target selectorTM biomarkerS

Test Menu

Biocept’s Target Selector™ platform features a range of liquid biopsy tests to assess NCCN guideline-driven-clinically actionable cancer biomarkers from a patient’s blood sample.

Increasing Access to Targeted Therapies via Liquid Biopsy
Test Technology Result Interpretation CPT Codes Method Targeted Therapies
ALK FISH Translocation 88377 CTC Xalkori®, Zykadia®, Alecensa®, Alunbrig®
AR Expression Expression 88346 or 88350 CTC Zytiga®, Xtandi®
BRAF Sequencing Mutation 81210 ctDNA Zelboraf®, Tafinlar®, Mekinist®
CTC Antibody
Enumeration 86152/86153 88346x1, 88350x2 CTC
Sequencing Mutation 81235 ctDNA Tarceva®, Gilotrif®, Iressa®, Tagrisso®
ER Expression Expression 88346 or 88350 CTC Nolvadex®, Aromatase Inhibitors
FGFR1 FISH Amplification 88377 CTC Nolvadex®, Faslodex®, Femara®, Arimidex®, Aromasin®
HER2 FISH Amplification 88377 CTC Herceptin®, Perjeta®, Tykerb®, Kadcyla®
KRAS Sequencing Mutation 81275 ctDNA Erbitux®, Vectibix®
MET FISH Amplification 88377 CTC Xalkori®, Cabometyx®, Exelixi®, Tivantinib®
NRAS Sequencing Mutation 81311 ctDNA Erbitux®, Vectibix®
PD-L1 Expression Expression 88346 or 88350 CTC Keytruda®, Opdivo®
PR Expression Expression 88346 or 88350 CTC Nolvadex®, Aromatase Inhibitors
RET FISH Translocation 88377 CTC Cabometyx®, Capresla®
ROS1 FISH Translocation 88377 CTC Xalkori®, Zykadia®, Alecensa®

ALK gene rearrangements are found in 2-7% of non-small cell lung cancer (NSCLC) cases, and detection is used to qualify patients for possible therapeutic intervention. In these rearrangements, the anaplastic lymphoma kinase (ALK) gene is fused to the echinoderm microtubule-associated protein-like 4 (EML4) gene. Multiple variants of this oncogenic EML4-ALK fusion have been reported; all involve the same cytoplasmic portion of the ALK protein, but with different truncations of EML4. Importantly, ALK rearrangements most commonly occur in the absence of EGFR or KRAS mutations.1

ALK gene rearrangements, or the resulting fusion proteins, may be detected in tumor specimens using fluorescence in situ hybridization (FISH), immunohistochemistry (IHC), or reverse transcription polymerase chain reaction (RT-PCR).2 Biocept’s Target Selector™ liquid biopsy platform has the ability to identify ALK gene translocations in patients using a simple blood sample.

Detection of an ALK fusion is used to determine the likelihood of response to crizotinib (Xalkori®) or ceritinib (Zykadia®), two commercially available tyrosine kinase inhibitors.3 Additionally, alectinib (Alecensa®) and brigatinib (Alunbrig®) are approved for patients with ALK-positive metastatic NSCLC who have progressed on or are intolerant to crizotinib.

Targeted Therapies: Crizotinib (Xalkori®), ceritinib (Zykadia®), alectinib (Alecensa®), and brigatinib (Alunbrig®).

Methodology: Biocept’s ALK liquid biopsy test is performed on circulating tumor cells (CTCs), using FISH analysis to identify ALK gene rearrangements.

