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Congenital Muscular Dystrophy Sequencing Panel

  • Summary and Pricing
  • Clinical Features and Genetics
  • Citations
  • Methods
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TEST METHODS

NGS Sequencing

Test Code Test Copy GenesCPT Code Copy CPT Codes
1301 B3GALNT2 81479 Add to Order
B4GAT1 81479
CHKB 81479
COL12A1 81479
COL6A1 81407
COL6A2 81407
COL6A3 81407
DAG1 81479
DMD 81408
DPM1 81479
DPM2 81479
DPM3 81479
EMD 81405
FKRP 81404
FKTN 81405
GMPPB 81479
ISPD 81405
ITGA7 81479
LAMA2 81408
LARGE1 81479
LMNA 81406
POMGNT1 81406
POMGNT2 81479
POMK 81479
POMT1 81406
POMT2 81406
TMEM5 81479
Full Panel Price* $2140.00
Test Code Test Copy Genes Total Price CPT Codes Copy CPT Codes
1301 Genes x (27) $2140.00 81404, 81405(x3), 81406(x4), 81407(x3), 81408(x2), 81479(x14) Add to Order

New York State Approved Test

Pricing Comment

If you would like to order a subset of these genes contact us to discuss pricing.

Targeted Testing

For ordering targeted known variants, please proceed to our Targeted Variants landing page.

Turnaround Time

The great majority of tests are completed within 28 days.

Clinical Sensitivity

Because of extensive phenotypic and locus heterogeneity for the congenital muscular dystrophies, over-all clinical sensitivity is difficult to estimate. Based on results from both the literature and PreventionGenetics, we estimate that this test will detect pathogenic variants in roughly 45% of patients (Sparks et al. 2012). Pathogenic variants in LAMA2, which cause merosin-deficient CMD, are over-all the most common subtype of CMD. In one study (Allamad et al. 2002) merosin-deficient CMD was found to account for about 30% of the CMD cases in Europe. In a cohort of ninety fetuses with severe cobblestone lissencephaly and associated findings consistent with Walker-Warburg syndrome, Vuillaumier-Barrot et al (2012), found a genetic diagnosis in 58, or 64%. These diagnosed cases had relative frequencies as follows: POMT1 (42%), POMT2 (17%), POMGNT1 (17%), TMEM5 (9%), ISPD (9%), LARGE1 (3%) and FKRP (3%). Sequence analysis using genomic DNA from peripheral blood was found to have clinical sensitivity of 66%, 56%, and 79% among patients classified as having typical Bethlem Myopathy, severe Bethlem Myopathy, and Ulrich Congenital Muscular Dystrophy, respectively (Lampe et al. 2005). Sequencing analysis should have high analytical sensitivity for all CMD genes with the exception of LARGE1, ISPD, LAMA2, which are known to harbor gross deletions and duplications.

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Deletion/Duplication Testing via aCGH

Test Code Test Copy GenesIndividual Gene PriceCPT Code Copy CPT Codes
600 B3GALNT2$690.00 81479 Add to Order
B4GAT1$690.00 81479
CHKB$690.00 81479
COL12A1$690.00 81479
COL6A1$690.00 81479
COL6A2$690.00 81406
COL6A3$690.00 81406
DAG1$690.00 81479
DMD$690.00 81161
DPM1$690.00 81479
DPM2$690.00 81479
DPM3$690.00 81479
EMD$690.00 81404
FKRP$690.00 81479
FKTN$690.00 81479
GMPPB$690.00 81479
ISPD$690.00 81479
ITGA7$690.00 81479
LAMA2$690.00 81479
LARGE1$690.00 81479
LMNA$690.00 81479
POMGNT1$690.00 81479
POMGNT2$690.00 81479
POMK$690.00 81479
POMT1$690.00 81479
POMT2$690.00 81479
TMEM5$690.00 81479
Full Panel Price* $1290.00
Test Code Test Copy Genes Total Price CPT Codes Copy CPT Codes
600 Genes x (27) $1290.00 81161, 81404, 81406(x2), 81479(x23) Add to Order
Pricing Comment

# of Genes Ordered

Total Price

1

$690

2

$730

3

$770

4-10

$840

11-30

$1,290

31-100

$1,670

Over 100

Call for quote

Turnaround Time

The great majority of tests are completed within 28 days.

