NexCourse® NSCLC

Choose the best treatment for your patient quickly and decisively

Problem Statement

Each year, over 225,000 people are diagnosed with lung cancer in the U.S.1
Aggressive Disease

Both non-small cell lung cancer (NSCLC) and small cell lung cancer are aggressive diseases with low survival rates. Because many tumors metastasize before diagnosis, it’s important that patients receive the correct targeted treatment as quickly as possible2, 3. The earlier lung cancer is caught, the better chance a patient has of surviving five years after being diagnosed. For lung cancer, only 15.3% are diagnosed at the local stage, and five-year relative survival for localized cancer is 53.5%. However, unfortunately 57% of patients are diagnosed at the distant stage where the cancer has metastasized, and the five-year relative survival is only 3.9%.1

A Range of Treatments

An unprecedented number of new, targeted therapies are available today. But prescribing a treatment that may improve patient care requires a nuanced understanding of his or her molecular profile.4

Clinical Need

With aggressive disease progression, comorbid medical diseases, and low survival, choosing the best treatment as quickly as possible is critical
Identifying Mutations and Assessing Likelihood of Response

Examining specific oncogenes for significant alterations is one method of evaluating how likely a patient is to respond to targeted therapy. Mutation, chromosomal rearrangement, or gene amplification analysis may be used when considering a treatment regimen.

Enter NexCourse Lung

For patients with non-small cell lung cancer, NexCourse NSCLC provides actionable results in a concise, patient-specific summary report that includes clinically relevant information to support your treatment decisions

How it works

NexCourse NSCLC is a suite of powerful molecular tests
Tissue Collection

We start with formalin-fixed, paraffin-embedded (FFPE) tissue and test samples for relevant biomarker expression.

Molecular Testing

Using a number of advanced molecular testing platforms, NexCourse NSCLC analyzes biomarkers relevant to your patient’s disease, including EGFR and K-RAS mutations, ALK, ROS1 and RET rearrangements, MET amplification, and FGFR1 amplification if squamous cell carcinoma is involved. Pick and choose the biomarkers to test—or test for the entire NSCLC profile.

Targeted Therapies

NexCourse NSCLC makes it easy to decide if targeted therapies are appropriate
Tyrosine Kinase Inhibitor (TKI)

Mutations in the EGFR gene are a positive predictor of the effectiveness of a TKI and may be prognostic for overall survival. KRAS mutations are associated with intrinsic TKI resistance.5-7

ALK Inhibitors

ALK rearrangements have been identified in a subset of patients with NSCLC for whom ALK inhibitors may represent a very effective therapeutic strategy.

Detection of ALK and ROS1 rearrangements predicts the likelihood of response to the ALK inhibitor crizotinib. De novo amplification of MET may be a predictor of response to crizotinib.8-11

Multi-targeted Kinase Inhibitors

Multi-kinase inhibitors may be effective for inhibiting oncogenic activity of RET rearrangements.

Amplifications of FGFR1 are predominately found in squamous cell lung cancers from former/current smokers.12

The NexCourse NSCLC Advantage

A comprehensive test for a confident course of treatment

NexCourse NSCLC helps you decide to which treatments your patient is likely to respond. You’ll also be able to assess predictive and prognostic molecular markers for many first- and second-line NSCLC treatments.2, 3

References

  1. Howlader N, et al. SEER Cancer Statistics Review, 1975-2010, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2010/, based on November 2012 SEER data submission, posted to the SEER web site, April 2013.
  2. NCCN Clinical Practice Guidelines in Oncology, Non-Small Cell Lung Cancer V.3.2014.
  3. von Dincklage JJ, Ball D, and Silvestri GA. A review of clinical practice guidelines for lung cancer. J Thorac Dis. 2013; 5(Suppl 5): S607–S622.
  4. Azzoli CG. American Society of Clinical Oncology Clinical Practice Guideline update on chemotherapy for stage IV non-small cell lung cancer. J Clin Oncol. 2010;6(1):39-43.
  5. Li T, Kung HJ, Mack PC, et al. Genotyping and genomic profiling of non-small-cell lung cancer: implications for current and future therapies J Clin Oncol. 2013 Mar 10;31(8):1039-49.
  6. Zhu CQ, da Cunha Santos G, Ding K, et al. Role of KRAS and EGFR as biomarkers of response to erlotinib in National Cancer Institute of Canada Clinical Trials Group Study BR.21. J Clin Oncol. 2008;26(26):4268-4275.
  7. Cataldo VD, Gibbons DL, Román Pérez-Soler, R, et al. Treatment of Non–Small-Cell Lung Cancer with Erlotinib or Gefitinib N Engl J Med 2011; 364:947-955.
  8. Lipson D, et al. Identification of new ALK and RET gene fusions from colorectal and lung cancer biopsies. Nat Med. 18:2012; 382-384.
  9. Shaw A, et al. Clinical Features and Outcome of Patients with Non-Small Cell Lung Cancer who harbor EML4-ALK. J Clin Onc 2009; 27, 4247-4253.
  10. Bergethon K, et al. ROS1 rearrangements define a unique molecular class of lung cancers. J Clin Oncol. 2012; 30:863-870.
  11. Ou SH, et al. Activity of crizotinib (PF02341066), a dual mesenchymal-epithelial transition (MET) and anaplastic lymphoma kinase (ALK) inhibitor, in a non-small cell lung cancer patient with de novo MET amplification. J Thorac Oncol 2011;6942-946.
  12. Weiss J, et al. Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer. Sci Transl Med 2010; 2:62ra93.

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