Order a Test
Requisition Form


  1. Inamura K, Takeuchi K, Togashi Y, et al. (2009). “EML4-ALK lung cancers are characterized by rare other mutations, a TTF-1 cell lineage, an acinar histology, and young onset.” Mod Pathol. 22(4):508–515.
  2. Weickhardt AJ, Aisner DL, Franklin WA, et al. (2013). “Diagnostic assays for identification of anaplastic lymphoma kinase-positive non-small cell lung cancer”. Cancer. 119(8):1467.
  3. Shaw AT, Yeap BY, Mino-Kenudson M, et al. (2009). “Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK.” J Clin Oncol. 27(26):4247–4253.
  4. Bono JS, Logothetis CJ, Molina A, et al. (2011). “Abiraterone and increased survival in metastatic prostate cancer”. N Engl J Med. 364:1995–2005.
  5. Sher H, Fizazi K, Saad F, et al. (2012). “Increased survival with enzalutamide in prostate cancer after chemotherapy”. N Engl J Med. 367:1187–1197.
  6. Zakaria, F, El-Mashad, N, Mohamed, D. (2016). “Androgen receptor expression as a prognostic and predictive marker in triple-negative breast cancer patients”. Alexandria J of Med. 52:131–140.
  7. Davies H, Bignell GR, Cox C, et al. (2002). “Mutations of the BRAF gene in human cancer”. Nature. 417(6892):949–54.
  8. Mao C, Liao RY, Qiu LX, et al. (2011). “BRAF V600E mutation and resistance to anti-EGFR monoclonal antibodies in patients with metastatic colorectal cancer: a meta-analysis”. Mol Biol Rep. 38(4):2219–2223.
  9. Roth AD, Tejpar S, Delorenzi M, et al. (2010). “Prognostic role of KRAS and BRAF in stage II and III resected colon cancer: results of the translational study on the PETACC-3, EORTC 40993, SAKK 60-00 trial”. J Clin Oncol. 28(3):466–474.
  10. Flaherty, KT. (2011). “Is It Good or Bad to Find a BRAF Mutation?”. Journal of Clinical Oncology. 29(10):1229–1230
  11. Chapman PB, Hauschild A, Robert C, et al. (2011). BRIM-3 Study Group. “Improved survival with vemurafenib in melanoma with BRAF V600E mutation”. N Engl J of Med. 364(26):2507–16.
  12. Lynch TJ, Bell DW, Sordella R, et al. (2004). “Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib”. N Engl J of Med. 350(21):2129–39.
  13. Ladanyi M, Pao W. (2008). “Lung adenocarcinoma: guiding EGFR-targeted therapy and beyond”. Mod Pathol. 21 Suppl 2:S16–22.
  14. Wonjun J, Chang-Min C, Jin KR, et al. (2013). “Mechanisms of acquired resistance to EGFR-tyrosine kinase inhibitor in Korean patients with lung cancer”. BMC Cancer. 13:606.
  15. Dahlman-Wright K, Cavailles V, Fuqua SA, et al. (2006). “International Union of Pharmacology. LXIV. Estrogen receptors”. Pharmacol Rev. 58 4):773–81.
  16. EBCTCG, Davies C, Godwin J, et al. (2011). “Relevance of breast cancer hormone receptors and other factors to the efficacy of adjuvant tamoxifen: patient-level meta-analysis of randomised trials”. Lancet. 378(9793):771–784.
  17. Hynes NE, Dey JH. (2010). “Potential for targeting the fibroblast growth factor receptors in breast cancer”. Cancer Res.70(13):5199–5202.
  18. Weiss J, Sos ML, Seidel D, et al. (2010). “Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1dependency in squamous cell lung cancer”. Sci Transl Med. 2(62):62ra93.
  19. Liang G, Liu Z, Wu J, et al. (2012). “Anticancer molecules targeting fibroblast growth factor receptors”. Trends Pharmacol Sci. 33(10):531–541.
  20. Rüschoff J, Hanna W, Bilous M, et al. (2012). “HER2 testing in gastric cancer: a practical approach”. Modern Pathology. 25(5):637–50.
  21. Meza-Junco J, Au HJ, Sawyer MB (2011). “Critical appraisal of trastuzumab in treatment of advanced stomach cancer”. Cancer Management and Research. 3(3):57–64.
  22. Incorvati J, Shah S, Mu Y, et al. (2013). “Targeted therapy for HER2 positive breast cancer”. J Hematol Oncol. 6:38.
