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Biocept’s CNSide™ platform features a range of tests to assess NCCN guideline-driven-clinically actionable cancer biomarkers from a patient’s cerebrospinal fluid sample.

Test Technology Result Interpretation CPT Codes* Method Targeted Therapies
ALK FISH Translocation 88377 CSF-TC Xalkori®, Zykadia® Alecensa®, Alunbrig®
CSF-TC Antibody Capture Enumeration 86152/86153 88346 x1, 88350 x2 CSF-TC
EGFR FISH Amplification 88377 CSF-TC Prognostic insights
ER Expression Expression 88346 or 88350 CSF-TC Nolvadex®, Faslodex®, Femara® Arimidex®, Aromasin®
FGFR1 FISH Amplification 88377 CSF-TC Iclusig®, Votrient®, Stivarga® Lenvima®
HER2 FISH Amplification 81479 or 88377 CSF-TC Herceptin®, Perjeta®, Tykerb® Kadcyla®
MET FISH Amplification 88377 CSF-TC Xalkori®, Cabometyx®
MYC FISH Amplification 88377 CSF-TC Prognostic insights
NTRK1 FISH Fusion 88377 CSF-TC Rozlytrek™, Vitrakvi®
NTRK3 FISH Fusion 88377 CSF-TC Rozlytrek™, Vitrakvi®
PD-L1 Expression Expression 88346 or 88350 CSF-TC Keytruda®, Opdivo® Tecentriq®
PR Expression Expression 88346 or 88350 CSF-TC Nolvadex®, Aromatase Inhibitors
PTEN FISH Gene Loss 88377 CSF-TC Prognostic insights
RET FISH Translocation 88377 CSF-TC Cabometyx®, Caprelsa®
ROS1 FISH Translocation 88377 CSF-TC Xalkori®

*These CPT Codes are only representative of general or usual CPT Code utilized for the test. They should not be used to select a CPT Code for any particular test or patient. Such CPT Code selection should be performed by a qualified, certified coder based on the patient’s individual medical file.


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.


EGFR is a member of the ErbB family of receptors that have been implicated in tumor progression of many cancer types. Data suggests that in prostate cancer, even minimal change in EGFR gene copy number may play a role in EGFR protein expression, and high-level expression is often caused by EGFR polysomy.43 Overexpression of EGFR contributes to progression of a broad continuum of prostate cancer – hormone dependent to castration resistant.

Methodology: Biocept’s EGFR gene amplification test is performed on circulating tumor cells (CTCs), using FISH analysis to identify changes in EGFR gene copy number.


Estrogen receptors (ERs) are a group of receptors that bind to and are activated by the hormone estrogen 17β-estradiol.15 Binding of estrogen to its receptor promotes cell growth, and ER is commonly expressed in both primary and metastatic breast cancers. In fact, ~75% of invasive breast cancers express ER. Thus, for patients with newly diagnosed or recurring metastatic breast cancer, the assessment of ER expression levels is standard of care, and accurate assessment can play a major role in treatment outcomes. This is because ER expression is a strong predictive factor for response to hormone therapies.16

Several drugs have been developed that inhibit ERs in different ways. Drugs that block estrogen from binding ER include tamoxifen (Nolvadex®) and fulvestrant (Faslodex®). Selective estrogen receptor modulators (SERMs) reduce estrogen levels, and include letrozole (Femara®), anastrozole (Arimidex®), and exemestane (Aromasin®). Importantly, these hormone therapies are recommended for women with ER-positive breast cancers, but they do not help women whose tumors lack ERs.

Targeted Therapies: Tamoxifen (Nolvadex®), fulvestrant (Faslodex®), letrozole (Femara®), anastrozole (Arimidex®), and exemestane (Aromasin®).

Methodology: Biocept’s ER CSF test is performed on circulating tumor cells (CTCs), using fluorescently labeled antibodies to detect ER protein.


