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Multiple Cutaneous and Mucosal Venous Malformations

Synonym: VMCM1

, MD, PhD and , MD, PhD.

Author Information
, MD, PhD
Center for Vascular Anomalies
Division of Plastic Surgery
Cliniques Universitaires Saint Luc &
Université catholique de Louvain
Brussels, Belgium
, MD, PhD
Human Molecular Genetics
de Duve Institute
Université catholique de Louvain
Brussels, Belgium

Initial Posting: ; Last Update: January 29, 2015.


Clinical characteristics.

The condition multiple cutaneous and mucosal venous malformations (VMCM) is characterized by the presence of small, multifocal bluish cutaneous and/or mucosal venous malformations. They are usually present at birth. New lesions appear with time. Small lesions are usually asymptomatic; larger lesions can invade subcutaneous muscle and cause pain. Malignant transformation has not been reported.


Diagnosis of VMCM is based on clinical evaluation of the cutaneous and mucosal lesions. Doppler ultrasound examination and MRI can be used to confirm the venous component and extent of lesions. TEK (also known as TIE2) is the only gene in which pathogenic variants are known to cause VMCM.


Treatment of manifestations: Sclerotherapy, alone or in combination with plastic and reconstructive surgery, is used depending on the size and location of the lesions. When D-dimers are elevated, low molecular-weight heparin can be used to treat the associated pain.

Prevention of secondary complications: If the D-dimer level is greater than twice the normal range, low molecular-weight heparin should be initiated before any surgery to avoid disseminated intravascular coagulopathy.

Agents/circumstances to avoid: Contraceptive pills with high estrogen levels.

Evaluation of relatives at risk: Physical examination of at-risk neonates to identify those who can benefit from early treatment.

Genetic counseling.

VMCM is inherited in an autosomal dominant manner. Most individuals diagnosed with VMCM have an affected parent; the proportion of cases caused by de novo mutation is unknown; none has been reported to date. Each child of an individual with VMCM has a 50% chance of inheriting the pathogenic variant. Prenatal testing for pregnancies at increased risk is possible if the TEK pathogenic variant has been identified in an affected family member.


Suggestive Findings

Diagnosis of multiple cutaneous and mucosal venous malformations (VMCM) should be suspected in individuals with the following clinical and laboratory findings.

Clinical. Small, multifocal cutaneous and/or mucosal bluish-purple vascular malformations are present (see Figure 1) [Wouters et al 2008, Dompmartin et al 2010, Wouters et al 2010, Boon et al 2011, Boon & Vikkula 2012, Boon & Vikkula 2013]:

Figure 1.

Figure 1.

Multifocal mucocutaneous venous malformations (marked by arrows): (A) on the tongue; (B) on the neck; (C) in the supraclavicular area (scar of a resected VMCM, arrow heads); (D) on the distal forearm/wrist

  • Lesions are soft and usually compressible.
  • Doppler ultrasound examination can be used to confirm slow blood flow.
  • Ultrasound examination reveals saccular compressible venous-like cavities.

Family history is consistent with autosomal dominant inheritance.

Laboratory. D-dimer concentration may be elevated in individuals with multifocal VMCM, whereas it is normal in individuals with multifocal glomuvenous malformations:

Establishing the Diagnosis

The diagnosis of VMCM is established in a proband with the identification of a heterozygous pathogenic variant in TEK (previously known as TIE2), the only gene in which pathogenic variants are known to cause VMCM [Vikkula et al 1996, Brouillard & Vikkula 2007, Wouters et al 2008, Wouters et al 2010] (see Table 1).

One genetic testing strategy is molecular genetic testing of TEK. Sequence analysis is performed first followed by deletion/duplication analysis if no pathogenic variant is found.

An alternative genetic testing strategy is use of a multi-gene panel that includes TEK and other genes of interest (see Differential Diagnosis). Note: The genes included and the methods used in multi-gene panels vary by laboratory and over time.

Table 1.

Summary of Molecular Genetic Testing Used in Multiple Cutaneous and Mucosal Venous Malformations

Gene 1Test MethodProportion of Probands with a Pathogenic Variant Detectable by This Method
TEKSequence analysis 232/32 3
Deletion/duplication analysis 4None reported

See Table A. Genes and Databases for chromosome locus and protein name. See Molecular Genetics for information on allelic variants.


