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Solid Tumor Gene Panel Assay

Indicated for the detection of variants that are targets for cancer therapeutic or prognosis

  • Indicated for the detection of variants that are targets for cancer therapeutic or prognosis.
  • Covers hotspots, full exons or the entire gene within 26 of the most relevant cancer genes involved in solid tumors.
  • Offers at least 94% sensitivity and 100% specificity and positive predictive values for SNVs and indels with ≥3% and 5% variant allele frequency, respectively.
  • Can be performed on DNA extracted from formalin-fixed, paraffin-embedded (FFPE).

Genes tested in the assay:

clinical utility

The clinical utility of mutations found in the genes included in this panel is well established. For examples, certain mutations in the kinase domains (TKD) of some genes predict response to therapy with tyrosine kinase inhibitors (TKIs) in different types of cancer. This includes, for example, mutations in the EGFR and ERBB2 TKD in nonesmall cell lung cancer (1-2), mutations in BRAF gene in melanoma (3), mutations in ALK gene in neuroblastoma (4), and mutations in KIT and PDGFRA in gastrointestinal stromal tumors (5). In contrast, other mutations predict resistance to therapy; for example, mutations in codon 12 mutations in KRAS gene predict resistance to treatment with EGFR tyrosine kinase inhibitors in lung cancer (6) and resistance to treatment with anti-EGFR monoclonal antibodies in colorectal cancer (7). In addition, unexpected findings, such as the discovery of BRAF V600E mutation in an ovarian cancer, with subsequent response to treatment with a BRAF inhibitor (8) support the utility of sequencing genes that are not strictly characteristic for the patient’s tumor type. Thus, the Solid Tumor Gene Panel assay that we have validated here provides actionable information to direct patient care in routine practice.

  1. Paez JG, Jänne PA, Lee JC, Tracy S, Greulich H, Gabriel S, Herman P, Kaye FJ, Lindeman N, Boggon TJ, Naoki K, Sasaki H, Fujii Y, Eck MJ, Sellers WR, Johnson BE, Meyerson M: EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science 2004, 304:1497e1500.
  2. Stephens P, Hunter C, Bignell G, Edkins S, Davies H, Teague J, et al: Lung cancer: intragenic ERBB2 kinase mutations in tumours. Nature 2004, 431:525e526.
    Davies H, Bignell GR, Cox C, Stephens P, Edkins S, Clegg S, et al: Mutations of the BRAF gene in human cancer. Nature 2002, 417: 949e954.
  3. Janoueix-Lerosey I, Lequin D, Brugières L, Ribeiro A, de Pontual L, Combaret V, Raynal V, Puisieux A, Schleiermacher G, Pierron G, Valteau-Couanet D, Frebourg T, Michon J, Lyonnet S, Amiel J, Delattre O: Somatic and germline activating mutations of the ALK kinase receptor in neuroblastoma. Nature 2008, 455:967e970.
  4. Hirota S, Isozaki K, Moriyama Y, Hashimoto K, Nishida T, Ishiguro S, Kawano K, Hanada M, Kurata A, Takeda M, Tunio GM, Matsuzawa Y, Kanakura Y, Shinomura Y, Kitamura Y: Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors.Science 1998, 279:577e580.
  5. Pao W, Wang TY, Riely GJ, Miller VA, Pan Q, Ladanyi M, Zakowski MF, Heelan RT, Kris MG, Varmus HE: KRAS mutations and primary resistance of lung adenocarcinomas to gefitinib or erlotinib. PLoS Med 2005, 2:e17.
  6. Karapetis CS, Khambata-Ford S, Jonker DJ, O’Callaghan CJ, Tu D, Tebbutt NC, Simes RJ, Chalchal H, Shapiro JD, Robitaille S, Price TJ, Shepherd L, Au HJ, Langer C, Moore MJ, Zalcberg JR: Kras mutations and benefit from cetuximab in advanced colorectal cancer. N Engl J Med 2008, 359:1757e1765.
  7. Falchook GS, Long GV, Kurzrock R, Kim KB, Arkenau TH, Brown MP, Hamid O, Infante JR, Millward M, Pavlick AC, O’Day SJ, Blackman SC, Curtis CM, Lebowitz P, Ma B, Ouellet D, Kefford RF: Dabrafenib in patients with melanoma, untreated brain metastases, and other solid tumours: a phase 1 dose-escalation trial. Lancet 2012, 379:1893e1901.


Each patient requisition is reviewed by a Clinical Coordinator to assure all necessary information is present. Patient eligibility includes an assessment of (but is not limited to) the following criteria:

The patient tumor is solid tissue or any tumor where one or more gene targets on the panel is known to be actionable for that specific tumor

Tumor biopsy is of sufficient tumor cellularity

Sufficient quantity and quality of FFPE biopsy material is available for testing

Patient and/or appropriate family member has provided consent to the testing


Sample Type:  FFPE biopsy of tumor.

Acceptable specimen:  Specimen contains tumor content at least 10% or higher as determined from a H&E slide review. Submitted specimen contains at least (6) – 10um slides (in exceptional cases (3) – 10um slides will be accepted) or at least (1) – 3mm punch.

This test is offered on tumor biopsies only.

Turnaround Time

15 business days – Times begin from receipt of the tissue sample(s) by UAGC-CS and are based on business hours of the laboratory: Monday through Friday, 9am-5pm Arizona Time.

Additional Details