Fibroblast growth factor receptor 1 (FGFR1) is one of four fibroblast growth factor receptors, which are involved in diverse cellular processes, such as cell division, cell growth and maturation, the formation of blood vessels, and wound healing. Up to 10% of breast cancer patients have tumors that overexpress FGFR117, and the FGFR1 gene is amplified in ~20% of patients diagnosed with squamous cell lung cancer (predominantly former/current smokers). In different types of lung cancer, such as adenocarcinoma, FGFR1 amplification is quite rare.18

Recent studies suggest that the FGFR pathway can be targeted by FGFR inhibitors, thus assessing the FGFR1 status of a tumor can help select the most beneficial pharmacologic intervention.19 There are several pharmacologic agents that have been, or are being developed to inhibit FGFR signaling. These include highly selective FGFR1 inhibitors, and multi-kinase inhibitors. Only four agents have been approved by the FDA for use in cancer, although their approvals were not based on their activity against FGFR. These multi-kinase inhibitors are ponatinib (Iclusig®), pazopanib (Votrient®), regorafenib (Stivarga®), and lenvatinib (Lenvima®).

Targeted Therapies: Ponatinib (Iclusig®), pazopanib (Votrient®), regorafenib (Stivarga®), and lenvatinib (Lenvima®).

Methodology: Biocept’s FGFR1 CSF test is performed on circulating tumor cells (CTCs), using FISH analysis to identify FGFR1 gene amplifications.


The human epidermal growth factor receptor 2 (HER2, also called ERBB2 or NEU) is associated with several forms of cancer. Approximately 15–30% of breast cancer patients have tumors that overexpress HER2, and 7–34% of gastric cancers are HER2 positive.20, 21 HER2 overexpression is also associated with salivary duct carcinomas.

By 1998, antibody therapy targeting the HER2 pathway was shown to significantly improve progression-free and overall survival in metastatic disease. In 2005, evidence of improvement in disease-free and overall survival from trastuzumab (Herceptin®) adjuvant trials, or administration after surgery, became available. However, not all patients with HER2 overexpression benefit from this widely used agent. Second-generation studies in metastatic disease led to the approval of several new HER2-targeted therapies using: 1) small molecule tyrosine kinase inhibitors, such as lapatinib (Tykerb®), 2) new HER2/HER3 antibodies, such as pertuzumab (Perjeta®), and 3) the antibody chemotherapy conjugate ado-trastuzumab emtansine (Kadcyla®). These successes supported the launch of second-generation adjuvant trials testing single and dual HER2-targeted agents, administered concomitantly or sequentially with chemotherapy. Because of these efforts, HER2-positive breast cancer is no longer associated with poor prognosis if HER2-targeted therapies are administered.22 Recent guidance by the US FDA suggests that pathologic response to HER2-targeted therapy given preoperatively may allow for an earlier assessment of clinical benefit in the adjuvant setting.

Targeted Therapies: Trastuzumab (Herceptin®), pertuzumab (Perjeta®), emtansine (Kadcyla®), and  lapatinib (Tykerb®).

Methodology: Biocept’s HER2 CSF test is performed on circulating tumor cells (CTCs), using FISH analysis to identify changes in HER2gene copy number.


MET (or c-MET) was first discovered as an oncogene that encodes the tyrosine kinase receptor for hepatocyte growth factor (HGF). MET can be mutated or overexpressed in a number of human epithelial cancers, including lung (3%), colon (5%), kidney (5%), and upper digestive system (10%). Activating the MET receptor in malignant cells activates a number of signaling transduction pathways, altering a number of biological process and driving metastasis.27, 28, 29

MET deregulation in lung cancer is associated with poor outcomes and resistance to anti-EGFR therapies.30 It is anticipated that targeted therapy against MET and its pathway will lead to significant inhibition of cancer growth and metastasis. Multiple antibodies against MET and small molecule MET inhibitors are currently in clinical trials for the treatment of various cancer types.

Currently, crizotinib (Xalkori®) and cabozantinib (Cabometyx®) are the only FDA-approved therapies that target MET. These agents are dual- or multi-TKIs, blocking MET together with other cancer-related pathways. Several compounds targeting the MET pathway are under investigation in clinical trials. These include foretinib (Exelixis®), capmatinib (Novartis), tivantinib (ArQule Inc.), and glesatinib (Mirati Therapeutics). Determining which patient harbor MET mutations, and are therefore more likely to respond to MET kinase inhibitors, could contribute to better clinical outcomes.

