skip to content »

Molecular and Human Genetics

Houston, Texas

Department of Molecular and Human Genetics
Department of Molecular and Human Genetics
not shown on screen

V. Reid Sutton, M.D.

V. Reid Sutton, M.D.

Associate Professor, Department of Molecular and Human Genetics

Other Positions

Medical Director, Biochemical Genetics Laboratory
Director, Medical Genetics Residency Program
Director, ABMG Diagnostic Laboratory Training Programs

Education

B.A.,Transylvania University, 1988
M.D., University of Kentucky, 1992
Resident, Pediatrics, Washington University, 1996
Fellow, Medical Genetics, Baylor College of Medicine, 1999

Board Certifications

American Board of Medical Genetics: Clinical Genetics and Clinical Biochemical Genetics

Professional Organizations

Member, American Society of Human Genetics
Fellow, American College of Medical Genetics; Member of Professional Practice and Guidelines Committee
Member, International Skeletal Dysplasia Society
Member, Society of Inherited Metabolic Diseases

Clinical Interests

Aicardi syndrome, Focal Dermal Hypoplasia (Goltz syndrome), skeletal dysplasias (Osteogenesis Imperfecta), and inborn errors of metabolism

Research Interests

I am a clinical geneticist with special interests in Aicardi syndrome, Focal Dermal Hypoplasia (Goltz syndrome), skeletal dysplasias (Osteogenesis Imperfecta), and inborn errors of metabolism.

Aicardi Syndrome: Aicardi syndrome is an x-linked disorder that affects multiple organ systems. Common features of Aicardi syndrome include absence or hypoplasia of the corpus callosum, chorioretinal lacunae, seizures, polymicrogyria, heterotopia and vertebral anomalies. Affected individuals are females or males who have a 47,XXY chromosome constitution. I am the clinical geneticist in a multidisciplinary effort to characterize the phenotype of Aicardi syndrome and identify the gene that causes Aicardi syndrome.

Focal Dermal Hypoplasia: Focal dermal hypoplasia (FDH), also known as Goltz syndrome (OMIM 305600), is a genetic disorder that affects multiple organ systems early in development. Features of FDH include skin abnormalities, (hypoplasia, atrophy, linear pigmentation and herniation of fat through dermal defects); papillomas of the mucous membranes; patterning defects of the hands and feet, including syndactyly, polydactyly, camptodactyly and oligodactyly; osteopathia striata; colobomas and other ocular abnormalities; and hypodontia/oligodontia. FDH displays X-linked dominant inheritance; 95 percent of cases are sporadic and only 10 percent of cases are males. We have recently demonstrated that most cases of FDH are due to mutations in PORCN, a gene that is required for the post-translational modification and secretion of Wnt proteins. I am the clinical geneticist in a multidisciplinary effort to characterize the phenotype of FDH.

Skeletal Dysplasias: I am the Co-Director for the Osteogenesis Imperfecta Foundation’s Linked Clinical Research Centers and one of three clinical geneticists who launched the multidisciplinary skeletal dysplasia clinic at Texas Children's Hospital. In conjunction with staff from orthopedics, radiology, endocrinology, and neurology, we provide care to children and adults with skeletal dysplasias and disorders of bone and mineral metabolism.

Inborn Errors of Metabolism: As an attending physician in the metabolic clinic at Texas Children's Hospital, I endeavor to provide state-of-the-art medical care and diagnostic services to patients with a broad range of metabolic diseases.

Selected Publications

  1. Sutton VR, Plunkett K, Dang DX, Lewis RA, Bree AF, Bacino CA (2009). Craniofacial and anthropometric phenotype in ankyloblepharon-ectodermal defects-cleft lip/palate syndrome (Hay-Wells syndrome) in a cohort of 17 patients. Am. J. Med. Genet. A. 149A(9): 1916-21. [Pub Med]
  2. Wang X*, Sutton VR*, Peraza O, Yu Z, Rosetta R, Kou YC, Eble TN, Patel A, Thaller C, Fang P, Van den Veyver IB (2007). Mutations in X-linked PORCN, a putative regulator of Wnt signaling, cause focal dermal hypoplasia. Nat. Genet. 39(7): 836-8. *Equal contribution [Pub Med]
  3. Cheung SW, Shaw CA, Scott DA, Patel A, Sahoo T, Bacino CA, Pursley A, Li J, Erickson R, Gropman AL, Miller DT, Seashore MR, Summers AM, Stankiewics P, Chinault AC, Lupski JR, Beaudet AL, Sutton VR (2007). Microarray-based CGH detects chromosomal mosaicism not revealed by conventional cytogenetics. Am. J. Med. Genet. A. 143A(15): 1679-86. [Pub Med]
  4. Glasmacher MAK, Sutton VR, Hopkins BJ, Eble T, Lewis RA, Park-Parsons D, Van den Veyver IB. Phenotype and management of Aicardi syndrome: New findings from a survey of 69 children. J. Child Neurol. 22(2): 176-84. [Pub Med]
  5. Sutton VR, Van den Veyver IB. Aicardi syndrome. In GeneReviews at GeneTests: Medical Genetics Information Resource (database online). Copyright, University of Washington, Seattle, 1997-2006. [GeneTests]
  6. Sutton VR, Hopkins BJ, Gambhir N, Lewis RA, Van den Veyver IB (2005). Facial and physical features of Aicardi syndrome: Infants to teenagers. Am. J. Med. Genet. A. 138A(3): 254-8. [Pub Med]
  7. Sutton VR, Hyland JC, Phillips WA, Schlesinger AE, Brill PW (2005). A Dominantly Inherited Spondylometaphyseal Dysplasia with “Corner Fractures” and Congenital Scoliosis. Am. J. Med. Genet. A. 133A(2): 209-12. [Pub Med]
  8. Sutton VR, McAlister WH, Bertin TK, Kaffe S, Wang JC, Yano S, Shaffer LG, Lee B, Epstein CJ, Villar AJ (2003). Skeletal Defects in Paternal Uniparental Disomy for Chromosome 14 are Recapitulated in the Mouse Model (Paternal Uniparental Disomy 12). Hum. Genet. 113(5): 447-51. [Pub Med]
  9. Sutton VR, Pan Y, Davis EC, Beaudet AL, Craigen WJ (2003). A Mouse Model of Argininosuccinic Aciduria: Biochemical Characterization. Mol. Genet. Metab. 78(1): 11-6. [Pub Med]

More Publications (PubMed)

Contact Information

V. Reid Sutton, M.D.
Director, ABMG Diagnostic Laboratory Training Programs
Texas Children's Hospital
6621 Fannin St. Mail Code: CC-1560
Houston, TX 77030, U.S.A.

Phone: 832-822-4292
Fax: 832-825-4294
E-mail:

E-mail this page to a friend