Sequence analysis detects variants that are benign, likely benign, of unknown significance, likely pathogenic, or pathogenic. Pathogenic variants may include small intragenic deletions/insertions and missense, nonsense, and splice site variants; typically, exonic or whole-gene deletions/duplications are not detected. For issues to consider in interpretation of sequence analysis results, click here.


Testing that identifies deletions/duplications not readily detectable by sequence analysis of the coding and flanking intronic regions of genomic DNA; included in the variety of methods that may be used are: quantitative PCR, long-range PCR, multiplex ligation-dependent probe amplification (MLPA), and chromosomal microarray (CMA) that includes this gene/chromosome segment.

Clinical Characteristics

Clinical Description

The most typical finding in multiple cutaneous and mucosal venous malformations (VMCM) is presence of small multifocal cutaneous and/or mucosal venous malformations of bluish color [Vikkula et al 1996, Brouillard & Vikkula 2007, Wouters et al 2010, Boon & Vikkula 2012]. They are usually present at birth and increase in size as the affected child grows. New lesions appear with time. Their size ranges from one millimeter up to one centimeter.

Small millimetric lesions are usually asymptomatic, but can be of aesthetic concern. They do not usually bleed or ulcerate. Larger lesions (up to a few centimeters in diameter) can invade subcutaneous muscles and cause pain.

The size, number, and localization of lesions vary within and between families. Often one individual in a family has more extensive lesions than other family members; conversely, some family members may have only a few small, clinically insignificant lesions. Lesions are randomly located throughout the body. In rare cases, they can affect the GI and/or anal mucosa (in contrast to the oral mucosa, which is more typically affected) [Vikkula et al 1996, Brouillard & Vikkula 2007, Wouters et al 2010, Boon & Vikkula 2012].

Malignant transformation of the vascular malformations has not been reported.

Histologic findings. Enlarged venous-like channels with walls of smooth muscle of variable thickness are observed [Vikkula et al 1996]. The endothelium is flattened but continuous. If rounded mural cells (glomus cells) are observed, the diagnosis is glomuvenous malformation [Boon et al 2004, Brouillard et al 2005, Brouillard et al 2008, Brouillard et al 2013] (see Differential Diagnosis).

Genotype-Phenotype Correlations

No genotype-phenotype correlation has been reported.

  • All pathogenic variants identified to date are located in the parts of the gene coding for the tyrosine kinase domains of the receptor.
  • Intra- and interfamilial variation in expression of the phenotype is wide.


Approximately 90% of individuals who have a pathogenic variant in TEK develop mucocutaneous venous malformations by age 20 years; conversely, approximately 10% of individuals with a TEK pathogenic variant are clinically unaffected [Boon et al 2004, Wouters et al 2010].


Terms used previously to describe venous malformation include “cavernous angioma” and sometimes “cavernous hemangioma.”

The term mucocutaneous venous malformation was coined by Boon et al [1994] for the lesions identified in a large multigenerational family from the US.

The abbreviation VMCM stands for venous malformation cutaneous and mucosal.


The prevalence of VMCM is unknown; however, it accounts for about 1% of individuals with venous anomalies followed in multidisciplinary centers specializing in vascular abnormalities [Boon et al 2004].

Differential Diagnosis

Glomuvenous malformations (OMIM 138000), like multiple cutaneous and mucosal venous malformations (VMCM), are multifocal, small cutaneous venous-like lesions, but they are not usually seen on mucous membranes. They have a cobblestone appearance [Boon et al 2004, Mallory et al 2006, Brouillard et al 2013]. Glomuvenous malformations are deeper purple in color than VMCM, are painful on palpation, and are less invasive than sporadic venous malformations. Most lesions are located on the extremities. Histologically, they are characterized by the presence of abnormal mural cells called “glomus cells.”

Glomuvenous malformations are caused by loss-of-function mutations in GLMN, the gene encoding the protein glomulin [Brouillard et al 2002, Brouillard et al 2005, Brouillard et al 2013]. Inheritance is autosomal dominant although the pathophysiologic mechanism is paradominant (i.e., disease caused by presence of a germline mutation and a somatic mutation), most frequently as a result of acquired uniparental isodisomy [Brouillard et al 2002, Amyere et al 2013].

Blue rubber bleb nevus (BRBN) syndrome (OMIM 112200) is characterized by small multifocal cutaneous and mucosal venous-like lesions. They are rubbery blebs, often round and hyperkeratotic. They are associated with gastrointestinal lesions that often cause bleeding and severe chronic anemia. BRBN occurs sporadically. The etiology is not known.


