Format

Send to:

Choose Destination

Tuberous sclerosis 2(TSC2)

MedGen UID:
348170
Concept ID:
C1860707
Disease or Syndrome
Synonyms: TSC2
Modes of inheritance:
Heterogeneous
MedGen UID:
67020
Concept ID:
C0242960
Organism Attribute
Source: HPO
The presence of apparently similar characters for which the genetic evidence indicates that different genes or different genetic mechanisms are involved in different pedigrees. In clinical settings genetic heterogeneity refers to the presence of a variety of genetic defects which cause the same disease, often due to mutations at different loci on the same gene, a finding common to many human diseases including ALZHEIMER DISEASE; CYSTIC FIBROSIS; LIPOPROTEIN LIPASE DEFICIENCY, FAMILIAL; and POLYCYSTIC KIDNEY DISEASES. (Rieger, et al., Glossary of Genetics: Classical and Molecular, 5th ed; Segen, Dictionary of Modern Medicine, 1992)
Autosomal dominant inheritance
MedGen UID:
141047
Concept ID:
C0443147
Intellectual Product
Sources: HPO, OMIM, Orphanet
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.
Autosomal dominant inheritance (HPO, OMIM, Orphanet)
 
Genes (locations): IFNG (12q15); TSC2 (16p13.3)
OMIM®: 613254

Disease characteristics

Excerpted from the GeneReview: Tuberous Sclerosis Complex
Tuberous sclerosis complex (TSC) involves abnormalities of the skin (hypomelanotic macules, facial angiofibromas, shagreen patches, cephalic plaques, ungual fibromas); brain (cortical dysplasias, subependymal nodules and subependymal giant cell astrocytomas [SEGAs], seizures, intellectual disability/developmental delay, psychiatric illness); kidney (angiomyolipomas, cysts, renal cell carcinomas); heart (rhabdomyomas, arrhythmias); and lungs (lymphangioleiomyomatosis [LAM]). CNS tumors are the leading cause of morbidity and mortality; renal disease is the second leading cause of early death. [from GeneReviews]
Authors:
Hope Northrup  |  Mary Kay Koenig  |  Deborah A Pearson, et. al.   view full author information

Additional descriptions

From OMIM
Tuberous sclerosis complex (TSC) is an autosomal dominant multisystem disorder characterized by hamartomas in multiple organ systems, including the brain, skin, heart, kidneys, and lung. These changes can result in epilepsy, learning difficulties, behavioral problems, and renal failure, among other complications (reviews by Crino et al., 2006 and Curatolo et al., 2008). For a general phenotypic description and a discussion of genetic heterogeneity of tuberous sclerosis, see tuberous sclerosis-1 (191100), caused by mutation in the TSC1 gene (605284) on chromosome 9q34. Approximately 10 to 30% of cases of tuberous sclerosis are due to mutations in the TSC1 gene: the frequency of cases due to mutations in the TSC2 gene is consistently higher. TSC2 mutations are associated with more severe disease (Crino et al., 2006) (see GENOTYPE/PHENOTYPE CORRELATIONS section).  http://www.omim.org/entry/613254
From GHR
Tuberous sclerosis complex is a genetic disorder characterized by the growth of numerous noncancerous (benign) tumors in many parts of the body. These tumors can occur in the skin, brain, kidneys, and other organs, in some cases leading to significant health problems. Tuberous sclerosis complex also causes developmental problems, and the signs and symptoms of the condition vary from person to person.Virtually all affected people have skin abnormalities, including patches of unusually light-colored skin, areas of raised and thickened skin, and growths under the nails. Tumors on the face called facial angiofibromas are also common beginning in childhood.Tuberous sclerosis complex often affects the brain, causing seizures, behavioral problems such as hyperactivity and aggression, and intellectual disability or learning problems. Some affected children have the characteristic features of autism, a developmental disorder that affects communication and social interaction. Benign brain tumors can also develop in people with tuberous sclerosis complex; these tumors can cause serious or life-threatening complications.Kidney tumors are common in people with tuberous sclerosis complex; these growths can cause severe problems with kidney function and may be life-threatening in some cases. Additionally, tumors can develop in the heart, lungs, and the light-sensitive tissue at the back of the eye (the retina).  https://ghr.nlm.nih.gov/condition/tuberous-sclerosis-complex