Clinical Sensitivity

Clinical sensitivity of deletion/duplication testing for most of the CMD genes is low, except for the DMD, ISPD, LAMA2 and LARGE1 genes (Human Gene Mutation Database). Approximately two-thirds of the pathogenic variants in Duchenne muscular dystrophy patients are deletions of one or more exons in the DMD gene. The occurrence of deletions is slightly higher in Becker muscular dystrophy patients. Duplications are found in approximately 10% of Duchenne muscular dystrophy patients and 20% of Becker muscular dystrophy patients. If a patient is highly suspicious for Duchenne/Becker muscular dystrophy, testing for deletions and duplications involving DMD should be performed first. 

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Clinical Features

The congenital muscular dystrophies are a clinically and genetically heterogeneous group of disorders characterized by elevated serum CK levels, muscle weakness, a dystrophic process observed in biopsied muscle, and variable associated findings such as central nervous system abnormalities, cardiac muscle involvement, skeletal effects, and developmental delay (Bertini et al. 2011). Onset of symptoms generally occurs at birth, although some symptoms do not manifest until later in life. This panel includes testing for Merosin-deficient congenital muscular dystrophy, dystroglycanopathies including Walker-Warburg syndrome (WWS), Ullrich congenital muscular dystrophy, Bethlem myopathy, dystrophinopathies, Emery-Dreifuss muscular dystrophy, LMNA-related muscular dystrophies, and other rare forms of muscular dystrophy. 

Genetics

Congenital muscular dystrophies caused by pathogenic variants in LAMA2, CHKB, ITGA7, B3GALNT2 , B4GAT1, DAG1 , DPM1, DPM2, DPM3, FKRP, FKTN, GMPPB, ISPD, LARGE1, POMGNT1, POMGNT2, POMK, POMT1, POMT2, and TMEM5 are inherited in an autosomal recessive manner. Pathogenic variants in these genes include missense, nonsense, splicing, and small deletions/insertions (http://www.dmd.nl/; Human Gene Mutation Database). Gross deletions/duplications have been commonly reported in the LAMA2, ISPD, and LARGE1 genes (Human Gene Mutation Database).

LMNA related congenital muscular dystrophy is inherited as autosomal dominant disorder and many times occurs as a result of de novo mutation.

DMD and EMD both cause X-linked recessive muscular dystrophies. Approximately two-thirds of the pathogenic variants in Duchenne muscular dystrophy patients are deletions of one or more exons in the DMD gene. The occurrence of deletions is slightly higher in Becker muscular dystrophy patients. Duplications are found in approximately 10% of Duchenne muscular dystrophy patients and 20% of Becker muscular dystrophy patients. Pathogenic variants detectable by sequence analysis are found in approximately one-third of Duchenne muscular dystrophy cases and in approximately 20% of Becker muscular dystrophy cases. Emery-Dreifuss muscular dystrophy is caused by pathogenic variants in the EMD gene which include missense, nonsense, and splicing variants and also small out-of-frame insertions/deletions and gross deletions (Human Gene Mutation Database). 

Most cases of Bethlem myopathy have autosomal dominant inheritance of COL6A1, COL6A2 or COL6A3 pathogenic variants (Lampe and Bushby 2005; Jobsis et al. 1999; Butterfield et al. 2013). Once thought to be strictly a recessive condition, Ullrich congenital muscular dystrophy has been shown to be inherited in a dominant manner in numerous cases (Pan et al. 2003). A dominant-negative effect underlies pathogenicity of dominantly inherited UCMD (Pan et al. 2003; Baker et al. 2005), while most cases of recessive UCMD result from truncating pathogenic variants. Recently, both dominant and recessive pathogenic variants in a fourth collagen gene, COL12A1, have been found in patients with Ullrich and Bethlem phenotypes (Hicks et al. 2014; Zou et al. 2014).

Testing Strategy

For this NGS test, the full coding regions plus ~20bp of non-coding DNA flanking each exon are sequenced for each of the congenital muscular dystrophy genes listed below. Sequencing is accomplished by capturing specific regions with an optimized solution-based hybridization method, followed by massively parallel sequencing of the captured DNA fragments. Additional Sanger sequencing is performed for any regions not captured or with insufficient number of sequence reads. All pathogenic, undocumented and questionable variant calls are confirmed by Sanger sequencing.

