Sotos Syndrome

Disease Overview

Sotos syndrome, also known as cerebral gigantism, is a rare genetic condition characterized by rapid physical growth during early childhood.¹ Newborns with Sotos syndrome tend to be larger, taller and heavier than other children. The head is large (macrocephalic), long and narrow (dolichocephalic), the forehead is prominent and broad, and hair is often thin surrounding the forehead and ears.^1,2 People affected with Sotos syndrome have characteristic facial features generally noticed at birth but become more noticeable between the ages of 1-6 years.^3,4 Other features may include developmental delay and intellectual disability. ^5,6

Diagnosis is based on clinical features including distinct craniofacial features, excessive growth, advanced bone age and developmental delay as well as genetic testing.⁷

There is no cure yet. Treatment is directed toward specific symptoms that are apparent in each individual.⁶

Introduction

Sotos syndrome was first recognized in 1964 by Juan Sotos, MD, who described a child with rapid growth and a large head.¹ The major criteria for diagnosis were established in 1994.⁸ In 2002, Japanese researchers identified a change (variant) in the NDS1 gene in people with Sotos syndrome. The symptoms of Sotos syndrome can vary from person to person, even when they have the same NSD1 gene variant.¹⁴

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Synonyms

• cerebral gigantism (outdated term)

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Subdivisions

• Sotos syndrome 1
• Sotos syndrome 2 (Malan syndrome)
• Sotos syndrome 3

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Signs & Symptoms

The following features are present in ≥ 90% of individuals with Sotos syndrome:^1,3,6,10

• Characteristic facial appearance
• Developmental delay and learning disability
• Overgrowth/advanced bone age

Characteristic facial appearance

The craniofacial features most characteristic are a prominent forehead and receding forehead hairline in 96% of individuals with Sotos syndrome.^5,11

○      long, narrow face (dolichocephalic head)

○      widely spaced eyes (hypertelorism)

○      down slanting eyelids and folds (palpebral features)

○      high narrow palate

○      pointed chin

The typical facial features are noticed at birth but become most apparent in childhood and as the child matures, the chin becomes more prominent and squarer in shape.^3,12 In adults, the craniofacial characteristics are less distinctive, but the chin is prominent, and the dolichocephalic and receding hairline (frontal bossing) remain.¹³

Developmental delay

Affected infants and children usually have a delay in achieving certain developmental milestones (e.g., sitting, crawling, walking, etc.). They may not begin to walk until approximately 15 to 17 months of age.^1,10 Affected children may also experience difficulty performing certain tasks requiring coordination (such as riding a bicycle or playing sports), fine motor skills (e.g., the ability to grasp small objects) and may have unusual clumsiness.⁶  Most children have low muscle tone (supranuclear hypotonia) which is a major contributor to motor delays. Children with this disorder typically have delays in obtaining language skills. Many affected children do not begin to speak until approximately two to three years of age.¹¹

Intellectual disability

Intellectual disability is present in 80 to 85% of the people affected with Sotos syndrome, with an average IQ of 72 and a range from 40 to borderline mild intellectual disability. About 15 to 20% may have normal intelligence.¹⁰ Intelligence quotient (IQ) is a standardized measure used to assess cognition and intelligence.

Overgrowth/advanced bone age

The main clinical finding is prenatal and postnatal overgrowth. The rate of growth is particularly excessive in the first 3 to 4 years of life and then proceeds at the normal rate but in the high percentiles. The mean height is usually 2 to 3 years ahead of peers during childhood.⁹ Weight is usually appropriate for the height and the bone age is advanced by 2 to 4 years over chronological age during childhood.⁶ Adult height is usually taller than average for males and females. Final adult height typically reaches 5-6” above the predicted adult height in males and 3-4” in females.⁸ Some individuals may reach excessive adult heights; males from 193 cm to 203 cm (6 ft. 4 in. to 6 ft. 8 in.) and females up to 188 cm (6 ft. 2 in.) are known.¹⁰

Other signs and symptoms in people with Sotos syndrome include:

• Behavioral findings
• Sleep disorders
• Heart (cardiac) anomalies
• Brain (cranial) MRI/CT anomalies
• Joint hyperlaxity
• Health complications in newborns
• Kidney (renal) anomalies
• Curved spine (scoliosis)
• Seizures