Clinical features

Astrocytoma
MedGen UID:
438
Concept ID:
C0004114
Neoplastic Process
A glial tumor of the brain or spinal cord showing astrocytic differentiation. It includes the following clinicopathological entities: pilocytic astrocytoma, diffuse astrocytoma, anaplastic astrocytoma, pleomorphic xanthoastrocytoma, subependymal giant cell astrocytoma, and glioblastoma.
Autistic disorder of childhood onset
MedGen UID:
13966
Concept ID:
C0004352
Mental or Behavioral Dysfunction
Autism, the prototypic pervasive developmental disorder (PDD), is usually apparent by 3 years of age. It is characterized by a triad of limited or absent verbal communication, a lack of reciprocal social interaction or responsiveness, and restricted, stereotypic, and ritualized patterns of interests and behavior (Bailey et al., 1996; Risch et al., 1999). 'Autism spectrum disorder,' sometimes referred to as ASD, is a broader phenotype encompassing the less severe disorders Asperger syndrome (see ASPG1; 608638) and pervasive developmental disorder, not otherwise specified (PDD-NOS). 'Broad autism phenotype' includes individuals with some symptoms of autism, but who do not meet the full criteria for autism or other disorders. Mental retardation coexists in approximately two-thirds of individuals with ASD, except for Asperger syndrome, in which mental retardation is conspicuously absent (Jones et al., 2008). Genetic studies in autism often include family members with these less stringent diagnoses (Schellenberg et al., 2006). Levy et al. (2009) provided a general review of autism and autism spectrum disorder, including epidemiology, characteristics of the disorder, diagnosis, neurobiologic hypotheses for the etiology, genetics, and treatment options. Genetic Heterogeneity of Autism Autism is considered to be a complex multifactorial disorder involving many genes. Accordingly, several loci have been identified, some or all of which may contribute to the phenotype. Included in this entry is AUTS1, which has been mapped to chromosome 7q22. Other susceptibility loci include AUTS3 (608049), which maps to chromosome 13q14; AUTS4 (608636), which maps to chromosome 15q11; AUTS5 (606053), which maps to chromosome 2q; AUTS6 (609378), which maps to chromosome 17q11; AUTS7 (610676), which maps to chromosome 17q21; AUTS8 (607373), which maps to chromosome 3q25-q27; AUTS9 (611015), which maps to chromosome 7q31; AUTS10 (611016), which maps to chromosome 7q36; AUTS11 (610836), which maps to chromosome 1q41; AUTS12 (610838), which maps to chromosome 21p13-q11; AUTS13 (610908), which maps to chromosome 12q14; AUTS14A (611913), which has been found in patients with a deletion of a region of 16p11.2; AUTS14B (614671), which has been found in patients with a duplication of a region of 16p11.2; AUTS15 (612100), associated with mutation in the CNTNAP2 gene (604569) on chromosome 7q35-q36; AUTS16 (613410), associated with mutation in the SLC9A9 gene (608396) on chromosome 3q24; AUTS17 (613436), associated with mutation in the SHANK2 gene (603290) on chromosome 11q13; and AUTS18 (615032), associated with mutation in the CHD8 gene (610528). (NOTE: the symbol 'AUTS2' has been used to refer to a gene on chromosome 7q11 (KIAA0442; 607270) and therefore is not used as a part of this autism locus series.) There are several X-linked forms of autism susceptibility: AUTSX1 (300425), associated with mutations in the NLGN3 gene (300336); AUTSX2 (300495), associated with mutations in NLGN4 (300427); AUTSX3 (300496), associated with mutations in MECP2 (300005); AUTSX4 (300830), associated with variation in the region on chromosome Xp22.11 containing the PTCHD1 gene (300828); AUTSX5 (300847), associated with mutations in the RPL10 gene (312173); and AUTSX6 (300872), associated with mutation in the TMLHE gene (300777). Folstein and Rosen-Sheidley (2001) reviewed the genetics of autism.
Renal cell carcinoma, papillary, 1
MedGen UID:
766
Concept ID:
C0007134
Neoplastic Process
Hereditary papillary renal cell carcinoma is characterized by the development of multiple, bilateral papillary renal tumors (Zbar et al., 1995). The transmission pattern is consistent with autosomal dominant inheritance with incomplete penetrance. Papillary renal cell carcinoma is histologically and genetically distinct from 2 other forms of inherited renal carcinoma, von Hippel Lindau disease (193300), caused by mutation in the VHL gene (608537) on chromosome 3, and a form associated with the chromosome translocation t(3;8), as described by Cohen et al. (1979). Bodmer et al. (2002) reviewed the molecular genetics of familial and nonfamilial cases of renal cell carcinoma, including the roles of VHL, MET, and translocations involving chromosomes 1, 3, and X. For background information and a discussion of genetic heterogeneity of nonpapillary renal cell carcinoma, see RCC (144700). See also a hereditary syndrome of predisposition to uterine leiomyomas and papillary renal cell carcinoma (HLRCC; 150800) caused by germline mutation in the FH gene (136850).