Targeted Therapies: Crizotinib (Xalkori®), cabozantinib (Cabometyx®), cabozantinib (Exelixis®) and (Tivantinib®)

Methodology: Biocept’s MET CSF test is performed on circulating tumor cells (CTCs), using FISH analysis to identify MET gene amplifications.


The MYC family oncogene is deregulated in >50% of human cancers – often associated with poorer outcomes. Clinical studies have shown promise to MYC – pathway inhibition as a strategy for cancer treatment.44 Amplification of the long arm of chromosome 8 (8q) occurs in prostate cancer45 and c-MYC can be found in circulating tumor cells (CTCs) of some patients with progressive castration – resistant metastatic prostate cancer.46 c-MYC over expression may lead to increased androgen – independent cell growth and proliferation.47 For those patents with ongoing and androgen receptor therapy, selective pressure may also change the MYC gene amplification status, identifiable in CTCs.48

Methodology: Biocept’s c-MYC CSF test is performed on circulating tumor cells (CTCs), using FISH analysis to identify changes in c-MYC gene amplification.


NTRK1, NTRK2, and NTRK3 genes encode for three transmembrane protein receptors, Trk A, Trk B, and Trk C, that are part of the tropomyosin receptor kinase (Trk) family. The Trk family play important roles in neuronal development, maintenance, and protection of cells. Potential oncogenesis may occur when gene fusions involving NTRK1, 2,and 3 result in overexpression of Trk receptors. Targeted inhibitor therapies of neurotropic tyrosine kinases can be efficacious in selected patients with NTRK1, NTRK2, or NTRK3 gene fusions.53

Targeted Therapies: Rozlytrek™ (entrectinib) and Vitrakvi® (larotrectinib)

Methodology: Biocept’s NTRK1 CSF test is performed on circulating tumor cells (CTCs), using FISH analysis to identify NTRK1 gene fusions/rearrangements.


NTRK1, NTRK2, and NTRK3 genes encode for three transmembrane protein receptors, Trk A, Trk B, and Trk C, that are part of the tropomyosin receptor kinase (Trk) family. The Trk family play important roles in neuronal development, maintenance, and protection of cells. Potential oncogenesis may occur when gene fusions involving NTRK1, 2,and 3 result in overexpression of Trk receptors. Targeted inhibitor therapies of neurotropic tyrosine kinases can be efficacious in selected patients with NTRK1, NTRK2, or NTRK3 gene fusions.53

Targeted Therapies: Rozlytrek™ (entrectinib) and Vitrakvi® (larotrectinib)

Methodology: Biocept’s NTRK3 liquid biopsy test is performed on circulating tumor cells (CTCs), using FISH analysis to identify NTRK3 gene fusions/rearrangements.


Programmed death-1 (PD-1) is an immune checkpoint receptor expressed by T cells. Expression of PD-L1 has been described for many tumor types, including melanoma, both squamous and non-squamous NSCLC, breast, ovarian, pancreatic, esophageal, kidney, bladder, and hematopoietic malignancies.35,36,37,38,39,40 Upregulation of PD-1 plays a key role in T-cell exhaustion, which hampers the ability of the immune system to destroy cancer cells. When PD-1 binds its ligand PD-L1 (programmed death ligand-1), a signal is transduced, telling the T-cell to leave other cells alone. This checkpoint is in place to protect normal cells from immune attack, but some cancer cells co-opted this system, expressing high levels of PD-L1 to evade the immune system. Detecting PD-L1 in tumor cells identifies cancer patients that may benefit from treatment with immunotherapy agents. These agents, called PD-1 or PD-L1 inhibitors (or checkpoint inhibitors) have been shown to increase immune responses to cancers and improve patient survival.41

In 2014, the FDA granted accelerated approval for pembrolizumab (Keytruda®) to treat advanced or unresectable melanoma, making it the first PD-1 inhibitor cleared in the US. Later the same year, the FDA approved nivolumab (Opdivo®) for melanoma. In 2015, nivolumab became the first immunotherapy agent approved for the treatment of lung cancer. Finally, in 2016 the FDA granted accelerated approval for the PD-L1 inhibitor, atezolizumab (Tecentriq®), to treat bladder cancer; this drug was subsequently approved for lung cancer. Other PD-1/PD-L1 targeted treatments are in clinical development, either alone or in combination with other agents, and in various types of cancer.