  23. Zhang Z, Wang Y, Vikis HG, et al. (2001). “Wildtype KRAS2 can inhibit lung carcinogenesis in mice”. Nature Genetics. 29(1):25–33.
  24. McCoy MS, Toole JJ, Cunningham JM, et al. (1983). “Characterization of a human colon/lung carcinoma oncogene”. Nature. 302(5903):79–81.
  25. Kranenburg O. (2005). “The KRAS oncogene: past, present, and future”. Biochimica et Biophysica Acta. 1756(2):81–82.
  26. Riely GJ, Marks J, Pao W. (2009). “KRAS mutations in non-small cell lung cancer”. Proc Am Thorac Soc. 6(2):201–205.
  27. Bottaro DP, Rubin JS, Faletto DL, et al. (1991). “Identification of the hepatocyte growth factor receptor as the c-met proto-oncogene product”. Science. 251:802–804.
  28. Di Renzo MF, Narsimhan RP, Olivero M, et al. (1991). “Expression of the Met/HGF receptor in normal and neoplastic human tissues”. Oncogene. 6:1997–2003.
  29. Benvenuti S, Comoglio PM. (2007). “The MET receptor tyrosine kinase in invasion and metastasis”. J Cell Physiol. 213:316–325.
  30. Turke AB, Zejnullahu K, Wu YL, et al. (2010). “Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC”. Cancer Cell. 17(1):77–88.
  32. Dang CV, Reddy EP, Shokat KM, et al. (2007). “Drugging the ‘undruggable’ cancer targets”. Nature Reviews Cancer. 17(8):502-508.
  33. Akinleye A, Furqan M, Mukhi N, et al. (2013). “MEK and the inhibitors: from bench to bedside”. Journal of Hematology & Oncology. 6:27.
  34. Johnson DB, Lovly CM, Flavin M, et al. (2015). “Impact of NRAS mutations for patients with advanced melanoma treated with immune therapies”. Cancer immunology research. 3(3):288–295.
  35. Ghebeh H, Mohammed S, Al-Omair A, et al. (2006). “The B7-H1 (PD-L1) T lymphocyte-inhibitory molecule is expressed in breast cancer patients with infiltrating ductal carcinoma: correlation with important high-risk prognostic factors”. Neoplasia. 8:190–8.
  36. Hamanishi J, Mandai M, Iwasaki M, et al. (2007). “Programmed cell death 1 ligand 1 and tumor-infiltrating CD8+ T lymphocytes are prognostic factors of human ovarian cancer”. Proc Natl Acad Sci USA. 104:3360–5.
  37. Nomi T, Sho M, Akahori T, et al. (2007). “Clinical significance and therapeutic potential of the programmed death-1 ligand/programmed death-1 pathway in human pancreatic cancer”. Clin Cancer Res. 13:2151–7.
  38. Ohigashi Y, Sho M, Yamada Y, et al. (2005). “Clinical significance of programmed death-1 ligand-1 and programmed death-1 ligand-2 expression in human esophageal cancer”. Clin Cancer Res. 11:2947–53.
  39. Hino R, Kabashima K, Kato Y, et al. (2010). “Tumor cell expression of programmed cell death-1 ligand 1 is a prognostic factor for malignant melanoma”. Cancer. 116:1757–66.
  40. Wilcox RA, Ansell SM, Lim MS, et al. (2012). “The B7 homologues and their receptors in hematologic malignancies”. Eur J Haematol. 88:465–75.
  41. Farkona S, Diamandis EP, Blasutig IM. (2016). “Cancer immunotherapy: the beginning of the end of cancer?” BMC Med. 14:73.
  42. Hammond ME, Hayes DF, Dowsett M, et al. (2010). “American Society of Clinical Oncology/College Of American Pathologists guideline recommendations for immunohistochemical testing of estrogen and progesterone receptors in breast cancer”. J Clin Oncol. 28(16):2784–2795.
  43. Ciampi R, Nikiforov YE. (2007). “RET/PTC rearrangements and BRAF mutations in thyroid tumorigenesis”. Endocrinology. 148(3):936–941.
  44. Davies KD, Le AT, Theodoro MF, et al. (2012). “Identifying and targeting ROS1 gene fusions in non-small cell lung cancer”. Clin Cancer Res. 18(17):4570–4579.

partner with biocept

Contact us to learn how Biocept can support your research and testing.