Molecular Genetics/DNA

The Molecular Genetics Laboratory of the Wake Forest University of the Health Sciences offers DNA testing for a variety of disorders. In addition, patient evaluation by a board-certified Clinical Geneticist and genetic counseling are available. This laboratory offers the latest in genetic testing with the most advanced technology currently in use.

Molecular Genetics Form for DNA Analysis

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Cystic Fibrosis Screening/Genotyping   

Clinical indicators of individuals for whom molecular genetic testing should be considered:

  • To establish or confirm the diagnosis of CF in symptomatic individuals
  • For carrier detection:
    • In population screening programs
    • In at-risk relatives, their reproductive partners, and in certain other individuals
    • In prenatal testing of at-risk pregnancies and for pregnancies in which fetal echogenic bowel has been identified

Cystic fibrosis needs to be considered in the following:

  • Infants with meconium ileus occurs in 10-20% of newborns diagnosed with CF
  • Infants with salt-loss syndromes (acute salt depletion, chronic metabolic alkalosis) hyponatremia and hypochloremia of unknown etiology with compensatory metabolic alkalosis
  • Infants with hypoproteinemia and anemia
  • Children with rectal prolapse
  • Children with failure to thrive, poor growth and weight gain, nutritional problems, chronic diarrhea, or malabsorption. Pancreatic insufficiency with malabsorption occurs in the great majority of patients with CF.
  • Children with refractory asthma (particularly at a young age), recurrent pneumonia, recurrent sinusitis, and/or nasal polyps. Alternatively, such children may have a spectrum of disorders not related to CF, including immunologic abnormalities, ciliary dysfunction, broncopulmonary anatomic abnormalities, and allergies. Though they may be present as sequelae of any of these conditions, gastroesophageal reflux and chronic tracheal aspiration also deserve to be considered as primary causes of such symptoms.
  • Adolescents or adults with recurrent pancreatitis
  • Adults with recurrent sinusitis/bronchitis or bronchiectasis, nasal polyps, recurrent pancreatitis
  • More than 95% of males with CF are infertile due to azoospermia resulting from absent, atrophic or fibrotic Wolffian duct structures.

Molecular genetic testing:

CFTR is the only gene associated with the CFTR-related disorders, cystic fibrosis and CBAVD. Over 1000 mutations have been identified in the CFTR gene although the vast majority are rare mutations and have only been detected in one family.

Mutation panel.  A 32 mutation panel is used which includes the 23 mutations recommended by the American College of Medical Genetics and the American College of Obstetricians and Gynecologists.  The mutation detection rate for this 32 mutation panel varies depending on an individual’s ethnic background.  In some symptomatic individuals, only one or neither mutation is detectable; in some carriers, the disease-causing mutation is not detectable.  Mutations analyzed:  deltaF508; deltaI507; G542X; G551D; W1282X; N1303K; R553X; 621+1G->T; R117H; 1717-1G->A; A455E; R560T; R1162X; G85E; R334W; R347P; R347H; 711+1G->T; 1898+1G->A; 2184delA; 1078delT; 3849+10kbC->T; 2789+5G->A; 3659delC; I148T; 3120+1G->A; V520F; S549N; S549R; 3905insT; 394delTT; 3876delA.

Poly T tract analysis.  The Poly T tract, a string of thymidine bases located in intron 8 of the CFTR gene, can be associated with CFTR-related disorders depending on its size. The three common variants of the poly T tract are 5T, 7T, and 9T. Both 7T and 9T are considered polymorphic variants and 5T is considered a variably penetrant mutation. Poly-T testing is appropriate as a reflex test when a R117H mutation is detected or an adult male is being evaluated for CBAVD.  Males with CBAVD or suspected CBAVD and individuals with non-classic CF are all appropriate for T tract typing.