Evaluations Following Initial Diagnosis

To establish the extent of disease and needs of an individual diagnosed with multiple cutaneous and mucosal venous malformations (VMCM), the following evaluations are recommended:

Biopsy is usually not necessary for diagnosis

Treatment of Manifestations

Management depends largely on the size and location of the lesions. Treatment is required for any symptomatic VMCM lesion. Although sclerotherapy is the treatment of choice, sclerosing agents are not specific and can lead to ulceration if the VMCM is mucosal or involves the epidermis [Hammer et al 2001, Dompmartin et al 2010, Boon et al 2011]. Foam aethoxysclerol and bleomycin are preferentially used as sclerosing agents. Surgery gives a consistently better result if it is performed after sclerotherapy.

If lesions are painful and D-dimers are elevated, low molecular-weight heparin can be used to alleviate pain [Dompmartin et al 2008].

Prevention of Secondary Complications

If VMCM is associated with localized intravascular coagulopathy (LIC) (D-dimer level greater than twice the normal range), treatment with low molecular-weight heparin should be initiated before any surgery in order to avoid perioperative decompensation of LIC into disseminated intravascular coagulopathy (DIC).


Because VMCM lesions can increase in size over time and become painful or symptomatic, affected individuals should be reevaluated yearly or whenever symptoms arise.

Agents/Circumstances to Avoid

Contraceptive pills with high estrogen levels should be avoided, as venous malformation lesions are estrogen dependent. Venous malformations can increase in size and become symptomatic, especially at initiation of estrogen-based contraception. (In some, but not all, instances, stabilization of a venous malformation lesion and diminution of pain may be observed after three months of contraceptive pill use.)

Evaluation of Relatives at Risk

Evaluating at-risk neonates by physical examination is appropriate in order to identify those who may benefit from early treatment.

Lesions arising after infancy usually stay small and therefore are rarely symptomatic. If no lesions are seen at birth, a second evaluation should be done around puberty.

If the TEK pathogenic variant has been identified in the family, molecular genetic testing can be used to evaluate at-risk relatives.

See Genetic Counseling for issues related to testing of at-risk relatives for genetic counseling purposes.

Pregnancy Management

During pregnancy, affected women may develop small new lesions; in addition, existing lesions may increase in size and become painful. If the D-dimer level is high, low molecular-weight heparin therapy may be used to alleviate pain.

Therapies Under Investigation

Search for access to information on clinical studies for a wide range of diseases and conditions. Note: There may not be clinical trials for this disorder.

Genetic Counseling

Genetic counseling is the process of providing individuals and families with information on the nature, inheritance, and implications of genetic disorders to help them make informed medical and personal decisions. The following section deals with genetic risk assessment and the use of family history and genetic testing to clarify genetic status for family members. This section is not meant to address all personal, cultural, or ethical issues that individuals may face or to substitute for consultation with a genetics professional. —ED.

Mode of Inheritance

Multiple cutaneous and mucosal venous malformations (VMCM) is inherited in an autosomal dominant manner.

Risk to Family Members

Parents of a proband

  • Most individuals diagnosed with VMCM have an affected parent.
    • The family history may appear to be negative because of failure to recognize the disorder in a parent because of:
      • A milder phenotypic presentation; or
      • Incomplete penetrance.
    • The family history may also appear to be negative because early death of the parent before the onset of symptoms or late onset of the disease in the affected parent.
  • An apparently negative family history cannot be confirmed until appropriate evaluations of the proband’s parents (testing for the TEK pathogenic variant identified in the proband and careful dermatologic evaluation) have been performed.
  • If neither parent of a proband has clinical evidence of VMCM and the TEK pathogenic variant found in the proband cannot be detected in leukocyte DNA of either parent, the proband’s mutation is likely de novo. The proportion of cases caused by de novo mutation is unknown; to date none has been reported.

Note: Somatic mosaicism for a TEK pathogenic variant causes either multifocal, sporadic venous malformations or a single venous malformation [Limaye et al 2009].

Sibs of a proband

  • The risk to the sibs of the proband depends on the genetic status of the proband’s parents.
  • If a parent of the proband is affected, the risk to the sibs is 50%.
  • Ten percent of individuals with a TEK pathogenic variant will not have findings of VMCM; therefore, when the parents of the proband are clinically unaffected the sibs of a proband may still be at risk.
  • Although no instances of germline mosaicism have been reported, it remains a possibility.