Behavioral findings: Individuals with Sotos syndrome can have behavioral problems at all ages that can make it difficult for them to develop relationships with others.¹⁵  These behavioral problems include an increased risk for autism spectrum disorder (ASD).¹⁵

Sleep disorders: Along with behavioral problems, many children have sleep disorders. ¹⁶

Cardiac anomalies: Heart defects are present in about 8 to 35% of children with Sotos syndrome but are usually not severe.¹⁰ The most commonly reported are a hole in the wall of the heart between chambers (septal defects) and a lack of enclosure of the blood vessel that connects the aorta and pulmonary arteries after birth (patent ductus arteriosus).¹⁷

Cranial anomalies: Some brain abnormalities (enlarged ventricles) may occur.^7,10 Characteristic MRI changes include increased size of extra-axial fluid spaces, increased size of ventricles with increased size of posterior aspects of lateral ventricles (like that of colpocephaly, when an area of the brain, called the occipital horn, is larger than expected), midline defects such as persistence of the cavum septum pellucidum, a normal space between the two leaflets of the septum pellucidum, a thin membrane in the brain, and thinning of the middle 1/3 of the corpus callosum, the brain structure that divides both of the cerebral hemispheres.¹⁸

Joint hyperlaxity: Low muscle tone (hypotonia) and lax joints are almost always present, and clumsiness is frequent (60 to 80%).⁴

Neonatal complications: Newborns often have jaundice, difficulty feeding and low muscle tone (hypotonia).

Renal anomalies: Abnormalities in the genital and/or urinary systems occur in about 20% of the affected people.⁴

Scoliosis: A curved spine is present in about 40% of those affected but is usually not severe enough to require bracing or surgery.⁶

Seizures: Seizures may occur in 30% of those affected.¹⁰

Additional symptoms¹⁹

The following features are seen in ≥2% and <15% of individuals with Sotos syndrome: ⁴

Eye problems

• Astigmatism: a problem where the eye isn’t perfectly round which can make things look blurry
• Cataract: when the lens of the eye becomes cloudy, making it hard to see clearly, like looking through foggy glass
• Hypermetropia (farsightedness): difficulty seeing things that are far away
• Myopia (nearsightedness): difficulty seeing things up close
• Nystagmus: fast, uncontrolled eye movements that make it hard for the eyes to focus
• Strabismus: when the eyes don’t line up properly, sometimes called “crossed eyes”

Ear and hearing problems

• Cholesteatoma: a growth in the ear that can cause hearing problems and sometimes infections
• Conductive hearing loss: hearing loss is caused by something blocking sound from reaching the inner ear like earwax or a bone problem

Digestive and abdominal conditions

• Constipation: when it’s hard to have a bowel movement
• Functional megacolon: when there is atypical enlargement of the colon without an identifiable cause
• Gastroesophageal reflux: when stomach acid flows back into the throat, causing a burning feeling, also known as heartburn
• Hirschsprung’s disease: a condition where part of the intestine doesn’t work right, making it hard to have a bowel movement
• Umbilical hernia: when a small part of the intestine pushes through the belly button causing a bulge
• Inguinal hernia: when part of the intestine pushes into the groin area causing a bulge there

Bone, muscle, and joint conditions

• Contractures: when muscles or joints get tight and hard to move
• Craniosynostosis: when a baby’s skull bones fuse too early, affecting the shape of the head
• Pectus excavatum: when the chest looks sunken or “caved in”
• Talipes equinovarus (clubfoot): when a baby is born with one or both feet twisted out of shape
• Vertebral anomalies: problems with the bones of the spine which can affect posture and movement

Skin and nail conditions

• Hypoplastic nails: nails that are underdeveloped or smaller than usual
• Skin hyperpigmentation: when parts of the skin are darker than the surrounding areas
• Skin hypopigmentation: when parts of the skin are lighter than the surrounding areas

Growth and development conditions

• Hemihypertrophy: when one side of the body is bigger than the other
• Neonatal hypoglycemia: low blood sugar levels in newborn babies which can make them weak or jittery
• Hypothyroidism: when the thyroid gland (in the neck) doesn’t make enough thyroid hormone which can slow down growth and energy levels
• Premature eruption of teeth in 60 to 80% of individuals