This panel provides 100% coverage of the aforementioned regions of the indicated genes. We define coverage as > 20X NGS reads for exons and 0-10 bases of flanking DNA, > 10X NGS reads for 11-20 bases of flanking DNA, or Sanger sequencing.

DMD seqencing is including in this testing; however, if a patient is highly suspicious for Duchenne/Becker muscular dystrophy, testing for deletions and duplications with a high-density gene-centric array comparative genomic hybridization (aCGH) Test #1200 should be performed first.

Indications for Test

Elevated serum CK at birth or early in life and/or muscle biopsy consistent with dystrophic process. This test especially aids in a differential diagnosis of similar phenotypes, rules out particular syndromes, and provides the analysis of multiple genes simultaneously. 

Diseases

Name Inheritance OMIM ID
Becker Muscular Dystrophy XL 300376
Bethlem Myopathy AR, AD 158810
Bethlem Myopathy 2 AR, AD 616471
Congenital Disorder Of Glycosylation Type 1E AR 608799
Congenital Disorder Of Glycosylation Type 1O AR 612937
Congenital Disorder of Glycosylation, Type Iu AR 615042
Congenital Muscular Dystrophy-Dystroglycanopathy (With Brain And Eye Anomalies) Type A5 AR 613153
Duchenne Muscular Dystrophy XL 310200
Emery-Dreifuss Muscular Dystrophy 1, X-Linked XL 310300
Fukuyama Congenital Muscular Dystrophy AR 253800
Merosin Deficient Congenital Muscular Dystrophy AR 607855
Muscle Eye Brain Disease AR 253280
Muscular Dystrophy, Congenital, Due To Integrin Alpha-7 Deficiency AR 613204
Muscular Dystrophy, Congenital, LMNA-Related AR, AD 613205
Muscular Dystrophy, Congenital, Megaconial Type AR 602541
Muscular Dystrophy-Dystroglycanopathy (Congenital with Brain and Eye Anomalies), Type A, 10; MDDGA10 AR 615041
Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A, 12 AR 615249
Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A, 13 AR 615287
Muscular Dystrophy-Dystroglycanopathy (Congenital With Brain And Eye Anomalies), Type A, 6 AR 613154
Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A, 7 AR 614643
Muscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies, type A, 11 AR 615181
Muscular dystrophy-dystroglycanopathy (limb-girdle), type C, 14 AR 615352
Muscular Dystrophy-Dystroglycanopathy (Limb-Girdle), Type C, 2 AR 613158
Muscular Dystrophy-Dystroglycanopathy (Limb-Girdle), Type C, 9 AR 613818
Ullrich Congenital Muscular Dystrophy AR, AD 254090
Ullrich Congenital Muscular Dystrophy 2 AR, AD 616470
Walker-Warburg Congenital Muscular Dystrophy AR, AD 236670