Offspring of a proband. Each child of an individual with VMCM has a 50% chance of inheriting the TEK pathogenic variant.

Other family members of a proband

  • The risk to other family members depends on the status of the proband's parents.
  • If a parent is affected, his or her family members are at risk.

Related Genetic Counseling Issues

See Management, Evaluation of Relatives at Risk for information on evaluating at-risk relatives for the purpose of early diagnosis and treatment.

Considerations in families with an apparent de novo mutation. When neither parent of a proband with VMCM has the pathogenic variant or clinical evidence of the disorder, the TEK mutation is likely de novo. However, possible non-medical explanations including alternate paternity or maternity (e.g., with assisted reproduction) or undisclosed adoption could also be explored.

Family planning

  • The optimal time for determination of genetic risk is before pregnancy.
  • It is appropriate to offer genetic counseling (including discussion of potential risks to offspring and reproductive options) to young adults who are affected.

DNA banking is the storage of DNA (typically extracted from white blood cells) for possible future use. Because it is likely that testing methodology and our understanding of genes, allelic variants, and diseases will improve in the future, consideration should be given to banking DNA of affected individuals.

Prenatal Testing

Molecular genetic testing. If the TEK pathogenic variant has been identified in an affected family member, prenatal testing for pregnancies at increased risk may be available from a clinical laboratory that offers either testing of this gene or custom prenatal testing.

Imaging studies. Prenatal diagnosis of VMCM has not been reported. The number and size of fetal lesions are variable and unpredictable. Doppler ultrasonography may be used to evaluate for fetal lesions in those fetuses at increased risk for VMCM but the small size of the lesions makes them difficult to detect.

Requests for prenatal testing for conditions which (like VMCM) do not affect intellect and have some treatment available are not common. Differences in perspective may exist among medical professionals and within families regarding the use of prenatal testing, particularly if the testing is being considered for the purpose of pregnancy termination rather than early diagnosis. Although most centers would consider decisions about prenatal testing to be the choice of the parents, discussion of these issues is appropriate.

Preimplantation genetic diagnosis (PGD) may be an option for some families in which the TEK pathogenic variant has been identified.


GeneReviews staff has selected the following disease-specific and/or umbrella support organizations and/or registries for the benefit of individuals with this disorder and their families. GeneReviews is not responsible for the information provided by other organizations. For information on selection criteria, click here.

  • Foundation for Faces of Children
    258 Harvard Street
    Brookline MA 02446-2904
    Phone: 617-355-8299
  • Vascular Anomaly Patient Association (VASCAPA)
    Avenue Hippocrate 75
    Brussels B-1200

Molecular Genetics

Information in the Molecular Genetics and OMIM tables may differ from that elsewhere in the GeneReview: tables may contain more recent information. —ED.

Table A.

Multiple Cutaneous and Mucosal Venous Malformations: Genes and Databases

Gene SymbolChromosomal LocusProtein NameLocus SpecificHGMD
TEK9p21​.2Angiopoietin-1 receptorTEK databaseTEK

Data are compiled from the following standard references: gene symbol from HGNC; chromosomal locus, locus name, critical region, complementation group from OMIM; protein name from UniProt. For a description of databases (Locus Specific, HGMD) to which links are provided, click here.

Table B.

OMIM Entries for Multiple Cutaneous and Mucosal Venous Malformations (View All in OMIM)


Gene structure. TEK has 24 exons. For a detailed summary of gene and protein information, see Table A, Gene Symbol.

Pathogenic allelic variants. Eight pathogenic variants have been reported (see Table 2; Table A, HGMD). The c.2545C>T substitution was detected in six families [Vikkula et al 1996, Wouters et al 2010, Boon et al 2011].

Paradominant inheritance (i.e., presence of a germline mutation and a somatic mutation) may be the mechanism of disease causation, as demonstrated by the somatic ‘second hit’ identified in one VMCM tissue [Limaye et al 2009].

Table 2.

TEK Pathogenic Allelic Variants Discussed in This GeneReview

DNA Nucleotide ChangeProtein Amino Acid ChangeReference Sequences

Note on variant classification: Variants listed in the table have been provided by the authors. GeneReviews staff have not independently verified the classification of variants.