Reproductive and urinary conditions

• Cryptorchidism: when a boy is born with one or both testicles not in the right place
• Hypospadias: when the opening of a boy’s urethra is in a different spot than usual
• Phimosis: when the foreskin on a boy’s penis is too tight to pull back
• Hydrocele: when fluid collects around a testicle causing swelling

Other conditions

• Hemangioma: a red or purple birthmark made of extra blood vessels
• Hypercalcemia: when there’s too much calcium in the blood which can make people feel sick or tired
• Hypodontia: when someone is born with fewer teeth than usual
• Subpleural blebs: small air bubbles that form on the surface of the lungs
• 2/3 toe syndactyly: when the second and third toes are fused together

Approximately 2.2 to 3.9% of people with Sotos syndrome develop tumors, including sacrococcygeal teratoma, neuroblastoma, presacral ganglioma and acute lymphoblastic leukemia.^5,6

Sotos syndrome is not a life-threatening disorder and individuals with the disorder may have a normal life expectancy.¹⁹

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Causes

Sotos syndrome can be caused by changes (variants) or deletions (losses) of the NSD1 gene, ^2,6 or by variants in the NFIX gene¹⁴ or the APC2 gene.¹⁴

•  The NSD1 gene controls when certain genes are turned on or off which affects how the body grows and develops.
• The NFIX gene helps manage the activity of other genes and is important for brain and muscle development as well as blood cell formation and blocks important proteins that help turn genes on or off.²⁰
• The APC2 gene supports brain development by helping nerve cells move to the right places and form connections which is key for a healthy nervous system.

Sotos syndrome 1 is caused by variants in the NSD1 gene or by deletions involving this gene. Variants in this gene have been identified in approximately 90% of people with Sotos syndrome 1.^2,6 The NSD1 gene is found on the long arm (q) of chromosome 5 in the q35 region, and, therefore, Sotos syndrome can also be  caused by a deletion of the NSD1 gene, which is missing when a person has a 5q35 deletion.

Sotos syndrome 2 is caused by variants in the NFIX gene. Variants in this gene have been identified in five individuals.¹⁴

Sotos syndrome 3 is caused by a loss-of-function variant in the APC2 gene. This was reported in two siblings with some neural features of Sotos syndrome including intellectual disability, abnormal brain structure and typical facial features but no other features such as bone or heart abnormalities.¹⁴ The parents were blood relatives (consanguineous). The APC2 gene is specifically expressed in the nervous system and is a crucial downstream gene of NSD1. In other words, variants in the NSD1 gene affect the APC2 gene and result in neural abnormalities.¹⁴

Inheritance

Sotos syndrome 1 and 2

Sotos syndrome 1 and 2 are autosomal dominant genetic conditions. Dominant genetic disorders occur when only a single copy of a disease-causing gene variant is necessary to cause the disease. The gene variant can be inherited from either parent or can be the result of a new (de novo) changed gene in the affected individual that is not inherited. Most people with Sotos syndrome have a de novo NSD1 gene variant. When the parents are unaffected, the risk of having another child with the syndrome is very low (<1%).⁴ The risk of passing the gene variant from an affected parent to a child is 50% for each pregnancy. The risk is the same for males and females.

Sotos syndrome 3

Sotos syndrome 3 is an autosomal recessive condition. Recessive genetic disorders occur when an individual inherits a disease-causing gene variant from each parent. If an individual receives one normal gene and one disease-causing gene variant, the person will be a carrier for the disease but usually will not show symptoms. The risk for two carrier parents to both pass the gene variant and have an affected child is 25% with each pregnancy. The risk of having a child who is a carrier like the parents is 50% with each pregnancy. The chance for a child to receive normal genes from both parents is 25%. The risk is the same for males and females.

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Affected populations

Sotos syndrome affects males and females in equal numbers, occurs in all ethnic groups and has been detected throughout the world. This condition occurs in about one in 14,000 live births.⁹ In patients of Japanese descent, people are more often affected by a gene deletion rather than disease-causing gene variant.

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Disorders with Similar Symptoms

Symptoms of the following disorders may be similar to those of Sotos syndrome. Comparisons may be useful for a differential diagnosis. Confirmation of any of the syndromes can be obtained by genetic testing.