Related Tests

Name
Autism Spectrum Disorders and Intellectual Disability (ASD-ID) Comprehensive Sequencing Panel with CNV Detection
Autosomal Dominant Limb Girdle Muscular Dystrophy (LGMD) Sequencing Panel
Autosomal Recessive Limb Girdle Muscular Dystrophy (LGMD) Sequencing Panel
Charcot Marie Tooth - Axonal Neuropathy Sequencing Panel
Charcot Marie Tooth - Comprehensive Sequencing Panel
Comprehensive Neuromuscular Sequencing Panel
Comprehensive Neuropathy Sequencing Panel
Congenital Disorders of Glycosylation (CDG) Sanger Sequencing Panel 2
Congenital Disorders of Glycosylation, Type Ie (CDG Ie) via the DPM1 Gene
Congenital Disorders of Glycosylation, Type Io Plus Secondary Dystroglycanopathy via the DPM3 Gene
Congenital Fiber Type Disproportion Sequencing Panel
Congenital Muscular Dystrophy, Megaconial Type via the CHKB Gene
Dystroglycan-Related Congenital Muscular Dystrophy Sequencing Panel
Dystroglycanopathies via the POMK Gene
Dystroglycanopathy via the B3GALNT2 Gene
Dystroglycanopathy via the DAG1 Gene
Dystroglycanopathy via the FKTN Gene
Dystroglycanopathy via the LARGE1/LARGE Gene
Dystroglycanopathy via the GMPPB Gene
Dystrophinopathy via the DMD Gene
Dystrophinopathy via the DMD Gene
Emery-Dreifuss Muscular Dystrophy (EDMD1) via the EMD Gene
Hutchinson-Gilford Progeria Syndrome (HGPS) via the LMNA Gene
Integrin Alpha 7-Related Congenital Myopathy via the ITGA7 Gene
Laminopathies via the LMNA Gene
Left Ventricular Noncompaction (LVNC) Sequencing Panel with CNV Detection
Limb Girdle Muscular Dystrophy Type 2I via the FKRP Gene
Limb-Girdle Muscular Dystrophy (LGMD) Sequencing Panel
Merosin-Deficient Congenital Muscular Dystrophy (MDC1A) via the LAMA2 Gene (Mexican Exon 55 Mutation)
Merosin-Deficient Congenital Muscular Dystrophy (MDC1A) via the LAMA2 Gene
Myofibrillar Myopathy Sequencing Panel
Type VI Collagenopathy via the COL6A1 Gene
Type VI Collagenopathy via the COL6A2 Gene
Type VI Collagenopathy via the COL6A3 Gene
Type VI-Related Collagenopathy Sequencing Panel
Type VI-Related Collagenopathy via the COL12A1 Gene
Walker-Warburg Syndrome via the B3GNT1(B4GAT1) Gene
Walker-Warburg Syndrome via the POMGNT1 Gene
Walker-Warburg Syndrome via the POMT1 Gene
Walker-Warburg Syndrome via the POMT2 Gene
Walker-Warburg Syndrome via the TMEM5 Gene
Walker-Warburg Syndrome via the Glycosyltransferase-Like Domain-Containing Protein 2 (POMGNT2) Gene
Walker-Warburg Syndrome via the Isoprenoid Synthase Domain Containing (ISPD) Gene

CONTACTS

Genetic Counselors
Geneticist
Citations
  • Allamand V., Guicheney P. 2002. European Journal of Human Genetics. 10: 91-4. PubMed ID: 11938437
  • Baker N.L. et al. 2005. Human Molecular Genetics. 14: 279-93. PubMed ID: 15563506
  • Bertini E. et al. 2011. Seminars in Pediatric Neurology. 18: 277-88. PubMed ID: 22172424
  • Butterfield R.J. et al. 2013. Human Mutation. 34: 1558-67. PubMed ID: 24038877
  • Hicks D. et al. 2014. Human Molecular Genetics. 23: 2353-63. PubMed ID: 24334769
  • Human Gene Mutation Database (Bio-base).
  • Jöbsis G.J. et al. 1999. Brain : a Journal of Neurology. 122 ( Pt 4): 649-55. PubMed ID: 10219778
  • Lampe A.K. et al. 2005. Journal of Medical Genetics. 42: 108-20. PubMed ID: 15689448
  • Lampe A.K., Bushby K.M. 2005. Journal of Medical Genetics. 42: 673-85. PubMed ID: 16141002
  • Pan T.C. et al. 2003. American Journal of Human Genetics. 73: 355-69. PubMed ID: 12840783
  • Sparks S. et al. 2012. Congenital Muscular Dystrophy Overview. In: Pagon RA, Adam MP, Bird TD, Dolan CR, Fong C-T, and Stephens K, editors. GeneReviews™, Seattle (WA): University of Washington, Seattle. PubMed ID: 20301468
  • Vuillaumier-Barrot S. et al. 2012. American Journal of Human Genetics. 91: 1135-43. PubMed ID: 23217329
  • Zou Y. et al. 2014. Human Molecular Genetics. 23: 2339-52. PubMed ID: 24334604
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TEST METHODS

NextGen Sequencing using PG-Select Capture Probes

Test Procedure

We use a combination of Next Generation Sequencing (NGS) and Sanger sequencing technologies to cover the full coding regions of the listed genes plus ~20 bases of non-coding DNA flanking each exon.  As required, genomic DNA is extracted from the patient specimen.  For NGS, patient DNA corresponding to these regions is captured using an optimized set of DNA hybridization probes.  Captured DNA is sequenced using Illumina’s Reversible Dye Terminator (RDT) platform (Illumina, San Diego, CA, USA).  Regions with insufficient coverage by NGS are covered by Sanger sequencing.  All pathogenic, likely pathogenic, or variants of uncertain significance are confirmed by Sanger sequencing.