Billing Information:

Initial CF Screening/Genotyping
·        cpt codes: 83907, 83890, 83909, 83900, 83901x14, 83914x30, 83912

Reflex test for R117H mutation - PolyT status
·        cpt codes: 83900, 83901x14, 83914, 83909, 83912

Reflex test for I148T mutation - sequence analysis
·        cpt codes: 83894, 83909x2, 83898, 83904x2, 83912

Reflex test for 506/507 polymorphism
·        cpt codes: 83900, 83901x14, 83914x2, 83909, 83912

Turn Around Time: 7-10 days

[PDF][Additional Clinical Information][Back to Top]

  Mental Retardation Testing 

Fragile X Syndrome  

Clinical indicators of individuals for whom molecular genetic testing should be considered:

  • Individuals of either sex with mental retardation, developmental delay, or autism, especially if they have a) any physical or behavioral characteristics of Fragile X syndrome; b) a family history of Fragile X syndrome; or c) male or female relatives with undiagnosed mental retardation
  • Individuals seeking reproductive counseling who have a family history of a) Fragile X syndrome or of b) undiagnosed mental retardation
  • Fetuses of known carrier mothers 
  • Patients who have a cytogenetic Fragile X test result that is discordant with their phenotype. These include patients who have a strong clinical indication (including risk of being a carrier) and who have had a negative or ambiguous cytogenetic test result, and patients with an atypical phenotype who have had a positive cytogenetic test result.

Molecular genetic testing:

FMR1 is the only gene known to be associated with FMR1-related disorders. The diagnosis of FMR1-related disorders rests on the detection of an alteration in the FMR1 gene. Greater than 99% of individuals with fragile X syndrome have an abnormal increase in the number of trinucleotide repeats (CGG) within the FMR1 gene and are considered a full mutation which is typically accompanied by aberrant methylation of the FMR1 gene.   All individuals with FXTAS and all females with FMR1-related Premature Ovarian Failure (POF) have an FMR1 premutation.

Allele sizes.   FMR1 alleles are categorized according to the repeat number. However, the distinction between allele categories is not absolute and must be made by considering both family history and repeat instability.

  • Normal alleles: Approximately 5-40 repeats.
  • Intermediate alleles (also termed "gray zone"): No consensus exists on the precise definition of intermediate alleles exists, but these may be broadly defined as 41-58 repeats.
  • Premutation alleles: Approximately 59-200 repeats.
  • Full mutation alleles: Over 200 repeats, with several hundred to several thousand repeats being typical.

Billing Information:

Initial testing by PCR
·        cpt codes: 83907, 83890, 83909, 83898, 83912

If PCR is not informative, reflex test Methylation-sensitive Southern Blot Analysis
·        cpt codes: 83892x2, 83894, 83896, 83897, 83912

Turn Around time: PCR 7-10 days; Southern Blot 21-28 days

[Additional Clinical Information][Back to Top]

Prader-Willi Syndrome  

Clinical indicators of individuals for whom molecular genetic testing should be considered:

Birth to two years

  • Hypotonia with poor suck in the neonatal period

Two to six years

  • Hypotonia with history of poor suck
  • Global developmental delay

Six to twelve years

  • History of hypotonia with poor suck (Hypotonia often persists.)
  • Global developmental delay
  • Excessive eating with central obesity if uncontrolled

Thirteen years to adulthood

  • Cognitive impairment, usually mild mental retardation
  • Excessive eating with central obesity if uncontrolled
  • Hypothalamic hypogonadism and/or typical behavior problems

Molecular genetic testing

Methylation-specific DNA testing is important to confirm the diagnosis of PWS in all individuals, but especially those who are too young to manifest sufficient features to make the diagnosis on clinical grounds or in those individuals who have atypical findings.

Over 99% of patients with PWS have a diagnostic abnormality in the parent-specific methylation imprint (maternal alleles only at 15q11q13) within the Prader-Willi critical region (PWCR).  Essentially all mechanisms leading to PWS can be detected by methylation-PCR analysis of the q11-q13 region of chromosome 15. Once the diagnosis of PWS is established by DNA methylation analysis, further testing is required to establish the molecular class of the mutation (i.e., deletion, UPD, or imprinting defect) for genetic counseling purposes.