Chordoma
MedGen UID:
40277
Concept ID:
C0008487
Neoplastic Process
Chordomas are rare, clinically malignant tumors derived from notochordal remnants. They occur along the length of the spinal axis, predominantly in the sphenooccipital, vertebral, and sacrococcygeal regions. They are characterized by slow growth, local destruction of bone, extension into adjacent soft tissues, and, rarely, distant metastatic spread (Stepanek et al., 1998). The incidence of chordoma is age-dependent, with fewer than 5% occurring in children and adolescents (summary by McMaster et al., 2011).
Ependymoma
MedGen UID:
41825
Concept ID:
C0014474
Neoplastic Process
Ependymomas are rare glial tumors of the brain and spinal cord (Yokota et al., 2003).
Gingival fibromatosis
MedGen UID:
42017
Concept ID:
C0016049
Finding
Generalized or localized diffuse fibrous overgrowth of the gingival tissue, usually transmitted as an autosomal dominant trait, but some cases are idiopathic and others produced by drugs. The enlarged gingiva is pink, firm, and has a leather-like consistency with a minutely pebbled surface and in severe cases the teeth are almost completely covered and the enlargement projects into the oral vestibule. (Dorland, 28th ed)
Hypothyroidism
MedGen UID:
6991
Concept ID:
C0020676
Disease or Syndrome
A syndrome that results from abnormally low secretion of THYROID HORMONES from the THYROID GLAND, leading to a decrease in BASAL METABOLIC RATE. In its most severe form, there is accumulation of MUCOPOLYSACCHARIDES in the SKIN and EDEMA, known as MYXEDEMA. It may be primary or secondary due to other pituitary disease, or hypothalamic dysfunction.
Precocious puberty
MedGen UID:
18752
Concept ID:
C0034013
Disease or Syndrome
Development of SEXUAL MATURATION in boys and girls at a chronological age that is 2.5 standard deviations below the mean age at onset of PUBERTY in the population. This early maturation of the hypothalamic-pituitary-gonadal axis results in sexual precocity, elevated serum levels of GONADOTROPINS and GONADAL STEROID HORMONES such as ESTRADIOL and TESTOSTERONE.
Wolff-Parkinson-White pattern
MedGen UID:
12162
Concept ID:
C0043202
Disease or Syndrome
Wolff-Parkinson-White syndrome is a condition characterized by abnormal electrical pathways in the heart that cause a disruption of the heart's normal rhythm (arrhythmia).The heartbeat is controlled by electrical signals that move through the heart in a highly coordinated way. A specialized cluster of cells called the atrioventricular node conducts electrical impulses from the heart's upper chambers (the atria) to the lower chambers (the ventricles). Impulses move through the atrioventricular node during each heartbeat, stimulating the ventricles to contract slightly later than the atria.People with Wolff-Parkinson-White syndrome are born with an extra connection in the heart, called an accessory pathway, that allows electrical signals to bypass the atrioventricular node and move from the atria to the ventricles faster than usual. The accessory pathway may also transmit electrical impulses abnormally from the ventricles back to the atria. This extra connection can disrupt the coordinated movement of electrical signals through the heart, leading to an abnormally fast heartbeat (tachycardia) and other changes in heart rhythm. Resulting symptoms include dizziness, a sensation of fluttering or pounding in the chest (palpitations), shortness of breath, and fainting (syncope). In rare cases, arrhythmias associated with Wolff-Parkinson-White syndrome can lead to cardiac arrest and sudden death. The most common arrhythmia associated with Wolff-Parkinson-White syndrome is called paroxysmal supraventricular tachycardia.Complications of Wolff-Parkinson-White syndrome can occur at any age, although some individuals born with an accessory pathway in the heart never experience any health problems associated with the condition.Wolff-Parkinson-White syndrome often occurs with other structural abnormalities of the heart or