For Sanger sequencing, Polymerase Chain Reaction (PCR) is used to amplify targeted regions.  After purification of the PCR products, cycle sequencing is carried out using the ABI Big Dye Terminator v.3.0 kit.  PCR products are resolved by electrophoresis on an ABI 3730xl capillary sequencer.  In nearly all cases, cycle sequencing is performed separately in both the forward and reverse directions.

Patient DNA sequence is aligned to the genomic reference sequence for the indicated gene region(s). All differences from the reference sequences (sequence variants) are assigned to one of five interpretation categories, listed below, per ACMG Guidelines (Richards et al. 2015).

(1) Pathogenic Variants
(2) Likely Pathogenic Variants
(3) Variants of Uncertain Significance
(4) Likely Benign Variants
(5) Benign, Common Variants

Human Genome Variation Society (HGVS) recommendations are used to describe sequence variants (http://www.hgvs.org).  Rare variants and undocumented variants are nearly always classified as likely benign if there is no indication that they alter protein sequence or disrupt splicing.

Analytical Validity

As of March 2016, 6.36 Mb of sequence (83 genes, 1557 exons) generated in our lab was compared between Sanger and NextGen methodologies. We detected no differences between the two methods. The comparison involved 6400 total sequence variants (differences from the reference sequences). Of these, 6144 were nucleotide substitutions and 256 were insertions or deletions. About 65% of the variants were heterozygous and 35% homozygous. The insertions and deletions ranged in length from 1 to over 100 nucleotides.

In silico validation of insertions and deletions in 20 replicates of 5 genes was also performed. The validation included insertions and deletions of lengths between 1 and 100 nucleotides. Insertions tested in silico: 2200 between 1 and 5 nucleotides, 625 between 6 and 10 nucleotides, 29 between 11 and 20 nucleotides, 25 between 21 and 49 nucleotides, and 23 at or greater than 50 nucleotides, with the largest at 98 nucleotides. All insertions were detected. Deletions tested in silico: 1813 between 1 and 5 nucleotides, 97 between 6 and 10 nucleotides, 32 between 11 and 20 nucleotides, 20 between 21 and 49 nucleotides, and 39 at or greater than 50 nucleotides, with the largest at 96 nucleotides. All deletions less than 50 nucleotides in length were detected, 13 greater than 50 nucleotides in length were missed. Our standard NextGen sequence variant calling algorithms are generally not capable of detecting insertions (duplications) or heterozygous deletions greater than 100 nucleotides. Large homozygous deletions appear to be detectable.   

Analytical Limitations

Interpretation of the test results is limited by the information that is currently available.  Better interpretation should be possible in the future as more data and knowledge about human genetics and this specific disorder are accumulated.

When Sanger sequencing does not reveal any difference from the reference sequence, or when a sequence variant is homozygous, we cannot be certain that we were able to detect both patient alleles.  Occasionally, a patient may carry an allele which does not amplify, due to a large deletion or insertion.   In these cases, the report will contain no information about the second allele.  Our Sanger and NGS Sequencing tests are generally not capable of detecting Copy Number Variants (CNVs).

We sequence all coding exons for each given transcript, plus ~20 bp of flanking non-coding DNA for each exon.  Test reports contain no information about other portions of the gene, such as regulatory domains, deep intronic regions or any currently uncharacterized alternative exons.

In most cases, we are unable to determine the phase of sequence variants.  In particular, when we find two likely causative mutations for recessive disorders, we cannot be certain that the mutations are on different alleles.

Our ability to detect minor sequence variants due to somatic mosaicism is limited.  Sequence variants that are present in less than 50% of the patient’s nucleated cells may not be detected.

Runs of mononucleotide repeats (eg (A)n or (T)n) with n >8 in the reference sequence are generally not analyzed because of strand slippage during PCR.

Unless otherwise indicated, DNA sequence data is obtained from a specific cell-type (usually leukocytes from whole blood).   Test reports contain no information about the DNA sequence in other cell-types.

We cannot be certain that the reference sequences are correct.

Rare, low probability interpretations of sequencing results, such as for example the occurrence of de novo mutations in recessive disorders, are generally not included in the reports.