  • Greater than 70% of Prader-Willi cases are due to a deletion of the chromosome 15q11-q13 region
  • Approximately 28% are due to maternal uniparental disomy of chromosome 15
  • Less than 2% have an abnormality in the chromosome 15 imprinting process

Billing Information:

Methylation-specific PCR testing
·        cpt codes: 83907, 83890, 83900, 83914x2, 83894, 83912

Turn Around Time: 10-14 days

[Additional Clinical Information][Back to Top]

Angelman Syndrome  

Clinical indicators of individuals for whom molecular genetic testing should be considered:

  • Severe developmental delay or mental retardation
  • Severe speech impairment
  • Gait ataxia and/or tremulousness of the limbs
  • A unique behavior with an inappropriate happy demeanor that includes frequent laughing, smiling, and excitability
  • Microcephaly and seizures are common

Molecular genetic testing

DNA methylation analysis is the single most sensitive test. Analysis of parent-specific DNA methylation imprints (paternal alleles only) in the 15q11.2-q13 chromosome region detects ~78% of patients with AS, including those with a deletion, uniparental disomy, or an imprinting defect.  Once the diagnosis of AS is established by DNA methylation analysis, further testing is required to establish the molecular class of the mutation (i.e., deletion, UPD, or imprinting defect) for genetic counseling purposes.

Billing Information:

Methylation-specific PCR testing
·        cpt codes: 83907, 83890, 83900, 83914x2, 83894, 83912

Turn Around Time: 10-14 days

[Additional Clinical Information][Back to Top]

X Chromosome Inactivation 

Clinical indicators of individuals for whom molecular genetic testing should be considered:

  • Females with suspected X-linked recessive disease including mental retardation (~50%) and muscular dystrophy
  • Females with recurrent spontaneous abortions (14%)

Molecular genetic testing

Normally females with a 46,XX karyotype, the inactivation process is random with either the maternally-derived or paternally-derived X chromosome having an equal likelihood for being inactivated.   In the general population there is a distribution along a bell-shaped curve such that most females have a 50/50 ratio between maternal and paternal X chromosomes, but some individuals may be slight skewing and a few women having dramatic skewing of X-inactivation.  Skewed X-inactivation typically will not have any consequence except in cases where the X chromosome selected to remain active has certain gene mutations.  Such situations can lead to a female expressing X-linked recessive disorders, e.g., color-blindness or muscular dystrophy, usually found in males only.  In cases of suspected X-inactivation skewing, it is possible to access the relative degree of skewing using a polymerase chain reaction based assay, restriction enzyme to detect the methylation changes associated with X-inactivation, and densitometry.  When used in combination with molecular diagnostic testing of X-linked disorders, this approach can determine if X-chromosome inactivation skewing has occurred.

Billing Information:

Methylation-sensitive PCR testing
·        cpt codes: 83907, 83890, 83892x2, 83909x2, 83898x2, 83912

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   Neuromuscular Disorders 

Myotonic Dystrophy   

Myotonic dystrophy (DM) is a multi-system disorder that affects skeletal muscle and smooth muscle, as well as the eye, heart, endocrine system, and central nervous system. The clinical findings, which span a continuum from mild to severe, have been categorized into three somewhat overlapping phenotypes: mild, classical, and congenital. Mild DM is characterized by cataract and mild myotonia (difficulty relaxing the muscles after contraction); life span is normal. Classical DM is characterized by muscle weakness and wasting, myotonia, cataract, and often by cardiac conduction abnormalities; adults may become physically disabled and may have a shortened life span. Congenital DM is characterized by hypotonia and severe generalized weakness at birth, often with respiratory insufficiency and early death; mental retardation is common.

Myotonic dystrophy is an autosomal dominant disorder characterized by myotonia, muscular dystrophy, cataracts, hypogonadism, frontal balding, and ECG changes. Myotonic dystrophy is the most prevalent inherited neuromuscular disorder in adults.  The disorder is characterized by myotonia, progressive muscle weakness, and atrophy.  Symptoms can be minimal with onset in adolescence or later life, or more severe with onset in early adulthood.  In addition, a severe congenital onset form accompanied by mental retardation occurs with inheritance nearly always through maternal transmission.

Diagnosis/testing.  The diagnosis of DM is suspected in individuals with characteristic muscle weakness and is confirmed by detection of an expansion of the CTG trinucleotide repeat in the DMPK gene (chromosomal locus 19q13.2-q13.3). CTG repeat length exceeding 37 repeats is abnormal. DNA-based testing is essentially 100% sensitive and is widely available.

The direct analysis of CTG repeats in the DMPK gene (chromosomal locus 19q13.2-q13.3) is clinically available. An increased number of CTG repeats is identified in essentially 100% of patients with DM. The number of CTG repeats ranges from 5 to 37 in normal alleles. GTG repeat lengths in the range from about 38 to 49 are considered "premutations." Persons with CTG expansions in the premutation range have not been reported as having developed symptoms, but their children are at risk of inheriting a larger repeat size. Persons with CTG repeat length greater than 50 are frequently symptomatic.