Note on nomenclature: GeneReviews follows the standard naming conventions of the Human Genome Variation Society (www​ See Quick Reference for an explanation of nomenclature.

Normal gene product. The normal gene product, TEK, is a dimeric receptor tyrosine kinase mostly expressed on vascular endothelial cells. TEK binds the ligands angiopoietin 1, 2, and 4. Its function is important for endothelial cell proliferation, survival, and migration during angiogenesis, and later for vascular stability.

Abnormal gene product. Mutant TEK has increased autophosphorylation (a gain-of-function mutation) and can activate STAT1 signaling, in contrast to wild-type TEK [Korpelainen et al 1999, Limaye et al 2009, Boon et al 2011]. PI3K-AKT-FOXO1 pathway is activated, leading to reduced PDGF-beta production [Uebelhoer et al 2013]. A somatic second hit identified in one VMCM tissue is a loss-of-function mutation [Limaye et al 2009].


Literature Cited

  1. Amyere M, Aerts V, Brouillard P, McIntyre BA, Duhoux FP, Wassef M, Enjolras O, Mulliken JB, Devuyst O, Antoine-Poirel H, Boon LM, Vikkula M. Somatic uniparental isodisomy explains multifocality of glomuvenous malformations. Am J Hum Genet. 2013;92:188–96. [PMC free article: PMC3567282] [PubMed: 23375657]
  2. Boon LM, Enjolras O, Mulliken JB, Vikkula M. Vascular malformations. In: Irvine A, Hoeger P, Yan A, eds. Harper’s Textbook of Pediatric Dermatology. 3 ed. Wiley-Blackwell; 2011:112.1-112.24.
  3. Boon LM, Vikkula M. Molecular genetics of vascular malformations. In: Mulliken JB, Burrown PE, Fishman SJ, eds: Mulliken and Young’s Vascular Anomalies: Hemangiomas and Malformations. 2 ed. New York, NY: Oxford University Press; 2013:327-75.
  4. Boon LM, Mulliken JB, Enjolras O, Vikkula M. Glomuvenous malformation (glomangioma) and venous malformation: distinct clinicopathologic and genetic entities. Arch Dermatol. 2004;140:971–6. [PubMed: 15313813]
  5. Boon LM, Mulliken JB, Vikkula M, Watkins H, Seidman J, Olsen BR, Warman ML. Assignment of a locus for dominantly inherited venous malformations to chromosome 9p. Hum Mol Genet. 1994;3:1583–7. [PubMed: 7833915]
  6. Boon LM, Vikkula M. Vascular anomalies. In: Fitzpatrick’s Dermatology in General Medicine. 8 ed. New York, NY: McGraw-Hill Professional Publishing; 2012.
  7. Brouillard P, Boon LM, Mulliken JB, Ghassibé M, Warman ML, Tan OT, Olsen BR, Vikkula M. Mutations in a novel factor, glomulin, are responsible for glomuvenous malformations ("glomangiomas"). Am J Hum Genet. 2002;70:866–74. [PMC free article: PMC379115] [PubMed: 11845407]
  8. Brouillard P, Boon LM, Revencu N, Berg J, Dompmartin A, Dubois J, Garzon M, Holden S, Kangesu L, Labrèze C, Lynch SA, McKeown C, Meskauskas R, Quere I, Syed S, Vabres P, Wassef M, Mulliken JB, Vikkula M., GVM Study Group. Genotypes and phenotypes of 162 families with a glomulin mutation. Mol Syndromol. 2013;4:157–64. [PMC free article: PMC3666456] [PubMed: 23801931]
  9. Brouillard P, Enjolras E, Boon LM, Vikkula M. Glomulin and glomuvenous malformation. In: Epstein CJ, Erickson RP, Wynshaw-Boris A, eds. Inborn Errors of Development. New York, NY: Oxford University Press; 2008.
  10. Brouillard P, Ghassibé M, Penington A, Boon LM, Dompmartin A, Temple IK, Cordisco M, Adams D, Piette F, Harper JI, Syed S, Boralevi F, Taïeb A, Danda S, Baselga E, Enjolras O, Mulliken JB, Vikkula M. Four common glomulin mutations cause two thirds of glomuvenous malformations ("familial glomangiomas"): evidence for a founder effect. J Med Genet. 2005;42:e13. [PMC free article: PMC1735996] [PubMed: 15689436]
