children Born with Omphalocele. J Pediatr Surg. 2023;58(11):2114-2118. PubMed PMID: 37355432
  18. Duffy KA, Cohen JL, Elci OU, Kalish JM. Development of the Serum α-Fetoprotein Reference Range in Patients with Beckwith-Wiedemann Spectrum. J Pediatr. 2019;212:195-200.e2. PubMed PMID: 31235384
  19. Mussa A, Ciuffreda VP, Sauro P, Pagliardini V, Pagliardini S, Carli D, et al. Longitudinal Monitoring of Alpha-Fetoprotein by Dried Blood Spot for Hepatoblastoma Screening in Beckwith-Wiedemann Syndrome. Cancers (Basel). 2019;11(1):86. PubMed PMID: 30646549
  20. Porteus MH, Narkool P, Neuberg D, Guthrie K, Breslow N, Green DM, et al. Characteristics and outcome of children with Beckwith-Wiedemann syndrome and Wilms' tumor: a report from the National Wilms Tumor Study Group. J Clin Oncol. 2000;18(10):2026-31. PubMed PMID: 10811666
  21. McNeil DE, Brown M, Ching A, DeBaun MR. Screening for Wilms tumor and hepatoblastoma in children with Beckwith-Wiedemann syndromes: a cost-effective model. Med Pediatr Oncol. 2001;37(4):349-56. PubMed PMID: 11568898
  22. Gazzin A, Carli D, Sirchia F, Molinatto C, Cardaropoli S, Palumbo G, et al. Phenotype evolution and health issues of adults with Beckwith-Wiedemann syndrome. Am J Med Genet A. 2019;179(9):1691-1702. PubMed PMID: 31339634
  23. Butti N, Urgesi C, Mussa A, Montirosso R. Cognitive, Social, and Emotional-Behavioral Outcomes in Children and Adolescents With Beckwith-Wiedemann Syndrome. Am J Med Genet B Neuropsychiatr Genet. 2025;198(2):e33006. PubMed PMID: 39320140
  24. Russo S, Milani D, Meossi C, Marcucci L, Pajno R, Butti N, et al. Beckwith-Wiedemann spectrum (BWSp): an update on diagnosis, management, and follow-up from the scientific committee of the Italian BWSp association. Ital J Pediatr. 2025;51(1):287. PubMed PMID: 41126215

PubMed Topic Searches

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  5. Beckwith-Wiedemann mosaicism at 11p15

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