The discovery that the genetic defect in one form of the disorder is an amplified trinucleotide repeat in the 3-prime untranslated region of a protein kinase gene on chromosome 19 explains many of the unusual features of the disorder. Severity varies with the number of repeats: normal individuals have from 5 to 30 repeat copies; mildly affected persons, from 50 to 80; and severely affected individuals, 2,000 or more copies. Amplification is frequently observed after parent-to-child transmission, but extreme amplifications are not transmitted through the male line.

Trinucleotide repeat expansion of a CTG repeat contained in the myotonin protein kinase gene located on chromosome 19 leads to the pathological changes in all forms.  Normal individuals have less then ~37 repeats.  In affected individuals the repeat copy number is correlated to disease severity and age of onset.  Symptoms appear in individuals with greater than approximately 50 repeats.  More severe pathology and earlier onset occur when an individual inherits an allele containing hundreds of repeats.  Repeat copy number reaches to 1000-3000 in most congenital cases but may overlap the adult onset form.  A polymerase chain reaction assay is used to determine repeat copy number of alleles in the normal range and Southern blot analysis is used to estimate repeats in larger alleles.

Billing Information:

Initial testing by PCR
·        cpt codes: 83907, 83890, 83909, 83898, 83912

If PCR is not informative, reflex test Southern Blot Analysis
·        cpt codes: 83892, 83894, 83896, 83897, 83912

[Additional Clinical Information][Back to Top]

Spinal Bulbar Muscular Atrophy (SBMA).....Kennedy Disease  

Spinal and bulbar muscular atrophy (SBMA) is a gradually progressive neuromuscular disorder in which degeneration of lower motor neurons results in proximal muscle weakness, muscle atrophy, and fasciculations. SBMA occurs only in males. Affected individuals often show gynecomastia, testicular atrophy, and reduced fertility as a result of mild androgen insensitivity.

Diagnosis/testing.  All males with SBMA have expansion of a CAG trinucleotide repeat (>35 CAGs) in the androgen receptor (AR) gene. Molecular genetic testing for the CAG trinucleotide repeat expansion is available on a clinical basis.

Males with spinal and bulbar muscular atrophy (SBMA/Kennedy disease) - expansion not skewing: normal 9-36 repeats, affected 38-62

Billing Information:

Testing by PCR
·        cpt codes: 83907, 83890, 83909, 83898, 83912

[Additional Clinical Information][Back to Top]

Fragile X-Associated Tremor/Ataxia Syndrome   

The Fragile X-associated tremor/ataxia syndrome (FXTAS) is characterized by late-onset, progressive cerebellar ataxia and intention tremor in males who have a permutation allele in the FMR1 gene (see Fragile X Syndrome pg XX). Other neurologic findings include short-term memory loss, executive function deficits, cognitive decline, Parkinsonism, peripheral neuropathy, lower-limb proximal muscle weakness, and autonomic dysfunction. Penetrance is age related; symptoms are seen in 17% of males ages 50-59 years, in 38% ages 60-69 years, in 47% ages 70-79 years, and in 75% ≥age 80 years. 

Billing Information:

Testing by PCR
·        cpt codes: 83907, 83890, 83909, 83898, 83912

[Additional Clinical Information][Back to Top]

Chimerism Studies For Same Sex Bone Marrow Transplantation  

Chimerism studies are generally performed for patients undergoing same sex bone marrow transplantation, the laboratory uses highly polymorphic markers to genotype the donor and recipient prior to transplantation. Following transplantation, genotype of the recipient is performed to determine for the presence or absence of donor markers

Billing Information:

Pretransplant testing - PCR-based genotyping analysis
·        cpt codes: 83907x2, 83890x2, 83909x2, 83900, 83901x30, 83912 

Posttransplant testing - PCR-based genotyping analysis
·        cpt codes: 83907, 83890, 83909, 83900, 83901x14, 83912

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UniParental Disomy (UPD) Studies for Imprinting Disorders

Uniparental disomy (UPD) occurs when a person receives two copies of a chromosome, or part of a chromosome, from one parent and no copies from the other parent. UPD can occur as a random event during the formation of egg or sperm cells or may happen in early fetal development.