underlying heart disease. The most common heart defect associated with the condition is Ebstein anomaly, which affects the valve that allows blood to flow from the right atrium to the right ventricle (the tricuspid valve). Additionally, the heart rhythm problems associated with Wolff-Parkinson-White syndrome can be a component of several other genetic syndromes, including hypokalemic periodic paralysis (a condition that causes episodes of extreme muscle weakness), Pompe disease (a disorder characterized by the storage of excess glycogen), Danon disease (a condition that weakens the heart and skeletal muscles and causes intellectual disability), and tuberous sclerosis complex (a condition that results in the growth of noncancerous tumors in many parts of the body).
Subcutaneous nodule
MedGen UID:
101803
Concept ID:
C0151811
Pathologic Function
A small palpable mass in the subcutaneous tissues.
Cafe-au-lait spot
MedGen UID:
113157
Concept ID:
C0221263
Finding
A light brown, sharply demarcated skin patch. It is a manifestation of neurofibromatosis type 1 and McCune-Albright syndrome.
Renal angiomyolipoma
MedGen UID:
69146
Concept ID:
C0241961
Neoplastic Process
A benign renal neoplasm composed of fat, vascular, and smooth muscle elements.
Adenoma sebaceum
MedGen UID:
75563
Concept ID:
C0265319
Neoplastic Process
Facial ANGIOFIBROMA in tuberous sclerosis
Subungual fibromas
MedGen UID:
82726
Concept ID:
C0266003
Finding
The presence of fibromata beneath finger or toenails.
Cerebral calcification
MedGen UID:
124360
Concept ID:
C0270685
Finding
Abnormal deposits of calcium in the cerebral tissue.
Optic nerve glioma
MedGen UID:
138056
Concept ID:
C0346326
Neoplastic Process
A glioma originating in the optic nerve or optic chiasm.
Shagreen patch
MedGen UID:
96599
Concept ID:
C0432363
Congenital Abnormality
A plaque representing a connective-tissue nevus. Connective tissue naevi are uncommon skin lesions that occur when the deeper layers of the skin do not develop correctly or the components of these layers occur in the wrong proportion. Shagreen patches are oval-shaped and nevoid, skin-colored or occasionally pigmented, smooth or crinkled, The word shagreen refers to a type of roughened untanned leather.
Attention deficit hyperactivity disorder
MedGen UID:
220387
Concept ID:
C1263846
Mental or Behavioral Dysfunction
A behavior disorder originating in childhood in which the essential features are signs of developmentally inappropriate inattention, impulsivity, and hyperactivity. Although most individuals have symptoms of both inattention and hyperactivity-impulsivity, one or the other pattern may be predominant. The disorder is more frequent in males than females. Onset is in childhood. Symptoms often attenuate during late adolescence although a minority experience the full complement of symptoms into mid-adulthood. (From DSM-V)
Cardiac rhabdomyoma
MedGen UID:
232027
Concept ID:
C1332852
Neoplastic Process
A benign tumor of cardiac striated muscle.
Achromatic retinal patches
MedGen UID:
348171
Concept ID:
C1860710
Finding
Areas of the retina lacking pigmentation. Punched out areas of chorioretinal hypopigmentation less than 1 disc diameter in size and tending to be located in the midperiphery of the retina.
Subependymal nodules
MedGen UID:
369895
Concept ID:
C1968958
Finding
Small nodular masses which originate in the subependymal region of the lateral ventricles and protrude into the ventricular cavity. They may represent subependymal hamartomas of tuberous sclerosis or nodular heterotopia of grey matter.
Cortical tubers
MedGen UID:
369896
Concept ID:
C1968959
Finding
Cortical tubers in the brain are hamartomatous lesions typically located at the gray-white matter interface, commonly in the frontal and parietal lobes. Cortical tubers are composed of abnormal glial and neural cells, and the size, number, and location vary among patients.
Renal cyst
MedGen UID:
854361
Concept ID:
C3887499
Disease or Syndrome
A fluid filled sac in the kidney.
Infantile spasms
MedGen UID:
854616
Concept ID:
C3887898
Disease or Syndrome
Infantile spasms represent a subset of "epileptic spasms". Infantile Spasms are epileptic spasms starting in the first year of life (infancy).
Specific learning disability
MedGen UID:
871302
Concept ID:
C4025790
Mental or Behavioral Dysfunction
Impairment of certain skills such as reading or writing, coordination, self-control, or attention that interfere with the ability to learn. The impairment is not related to a global deficiency of intelligence.