• Weaver syndrome, also known as Weaver-Smith syndrome, is an extremely rare disorder characterized by accelerated growth. Affected individuals have a particular facial appearance that is similar to Sotos syndrome in that a high broad forehead is often present, but the face is usually round (not elongated) with widely spaced eyes (ocular hypertelorism) and an abnormally small jaw. Children often have increased muscle tone (hypertonia) and joint problems. The cause is now known to be variants in the EXH2 gene.
• Bekwith-Wiedemann syndrome (BWS) is a rare inherited disorder characterized by overgrowth, an abnormally large tongue (macroglossia), abnormal creases on the earlobes, protrusion of part of the intestines through an abnormal opening in the muscular abdominal wall near the umbilical cord (omphalocele) and abnormal enlargement of certain abdominal organs (visceromegaly) such as the liver, kidney and/or pancreas and hypoglycemia (low blood glucose) early in life. Most people with BWS have an abnormality in one of several genes located on the number 11 chromosome.
• Simpson-Golabi-Behmel syndrome is an X-linked recessive genetic disorder characterized by overgrowth before and after birth, a particular facial appearance that is different from Sotos syndrome, extra fingers and toes, extra nipples, separation of muscles in the abdominal wall (diastasis recti) and a skeletal abnormality in which the chest bone is depressed (pectus excavatum). This syndrome results from abnormalities (variations or microdeletions) of one of two genes on chromosome X.
• Fragile X syndrome is a genetic disorder caused by an abnormality in a gene on the X chromosome, with more severe symptoms in males and is characterized by intellectual disability, language delays, behavioral problems, autism, or autistic-like behavior (including poor eye contact and hand-flapping), enlarged external genitalia (macroorchidism), large or prominent ears, hyperactivity, delayed motor development and/or poor sensory skills. Affected individuals may also have an abnormally increased growth rate before puberty.

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Diagnosis

Doctors may first suspect Sotos syndrome before birth if unusual features show up during a prenatal ultrasound, such as grooves or indentations in the baby’s developing brain.²¹

After birth, the most recognizable signs and symptoms include:

• A distinct facial appearance
• Rapid growth in height and weight
• Developmental delays

The facial features are the most consistent feature and almost all children with Sotos syndrome have them.^1,4About 10% of children may be shorter than expected, and around 10–15% might not have any developmental delays.⁶

Other signs doctors may look for include:

• Advanced bone age (bones develop faster than typical) occurs in about 76–86% of people with Sotos syndrome.⁶
• Changes in brain structure are seen in over 93% of individuals with Sotos syndrome.
  • The space between the brain and the skull (extra-axial space) may appear larger on imaging which can be misinterpreted as communicating hydrocephalus (a condition where the brain is swollen due to excess fluid).
  • A defining feature of Sotos syndrome is that the increased head size (macrocrania) is not due to increased brain tissue size (megalencephaly).

Genetic testing can confirm the diagnosis of Sotos syndrome.

• DNA studies by FISH (fluorescence in situ hybridization) analysis and MLPA (multiplex ligation-dependent probe amplification) to detect chromosome 5q35 microdeletions and partial NSD1 gene deletions, which account for approximately 10-15% of the cases of Sotos syndrome in western populations.^4,7
• DNA analysis by genome sequencing which can determine the specific NSD1 gene variants.⁵

In people without NSD1 gene variants, genetic testing for variants in NFIX and APC2 genes should be done.¹⁴

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Standard Therapies

Treatment

The treatment of Sotos syndrome is directed toward the specific symptoms that are apparent in each individual. Treatment may require the coordinated efforts of several specialists who should work together as a team in a coordinated way. The team may include pediatricians, pediatric endocrinologists, geneticists, neurologists, surgeons, speech pathologists, specialists who diagnose and treat skeletal disorders (orthopedists), physicians who diagnose and treat eye disorders (ophthalmologists), physical therapists and/or other health care professionals. The team may need to systematically and comprehensively plan an affected child’s treatment.^5,6

Management

To establish the extent of the disease and needs in a person diagnosed with Sotos syndrome, the following evaluations are recommended:

• A detailed medical history to identify known features of Sotos syndrome such as learning difficulties, heart and kidney anomalies, seizures and scoliosis
• Clinical evaluation conducted early in development and on a continuing basis to confirm the presence and extent of developmental delay, psychomotor delay and/or intellectual disability to ensure that appropriate steps are taken to help affected individuals reach their highest potential.⁴
• A detailed physical examination including cardiac auscultation, blood pressure measurement and back examination for scoliosis
• Specific exams to detect abnormalities as soon as possible, before complications occur, such as echocardiogram and renal ultrasound examination and renal ultrasound examination to evaluate for kidney damage and referral for hearing assessment.⁵
• When clinical manifestations (e.g., cardiac anomalies, renal anomalies, scoliosis or seizures) are identified, referral to the appropriate specialist is recommended.
• Physical therapy is recommended to maximize mobility and to reduce the risk for later-onset orthopedic complications (e.g., contractures, scoliosis, hip dislocation).
• Growth-friendly surgery remains an effective treatment method for individuals with Sotos syndrome.^22,23
• Management in consultation with neurologists and neurosurgeons, recommended when raised intracranial pressure is suspected.²³
• Sleep disorders evaluation, which have a great impact on quality of life for patients and their families.¹⁶
• Assessment for symptoms of autism spectrum disordershould be done regularly in children with Sotos syndrome.¹⁵
• Special services that may be beneficial include infant stimulation, special education, special social support, physical therapy, occupational therapy, speech therapy and adaptive physical education.¹⁰
• Muscle stiffness and unusual muscle movements (like tight muscles or jerky movements), may need treatment with medications like baclofen (Botox) or even surgery if needed.²³
• Feeding difficulties including trouble chewing or controlling food in the mouth may be treated with help from a feeding therapist (usually an occupational or speech therapist) ²³
• Communication issues such as trouble speaking may be treated with tools or devices that help people communicate in other ways (like pictures, tablets, or speech-generating devices)²³
• Behavioral problems such as autistic behaviors may be addressed with applied behavior analysis (ABA) which helps with behavior, social skills and daily routines. A developmental pediatrician can also help with behavior strategies or medications if needed. For more serious behavior issues like aggression, a child psychiatrist may be needed.²³
• Antibiotic prophylaxis treatment is indicated in people with vesicoureteral reflux.²³
• Genetic counseling is recommended for families with an affected child.

A small percentage (2.2 to 3.9%) of people with Sotos syndrome may be more prone to developing certain benign tumors and malignancies than the general population, but because the risk of developing tumors or malignancies is low, routine screening is not recommended.^5,6

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Clinical Trials and Studies

Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. Government funding, and some supported by private industry, are posted on this government website.

For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:

Tollfree: (800) 411-1222
TTY: (866) 411-1010
Email: [email protected]

Some current clinical trials also are posted on the following page on the NORD website:
https://rarediseases.org/living-with-a-rare-disease/find-clinical-trials/

For information about clinical trials sponsored by private sources, contact:
www.centerwatch.com

For information about clinical trials conducted in Europe, contact:
https://www.clinicaltrialsregister.eu/