In many cases, UPD likely has no effect on health or development. Because most genes are not imprinted, it doesn’t matter if a person inherits both copies from one parent instead of one copy from each parent. In some cases, however, it does make a difference whether a gene is inherited from a person’s mother or father. A person with UPD may lack any active copies of essential genes that undergo genomic imprinting. This loss of gene function can lead to delayed development, mental retardation, or other medical problems.

Several genetic disorders can result from UPD or a disruption of normal genomic imprinting. The most well-known conditions include Prader-Willi syndrome, which is characterized by uncontrolled eating and obesity, and Angelman syndrome, which causes mental retardation and impaired speech. Both of these disorders can be caused by UPD or other errors in imprinting involving genes on the long arm of chromosome 15. Other conditions, such as Beckwith-Wiedemann syndrome (a disorder characterized by accelerated growth and an increased risk of cancerous tumors).

Billing Information:

Proband and Parents - PCR-based genotyping analysis
·        cpt codes: 83907x3, 83890x3, 83894x3, 83998x6, 83900, 83901x13, 83912

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  Infertility 

Premature Ovarian Failure 

Premature ovarian failure (POF), defined as cessation of menses before age 40 years, has been observed in female carriers of a premutation FMR1 allele (see Fragile X Syndrome pg XX).  Ovarian failure occurred as early as 11 years. The risk for POF was 21% (estimates ranged from 15-27% in various studies) in premutation carriers compared to a 1% background risk. In contrast, carriers of full mutation alleles are not at increased risk for POF.

Billing Information:

Testing by PCR
·        cpt codes: 83907, 83890, 83909, 83898, 83912

[Additional Clinical Information][Back to Top]

CBAVD 

Congenital bilateral aplasia of the vas deferens (CBAVD), which leads to male infertility, may occur in isolation or as a manifestation of cystic fibrosis. Kaplan et al. (1968) found that males with cystic fibrosis are infertile because of failure of normal development of the vas deferens. The diagnosis of congenital bilateral absence of the vas deferens (CBAVD) caused by mutations of CFTR is established in males with:

  • Azoospermia (absence of sperm in the semen)
  • A low volume of ejaculated semen (<2 ml; normal 3-5 ml) with a specific chemical profile 
  • Absence of the vas deferens on palpation. Rarely a thin fibrous cord representing a rudimentary vas deferens may be present.
  • An identifiable mutation in one or both CFTR genes.
  • Evidence of abnormalities of seminal vesicles or vas deferens upon rectal ultrasound examination.

Molecular genetic testing of men with isolated congenital absence of the vas deferens. Routine clinical test panels detect about 80% of the CFTR mutations that can be detected in patients with CBAVD identified in research studies using extensive laboratory screening methods. In addition, a variant called the 5T allele is frequently found in this patient population. The 5T allele, a variably penetrant mutant allele in which five thymidines occur near the 3' end of intron 8 in the CFTR gene, is observed in about 10% (5% allele frequency) of the general population and has been associated with mild CF. This variant alone does not cause cystic fibrosis, but can cause CBAVD in trans combination with disease-causing CFTR mutation.

Billing Information:

Initial CF Screening/Genotyping
·        cpt codes: 83907, 83890, 83909, 83900, 83901x14, 83914x30, 83912

Reflex test for R117H mutation - PolyT status
·        cpt codes: 83900, 83901x14, 83914, 83909, 83912

[Additional Clinical Information][Back to Top]

  DNA Isolation And Storage For Future Testing 

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, mutations, and diseases will improve in the future, consideration should be given to banking DNA of affected individuals.

The WFUHS Molecular Genetics Laboratory will isolate and store DNA specimens for up to 5 years.  DNA may be collected and stored because current testing is not available for certain disorders but possibly may become available at a later date.  DNA storage is confidential specimens are coded for security.

Billing Information:
·        cpt codes: 83907, 83890, 83912

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Test: Prenatal DNA Analysis - Amniotic Fluid / CVS / Fetal Blood 
Molecular Genetic Testing

Purpose of Test: To identify specific DNA anomalies that are specifically associated with a genetic defect and/or clinical syndrome.