We have confidence in our ability to track a specimen once it has been received by PreventionGenetics.  However, we take no responsibility for any specimen labeling errors that occur before the sample arrives at PreventionGenetics.

Deletion/Duplication Testing Via Array Comparative Genomic Hybridization

Test Procedure

Equal amounts of genomic DNA from the patient and a gender matched reference sample are amplified and labeled with Cy3 and Cy5 dyes, respectively. To prevent any sample cross contamination, a unique sample tracking control is added into each patient sample. Each labeled patient product is then purified, quantified, and combined with the same amount of reference product. The combined sample is loaded onto the designed array and hybridized for at least 22-42 hours at 65°C. Arrays are then washed and scanned immediately with 2.5 µM resolution. Only data for the gene(s) of interest for each patient are extracted and analyzed.

Analytical Validity

PreventionGenetics' high density gene-centric custom designed aCGH enables the detection of relatively small deletions and duplications within a single exon of a given gene or deletions and duplications encompassing the entire gene. PreventionGenetics has established and verified this test's accuracy and precision.

Analytical Limitations

Our dense probe coverage may allow detection of deletions/duplications down to 100 bp; however due to limitations and probe spacing this cannot be guaranteed across all exons of all genes. Therefore, some copy number changes smaller than 100-300 bp within a targeted large exon may not be detected by our array.

This array may not detect deletions and duplications present at low levels of mosaicism or those present in genes that have pseudogene copies or repeats elsewhere in the genome.

aCGH will not detect balanced translocations, inversions, or point mutations that may be responsible for the clinical phenotype.

Breakpoints, if occurring outside the targeted gene, may be hard to define.

The sensitivity of this assay may be reduced when DNA is extracted by an outside laboratory.

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Ordering Options


myPrevent - Online Ordering
  • The test can be added to your online orders in the Summary and Pricing section.
  • Once the test has been added log in to myPrevent to fill out an online requisition form.
REQUISITION FORM
  • A completed requisition form must accompany all specimens.
  • Billing information along with specimen and shipping instructions are within the requisition form.
  • All testing must be ordered by a qualified healthcare provider.

SPECIMEN TYPES
WHOLE BLOOD

(Delivery accepted Monday - Saturday)

  • Collect 3 ml -5 ml (5 ml preferred) of whole blood in EDTA (purple top tube) or ACD (yellow top tube). For Test #500-DNA Banking only, collect 10 ml -20 ml of whole blood.
  • For small babies, we require a minimum of 1 ml of blood.
  • Only one blood tube is required for multiple tests.
  • Ship blood tubes at room temperature in an insulated container. Do not freeze blood.
  • During hot weather, include a frozen ice pack in the shipping container. Place a paper towel or other thin material between the ice pack and the blood tube.
  • In cold weather, include an unfrozen ice pack in the shipping container as insulation.
  • At room temperature, blood specimen is stable for up to 48 hours.
  • If refrigerated, blood specimen is stable for up to one week.
  • Label the tube with the patient name, date of birth and/or ID number.

DNA

(Delivery accepted Monday - Saturday)

  • Send in screw cap tube at least 5 µg -10 µg of purified DNA at a concentration of at least 20 µg/ml for NGS and Sanger tests and at least 5 µg of purified DNA at a concentration of at least 100 µg/ml for gene-centric aCGH, MLPA, and CMA tests, minimum 2 µg for limited specimens.
  • For requests requiring more than one test, send an additional 5 µg DNA per test ordered when possible.
  • DNA may be shipped at room temperature.
  • Label the tube with the composition of the solute, DNA concentration as well as the patient’s name, date of birth, and/or ID number.
  • We only accept genomic DNA for testing. We do NOT accept products of whole genome amplification reactions or other amplification reactions.

CELL CULTURE

(Delivery preferred Monday - Thursday)

  • PreventionGenetics should be notified in advance of arrival of a cell culture.
  • Culture and send at least two T25 flasks of confluent cells.
  • Some panels may require additional flasks (dependent on size of genes, amount of Sanger sequencing required, etc.). Multiple test requests may also require additional flasks. Please contact us for details.
  • Send specimens in insulated, shatterproof container overnight.
  • Cell cultures may be shipped at room temperature or refrigerated.
  • Label the flasks with the patient name, date of birth, and/or ID number.
  • We strongly recommend maintaining a local back-up culture. We do not culture cells.
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