Term Hierarchy

Professional guidelines

PubMed

ACMG Board of Directors.
Genet Med 2015 Jan;17(1):68-9. Epub 2014 Nov 13 doi: 10.1038/gim.2014.151. PMID: 25356965
Green RC, Berg JS, Grody WW, Kalia SS, Korf BR, Martin CL, McGuire AL, Nussbaum RL, O'Daniel JM, Ormond KE, Rehm HL, Watson MS, Williams MS, Biesecker LG; American College of Medical Genetics and Genomics.
Genet Med 2013 Jul;15(7):565-74. Epub 2013 Jun 20 doi: 10.1038/gim.2013.73. PMID: 23788249Free PMC Article
Schaefer GB, Mendelsohn NJ; Professional Practice and Guidelines Committee.
Genet Med 2013 May;15(5):399-407. Epub 2013 Mar 21 doi: 10.1038/gim.2013.32. PMID: 23519317

External

Recommendations for reporting of secondary findings in clinical exome and genome sequencing, 2016 update (ACMG SF v2.0): a policy statement of the American College of Medical Genetics and Genomics.

Orphanet, Tuberous sclerosis, 2007

Recent clinical studies

Etiology

Maiese K
Curr Neurovasc Res 2017;14(3):299-304. doi: 10.2174/1567202614666170718092010. PMID: 28721811Free PMC Article
Yamanaka S, Mizobuchi T, Kurihara M
Ann Thorac Cardiovasc Surg 2017 Feb 20;23(1):36-39. Epub 2016 Jun 27 doi: 10.5761/atcs.cr.16-00095. PMID: 27349306Free PMC Article
Cristescu M, Abel EJ, Wells S, Ziemlewicz TJ, Hedican SP, Lubner MG, Hinshaw JL, Brace CL, Lee FT Jr
Cardiovasc Intervent Radiol 2016 Mar;39(3):433-40. Epub 2015 Sep 21 doi: 10.1007/s00270-015-1201-5. PMID: 26390876
Gilbert JR, Guy V, Kumar A, Wolpert C, Kandt R, Aylesworth A, Roses AD, Pericak-Vance MA
Neurogenetics 1998 Aug;1(4):267-72. PMID: 10732801
Platten M, Meyer-Puttlitz B, Blümcke I, Waha A, Wolf HK, Nöthen MM, Louis DN, Sampson JR, von Deimling A
J Neuropathol Exp Neurol 1997 Jul;56(7):806-10. PMID: 9210877

Diagnosis

Maiese K
Curr Neurovasc Res 2017;14(2):184-189. doi: 10.2174/1567202614666170313105337. PMID: 28294062Free PMC Article
Cinalli G, Imperato A, Mirone G, Di Martino G, Nicosia G, Ruggiero C, Aliberti F, Spennato P
J Neurosurg Pediatr 2017 Mar;19(3):325-332. Epub 2017 Jan 13 doi: 10.3171/2016.10.PEDS16352. PMID: 28084922
Yamanaka S, Mizobuchi T, Kurihara M
Ann Thorac Cardiovasc Surg 2017 Feb 20;23(1):36-39. Epub 2016 Jun 27 doi: 10.5761/atcs.cr.16-00095. PMID: 27349306Free PMC Article
Filipczak PT, Thomas C, Chen W, Salzman A, McDonald JD, Lin Y, Belinsky SA
Cancer Res 2016 Dec 15;76(24):7130-7139. Epub 2016 Oct 18 doi: 10.1158/0008-5472.CAN-16-1052. PMID: 27756752
Hernández-Breijo B, Monserrat J, Román ID, González-Rodríguez Á, Fernández-Moreno MD, Lobo MV, Valverde ÁM, Gisbert JP, Guijarro LG
Toxicol Appl Pharmacol 2013 Nov 1;272(3):568-78. Epub 2013 Aug 16 doi: 10.1016/j.taap.2013.07.024. PMID: 23958494