Targeted Therapies: Pembrolizumab (Keytruda®), nivolumab (Opdivo®), and atezolizumab (Tecentriq®)

Methodology: Biocept’s PD-L1 test is performed on circulating tumor cells (CTCs), using fluorescently labeled antibodies to detect PD-L1 protein.


The progesterone receptor (PR), much like the estrogen receptor, is a nuclear receptor that is frequently expressed in breast cancer cells. Cancer cells that express PR depend on progesterone to grow, and are therefore susceptible to hormone therapy. Determining the hormone receptor status of a breast tumor is therefore an important step toward determining whether the patient is likely to respond to a targeted therapy.42Common therapies for PR-positive breast tumors either lower estrogen/progesterone levels (e.g., aromatase inhibitors) or prevent estrogen/progesterone from binding their receptors (e.g.,Tamoxifen).

Targeted Therapies: Tamoxifen (Nolvadex®) and Aromatase Inhibitors

Methodology: Biocept’s PR test is performed on circulating tumor cells (CTCs), using fluorescently labeled antibodies to detect PR protein.


Phosphatase with tensin homology (PTEN) is a frequently inactivated tumor suppressor gene in human cancers. PTEN gene loss is found in up to 20% of localized prostate tumors and more than 40% for metastatic castrate-resistant prostate cancer.49 PTEN gene loss may drive progression through activation of the PI3K/AKT pathway.51 PTEN loss/deletion has been shown to be associated with poorer outcomes, including more advanced disease at surgery and shorter time to biochemical recurrence.49,50 Overall survival decreased in patients with PTEN loss versus those with no PTEN deletion (7 mo. vs. 12.1 mo.).51

Methodology: Biocept’s PTEN is performed on circulating tumor cells, using FISH analysis to identify PTEN gene loss.


The RET proto-oncogene encodes a receptor tyrosine kinase whose ligand is glial cell line-derived neurotrophic factor (GDNF), as well as two other proteins highly related to GDNF. The RET gene is susceptible to rearrangements, resulting in growth-promoting chimeric or fusion proteins that are found in 10–20% of sporadic papillary thyroid carcinomas (PTCs),43 and 1–2% of NSCLCs. In NSCLC, RET rearrangements most commonly occur in the absence of mutations in EGFR, KRAS, ALK, or ROS1, and tend to affect young never-smokers. Sporadic PTC is the most common type of thyroid cancer, representing 75–80% of all thyroid cancer cases. The close association between RET rearrangements and PTC strongly suggests that they play a causative role in tumor development.

The FDA has approved multi-kinase inhibitors that exhibit activity in cancers harboring RET alterations, including cabozantinib (Cabometyx®) and vandetanib (Caprelsa®). Searches are ongoing for additional compounds that can effectively counteract RET gene rearrangements or fusions.

Targeted Therapies: Cabozantinib (Cabometyx®) and vandetanib (Caprelsa®)

Methodology: Biocept’s RET is performed on circulating tumor cells, using FISH analysis to identify RET gene rearrangements.


The proto-oncogene ROS1 encodes a protein tyrosine kinase. The ROS1 gene is structurally similar to ALK, and ROS1 gene rearrangements are found in 1–2% of NSCLC cases. While the precise role played by ROS1 during normal development has not been identified, tumors harboring ROS1 fusions are remarkably responsive to TKIs.44 As a result, there is great interest in identifying ROS1 rearrangements in patients to determine which should receive TKI-based therapies. Pre-clinical and early clinical evidence suggest that tumors associated with a ROS1 rearrangement may be sensitive to dual ALK/MET inhibitors. Recently, the small molecule tyrosine kinase inhibitor, crizotinib (Xalkori®), was approved for the treatment of patients with metastatic NSCLC whose tumors are ROS1-positive.

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

Methodology: Biocept’s ROS1 test is performed on circulating tumor cells (CTCs), using FISH analysis to identify ROS1 gene rearrangements.


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