Specimen Required: Please provide indications for testing on our referral form with each specimen. Label each sample with the individual’s full name. Accurate testing and interpretation may otherwise be compromised. Include the appropriate requisition form and billing instructions

SUBMIT 1 OF THE FOLLOWING SPECIMENS:
Prenatal Specimens
- All prenatal specimens must be accompanied by a maternal blood specimen.

Amniotic Fluid - Obtain 20 mL of amniotic fluid. Transfer specimen to 2 screw-capped, sterile centrifuge tubes. Send specimen refrigerated. A separate culture charge will be assessed under "Amniotic Fluid Culture for Genetic Testing".
SPECIMEN CANNOT BE FROZEN.

Chorionic Villus - Obtain 20 mg of chorionic villus specimen. Send specimen refrigerated in transport media in 15-mL centrifuge tube. A separate culture charge will be assessed under "Fibroblast Culture for Genetic Testing".
SPECIMEN CANNOT BE FROZEN.

Fetal Blood (PUBS) - Draw 1 lavender-top (EDTA) tubes or 1 yellow-top (ACD) tubes of whole blood (1 mL) and send in the original VACUTAINERS.  Invert several times to mix blood. Forward unprocessed whole blood promptly at ambient temperature.

Average Turn Around Time: 1-2 weeks from receipt of specimen is typical.

[Lab Referral Form][Printable PDF File][Back to Top]

Test: Postnatal/Congenital DNA Analysis - Blood / Tissue / Buccal Smear  
Molecular Genetic Testing

Purpose of Test: To identify specific DNA anomalies that are specifically associated with a genetic defect and/or clinical syndrome.

Specimen Required:  Please provide indications for testing on our referral form with each specimen. Label each sample with the individual’s full name. Accurate testing and interpretation may otherwise be compromised. Include the appropriate requisition form and billing instructions

SUBMIT 1 OF THE FOLLOWING SPECIMENS:
Blood

  • Draw 2 lavender-top (EDTA) tubes or 2 yellow-top (ACD) tubes of whole blood (10 mL) and send in the original VACUTAINERS.  Invert several times to mix blood. Forward unprocessed whole blood promptly at ambient temperature.

Tissue

  • Obtain 200 mg of tissue. Specimen must be frozen within 1 hour of collection. Send specimen frozen in plastic container

Buccal Smear

  • Patient should rinse out mouth vigorously with water before obtaining specimen. Remove the Cyto-Pak Brush from the container; touch only the "stick" end. Using MEDIUM pressure, swab inside of cheek with a Cyto-Pak Brush by rapidly rotating bristles across cheek surface for 10 seconds.  Place brush back into the original container, re-cap, and seal with tape. Repeat collection of specimen from the other cheek.

Average Turn Around Time: 1-2 weeks from receipt of specimen is typical.

[Lab Referral Form][Printable PDF File][Back to Top]

Test: Hematologic DNA Analysis - Blood / Bone Marrow 
Molecular Genetic Testing

Purpose of Test: To identify specific DNA anomalies that are specifically associated with a genetic defect and/or clinical syndrome.

Specimen Required:  Please provide indications for testing on our referral form with each specimen. Label each sample with the individual’s full name. Accurate testing and interpretation may otherwise be compromised. Include the appropriate requisition form and billing instructions

SUBMIT 1 OF THE FOLLOWING SPECIMENS:
Blood

  • Draw 2 lavender-top (EDTA) tubes or 2 yellow-top (ACD) tubes of whole blood (10 mL) and send in the original VACUTAINERS.  Invert several times to mix blood. Forward unprocessed whole blood promptly at ambient temperature.

Bone Marrow

  • Place 2.0 mL of bone marrow in a lavender-top (EDTA) tube(s) and send in the original VACUTAINER(S). Invert several times to mix bone marrow. Forward unprocessed bone marrow promptly at ambient temperature.

Average Turn Around Time: 1-2 weeks from receipt of specimen is typical.

[Lab Referral Form][Printable PDF File][Back to Top]

 

Quick Reference

Medical Genetics Contact Information
Clinical Genetics Services

Phone 336-713-7573
Fax 336-713-7577

Genetic Laboratory Services

Phone 336-716-4321
Fax 336-716-2554

Maternal Serum Screening

Phone 336-713-7530
Fax 336-713-7577

Hours
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Last Updated: 11-18-2013
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