  11. Brouillard P, Vikkula M. Genetic causes of vascular malformations. Hum Mol Genet. 2007;16 Spec No. 2:R140-9. [PubMed: 17670762]
  12. Calvert JT, Riney TJ, Kontos CD, Cha EH, Prieto VG, Shea CR, Berg JN, Nevin NC, Simpson SA, Pasyk KA, Speer MC, Peters KG, Marchuk DA. Allelic and locus heterogeneity in inherited venous malformations. Hum Mol Genet. 1999;8:1279–89. [PubMed: 10369874]
  13. Dompmartin A, Acher A, Dompmartin A, Acher A, Thibon P, Tourbach S, Hermans C, Deneys V, Pocock B, Lequerrec A, Labbé D, Barrellier M-T, Vanwijck R, Vikkula M, Boon LM. Association of localized intravascular coagulopathy with venous malformations. Arch Dermatol. 2008;144:873–7. [PubMed: 18645138]
  14. Dompmartin A, Vikkula M, Boon LM. Venous malformation: update on aetiopathogenesis, diagnosis and management. Phlebology. 2010;25:224–35. [PMC free article: PMC3132084] [PubMed: 20870869]
  15. Hammer FD, Boon LM, Mathurin P, Vanwijck RR. Ethanol sclerotherapy of venous malformations: evaluation of systemic ethanol contamination. J Vasc Interv Radiol. 2001;12:595–600. [PubMed: 11340138]
  16. Korpelainen EI, Karkkainen M, Gunji Y, Vikkula M, Alitalo K. Endothelial receptor tyrosine kinases activate the STAT signaling pathway: mutant Tie-2 causing venous malformations signals a distinct STAT activation response. Oncogene. 1999;18:1–8. [PubMed: 9926914]
  17. Limaye N, Wouters V, Uebelhoer M, Tuominen M, Wirkkala R, Mulliken JB, Eklund L, Boon LM, Vikkula M. Somatic mutations in angiopoietin receptor gene TEK cause solitary and multiple sporadic venous malformations. Nat Genet. 2009;41:118–24. [PMC free article: PMC2670982] [PubMed: 19079259]
  18. Mallory SB, Enjolras O, Boon LM, Rogers E, Berk DR, Blei F, Baselga E, Ros AM, Vikkula M. Congenital plaque-type glomuvenous malformations presenting in childhood. Arch Dermatol. 2006;142:892–6. [PubMed: 16847206]
  19. Uebelhoer M, Nätynki M, Kangas J, Mendola A, Nguyen HL, Soblet J, Godfraind C, Boon LM, Eklund L, Limaye N, Vikkula M. Venous malformation-causative TIE2 mutations mediate an AKT-dependent decrease in PDGFB. Hum Mol Genet. 2013;22:3438–48. [PMC free article: PMC3736867] [PubMed: 23633549]
  20. Vikkula M, Boon LM, Carraway KL III, Calvert JT, Diamonti AJ, Goumnerov B, Pasyk KA, Marchuk DA, Warman ML, Cantley LC, Mulliken JB, Olsen BR. Vascular dysmorphogenesis caused by an activating mutation in the receptor tyrosine kinase TIE2. Cell. 1996;87:1181–90. [PubMed: 8980225]
  21. Wouters V, Boon LM, Vikkula M. TIE2 and cutaneomucosal venous malformation. In: Epstein CJ, Erickson RP, Wynshaw-Boris A, eds. Inborn Errors of Development. New York, NY: Oxford University Press; 2008.
  22. Wouters V, Limaye N, Uebelhoer M, Irrthum A, Boon LM, Mulliken JB, Enjolras O, Baselga E, Berg J, Dompmartin A, Ivarsson SA, Kangesu L, Lacassie Y, Teebi AS, Pennington A, Rieu P, Vikkula M. Hereditary cutaneomucosal venous malformations are caused by TIE2 mutations with widely variable hyper-phosphorylating effects. Eur J Hum Genet. 2010;18:414–20. [PMC free article: PMC2841708] [PubMed: 19888299]

Chapter Notes

Author Notes

Centre for Vascular Anomalies, Cliniques Universitaires St Luc
Dr. Vikkula, de Duve Institute

Revision History

  • 29 January 2015 (me) Comprehensive update posted live
  • 23 August 2012 (me) Comprehensive update posted live
  • 18 September 2008 (me) Review posted live
  • 17 January 2008 (mv) Original submission
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