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References

1. Sotos JF, Dodge PR, Muirhead D, et al. Cerebral gigantism in childhood: a syndrome of excessively rapid growth and acromegalic features and a nonprogressive neural disorder. N Engl J Med. 1964;271:109-116. doi: 10.1056/NEJM196407162710301
2. Kurotaki N, Imaizumi K, Harada N, et al. Haploinsufficiency of NSD1 causes Sotos syndrome. Nat Genet. 2002;30(4):365-366. doi:10.1038/ng863
3. Tatton-Brown K, Rahman N. Clinical features of NSD1-positive Sotos syndrome. Clin Dysmophol. 2004;13:199-204.
4. Sotos JF, Argente J. Overgrowth disorders associated with tall stature. Adv Pediatr. 2008;55:213-254. doi:10.1016/j.yapd.2008.07.019
5. Tatton-Brown K, Douglas J, Coleman K, et al. Genotype-phenotype associations in Sotos syndrome: an analysis of 266 individuals with NSD1 aberrations. Am J Hum Genet. 2005;77(2):193-204. doi:10.1086/432082
6. Visser R, Kant SG, Wit JM, Breuning MH. Overgrowth syndromes: from classical to new. Pediatr Endocrinol Rev. 2009;6(3):375-94.
7. Visser R. NSD1 and Sotos Syndrome, Chapter 113. In Eds.: Epstein CJ, Erickson RP, Wynshaw-Boris A. Inborn errors of development: the molecular basis of clinical disorders of morphogenesis. New York, NY: Oxford University Press: 2008:1032-1037.
8. Cole TR, Hughes HE. Sotos syndrome: a study of the diagnostic criteria and natural history. J Med Genet. 1994;31(1):20-32. doi:10.1136/jmg.31.1.20
9. Sotos JF. Sotos Syndrome. In: The NORD Guide to Rare Disorders, Philadelphia, PA: Lippincott, Williams and Wilkins: 2003:255-6.
10. Lane C, Milne E, Freeth M. Cognition and Behaviour in Sotos Syndrome: A Systematic Review. PLoS One. 2016 Feb 12;11(2):e0149189. doi:10.1371/journal
11. Sotos JF. Sotos syndrome 1 and 2. Pediatric Endocrine Reviews (PER). 2014 Sept;12(1):374-388.
12. Online Mendelian Inheritance in Man, OMIM. Johns Hopkins University, Baltimore, MD. SOTOS SYNDROME 1; SOTOS1. MIM Number: 117550. Date last edited: 05/23/2022. Available at https://omim.org/entry/117550. Accessed March 25, 2025.
13. Novara F, Stanzial F, Rossi E, Benedicenti F, Inzana F, Di Gregorio E, Brusco A, Graakjaer J, Fagerberg C, Belligni E, Silengo M, Zuffardi O, Ciccone R. Defining the phenotype associated with microduplication reciprocal to Sotos syndrome microdeletion. Am J Med Genet A. 2014 Aug;164A(8):2084-90. doi: 10.1002/ajmg.a.36591
14. Almuriekhi M, Shintani T, Fahiminiya S, et al. Loss-of-Function Mutation in APC2 Causes Sotos Syndrome Features. Cell Rep. 2015;10(9):1585-1598. doi:10.1016/j.celrep.2015.02.011
15. Riccioni A, Siracusano M, Arturi L, et al. Short report: Autistic symptoms in Sotos syndrome, preliminary results from a case-control study. Res Dev Disabil. 2024;145:104655. doi:10.1016/j.ridd.2023.104655
16. Frattale I, Sarnataro R, Siracusano M, et al. Sleep disturbances and behavioral symptoms in pediatric Sotos syndrome. Front Neurol. 2024;15:1360055. Published 2024 Feb 16. doi:10.3389/fneur.2024.1360055
17. Calcagni G, Ferrigno F, Franceschini A, et al. Congenital Heart Defects in Patients with Molecularly Confirmed Sotos Syndrome. Diagnostics (Basel). 2024;14(6):594. Published 2024 Mar 11. doi:10.3390/diagnostics14060594
18. ​​Schaefer GB, Bodensteiner JB, Buehler BA, Lin A, Cole TR. The neuroimaging findings in Sotos syndrome. Am J Med Genet. 1997;68(4):462-465. doi:10.1002/(sici)1096-8628(19970211)68:4<462::aid-ajmg18>3.0.co;2-q
19. National Institute of Neurological Disorders and Stroke. Sotos Syndrome. National Institutes of Health. Feb 5, 2021 https://www.ninds.nih.gov/health-information/disorders/sotos-syndrome Accessed May 7, 2025.
20. Tauchmann S, Schwaller J. NSD1: A Lysine Methyltransferase between Developmental Disorders and Cancer. Life (Basel). 2021;11(9):877. Published 2021 Aug 25. doi:10.3390/life11090877
21. Luo C, Liu Y, Wang H, et al. Aberrant Fetal Brain Sulcus Formation: A Clue to the Diagnosis of Sotos Syndrome. Prenat Diagn. Published online October 19, 2024. doi:10.1002/pd.6686
22. Verhofste BP, Glotzbecker MP, Marks DS, et al. Spinal Deformity in Sotos Syndrome: First Results of Growth-friendly Spine Surgery. J Pediatr Orthop. 2020;40(9):453-461. doi:10.1097/BPO.0000000000001554
23. Adam MP, Feldman J, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2025. Available from: https://www.ncbi.nlm.nih.gov/sites/books/NBK1116/Accessed May 7, 2025.

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