Therapy

Yamanaka S, Mizobuchi T, Kurihara M
Ann Thorac Cardiovasc Surg 2017 Feb 20;23(1):36-39. Epub 2016 Jun 27 doi: 10.5761/atcs.cr.16-00095. PMID: 27349306Free PMC Article
Cristescu M, Abel EJ, Wells S, Ziemlewicz TJ, Hedican SP, Lubner MG, Hinshaw JL, Brace CL, Lee FT Jr
Cardiovasc Intervent Radiol 2016 Mar;39(3):433-40. Epub 2015 Sep 21 doi: 10.1007/s00270-015-1201-5. PMID: 26390876
Hernández-Breijo B, Monserrat J, Román ID, González-Rodríguez Á, Fernández-Moreno MD, Lobo MV, Valverde ÁM, Gisbert JP, Guijarro LG
Toxicol Appl Pharmacol 2013 Nov 1;272(3):568-78. Epub 2013 Aug 16 doi: 10.1016/j.taap.2013.07.024. PMID: 23958494
Riikonen R
J Child Neurol 2004 Jun;19(6):401-4. doi: 10.1177/088307380401900601. PMID: 15446386
Astrinidis A, Kouvatsi A, Nahmias J, Povey S, Pandeliadis C, Danzaki A, Schneider M, Triantaphyllidis C
Hum Mutat 1998;12(3):217. PMID: 10660335

Prognosis

Fettweis G, Di Valentin E, L'homme L, Lassence C, Dequiedt F, Fillet M, Coupienne I, Piette J
Biochim Biophys Acta 2017 Jan;1864(1):113-124. Epub 2016 Oct 27 doi: 10.1016/j.bbamcr.2016.10.014. PMID: 27984090
Yamanaka S, Mizobuchi T, Kurihara M
Ann Thorac Cardiovasc Surg 2017 Feb 20;23(1):36-39. Epub 2016 Jun 27 doi: 10.5761/atcs.cr.16-00095. PMID: 27349306Free PMC Article
Maheshwar MM, Sandford R, Nellist M, Cheadle JP, Sgotto B, Vaudin M, Sampson JR
Hum Mol Genet 1996 Jan;5(1):131-7. PMID: 8789450
Geist RT, Gutmann DH
Cell Growth Differ 1995 Nov;6(11):1477-83. PMID: 8562486
Xu L, Sterner C, Maheshwar MM, Wilson PJ, Nellist M, Short PM, Haines JL, Sampson JR, Ramesh V
Genomics 1995 Jun 10;27(3):475-80. doi: 10.1006/geno.1995.1079. PMID: 7558029

Clinical prediction guides

Cai S, Everitt JI, Kugo H, Cook J, Kleymenova E, Walker CL
Am J Pathol 2003 Feb;162(2):457-68. doi: 10.1016/S0002-9440(10)63840-0. PMID: 12547704Free PMC Article
Astrinidis A, Kouvatsi A, Nahmias J, Povey S, Pandeliadis C, Danzaki A, Schneider M, Triantaphyllidis C
Hum Mutat 1998;12(3):217. PMID: 10660335
Kerfoot C, Wienecke R, Menchine M, Emelin J, Maize JC Jr, Welsh CT, Norman MG, DeClue JE, Vinters HV
Brain Pathol 1996 Oct;6(4):367-75. PMID: 8944308
Maheshwar MM, Sandford R, Nellist M, Cheadle JP, Sgotto B, Vaudin M, Sampson JR
Hum Mol Genet 1996 Jan;5(1):131-7. PMID: 8789450
Xu L, Sterner C, Maheshwar MM, Wilson PJ, Nellist M, Short PM, Haines JL, Sampson JR, Ramesh V
Genomics 1995 Jun 10;27(3):475-80. doi: 10.1006/geno.1995.1079. PMID: 7558029

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center