VistaSeq Hereditary Cancer Panel
81201; 81203; 81211; 81213; 81292; 81294; 81295; 81297; 81298; 81300; 81317; 81319; 81321; 81323; 81403; 81404(x2); 81405(x3); 81406(x4); 81408; 81479
VistaSeq Hereditary Cancer Panel is a multi-gene test that detects inherited mutations in genes which have been associated with an increased risk of developing hereditary cancers syndromes. The test provides an assessment of inherited genetic mutations within a panel of 27 genes. Mutations in different genes can cause the same type of cancer; conversely, one gene may be associated with multiple hereditary cancers. NCCN Guidelines® and The Society of Gynecologic Oncology (SGO) note that hereditary multi-gene panels may be an efficient and cost–effective approach to genetic cancer testing when used in appropriate clinical settings.1,2
VistaSeq provides an assessment of inherited genetic mutations within a panel of 27 genes known to be associated with hereditary cancer syndromes.
The following genes are assessed: APC, ATM, BARD1, BMPR1A, BRCA1, BRCA2, BRIP1, CDH1, CDK4, CDKN2A, CHEK2, EPCAM, FAM175A, MLH1, MSH2, MSH6, MUTYH, NBN, PALB2, PMS2, PRKAR1A, PTEN, RAD51C, RAD51D, SMAD4, STK11, TP53.
Next generation sequencing, array-based comparative genomic hybridization (aCGH), and multiplex ligation-dependent probe amplification (MLPA) platforms. The entire coding regions, as well as all flanking noncoding regions, of 27 cancer genes known to be involved in the development and progression of cancers are analyzed by next-generation sequencing. Flanking regions for the BRCA1 and BRCA2 genes include ±20 bp and ±10 bp for all other genes. Copy number variations are assessed by aCGH or MLPA to detect deletions and duplications.
Lavender-top (EDTA) tube or yellow-top (ACD) tube
A Clinical Questionnaire for VistaSeq should be submitted with specimens.
Causes for Rejection
Frozen specimen; leaking tube; clotted specimen; grossly hemolyzed specimen; incorrect anticoagulant
Store at room temperature.
Each gene sequence is interpreted independently of all other gene sequences; however, variants in different genes may sometimes interact to cause or modify a typically monogenic disease phenotype. It cannot be excluded that pathogenic variants were missed due to limitations inherent in the sequence analysis method used here. In addition, the presence of an inherited cancer syndrome due to a different genetic cause cannot be ruled out. Any interpretation given here should be clinically correlated with available information about presentation and the patient's relevant family history.