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NexCourse for colorectal cancer (CRC) provides actionable results in a concise, patient-specific, summary report with clinically relevant information to assist treatment decisions.

NexCourse CRC helps you:

  • Identify important biomarkers that predict therapy response and add prognostic information
  • Determine treatments to which each patient is more likely to respond favorably
  • Detect which therapies are more likely to cause severe toxic side effects

Select from our suite of molecular tests to receive the necessary information for a treatment course of action. When two or more molecular tests are ordered, you will receive a concise summary of results.

NexCourse CRC test offering and treatment direction.

With a number of therapies available, our NexCourse CRC assays are the right ones to reveal the answer and give you clear direction.

NEXCOURSE CRC TEST OFFERING AND TREATMENT DIRECTION
Prognosis (treatment naive) MSI expression can help identify the likelihood of benefit from 5-FU or capecitabine MSI in patients with Stage II disease.
5-FU and capecitabine response and toxicity TS expression can help determine the likelihood of response to 5-FU and capecitabine.
DPD can help determine the likelihood of toxicity from 5-FU and capecitabine.
Oxaliplatin response ERCC1 expression can help determine the likelihood of response to oxaliplatin.
Irinotecan toxicity UGT1A1 can help determine the likelihood of toxicity from irinotecan.
EGFR-inhibitor response
(cetuximab and panitumumab)
K-RAS mutation can help determine the likelihood of response to treatment with EGFR inhibitors cetuximab and panitumumab.
Prognosis B-RAF mutation is prognostic for survival of patients regardless of treatment.
Monitoring CTC CTCs provide helpful insights into metastatic CRC status and prognosis.

5-FU AND CAPECITABINE1-3

TS, MSI, and DPD indicate likelihood of 5-FU-based treatment effectiveness and toxicity

  • Low levels of TS expression in tumors are associated with better patient response to 5-FU and capecitabine1-3
  • Patients with DPD deficiency cannot metabolize 5-FU as effectively, which predicts a higher chance of toxicity4-7
  • Stage II CRC patients with MSI HIGH status tend to not benefit from 5-FU adjuvant therapy8-10

FOLFOX VS. FOLFIRI

ERCC1 and UGT1A1 help in the decision between FOLFOX and FOLFIRI treatment to increase potential effectiveness and decrease toxicity

  • High levels of ERCC1 are associated with oxaliplatin resistance1
  • A positive UGT1A1 mutation is associated with a decreased ability to metabolize irinotecan in FOLFIRI, resulting in an increased likelihood of severe toxicity11
  • Mutations in the EGFR are prognostic with or without chemotherapy.

EGFR INHIBITORS (cetuximab and panitumumab)

K-RAS indicates likelihood of metastatic tumor response to EGFR inhibitors

  • Positive K-RAS results are predictive that a patient's metastatic tumor will not respond to EGFR inhibitors12-14
  • Positive B-RAF mutation is an unfavorable prognostic indicator for patients regardless of treatment

SERIAL MONITORING

Our CTC test results:

  • Provide helpful insights into metastatic CRC status and prognosis15
  • Are a valuable adjunct to imaging and provide similar predictive and prognostic information to imaging, but earlier15
  • Can be followed over time

And, we keep your patients' test results on file so that every time you reorder their CTC, we send you a report charting their progress over time.

  1. Shirota Y, et al. ERCC1 and thymidylate synthase mRNA levels predict survival for colorectal cancer patients receiving combination oxaliplatin and fluorouracil chemotherapy. J Clin Oncol. 2001;19(23):4298-304.
  2. U chida K, et al. Thymidylate synthase, dihydropyrimidine dehydrogenase, ERCC1, and thymidine phosphorylase gene expression in primary and metastatic gastrointestinal adenocarcinoma tissue in patients treated on a phase I trial of oxaliplatin and capecitabine. BMC Cancer. 2008;8:386.
  3. Soong R, et al. Prognostic significance of thymidylate synthase, dihydropyrimidine dehydrogenase and thymidine phosphorylase protein expression in colorectal cancer patients treated with or without 5-fluorouracil-based chemotherapy. Ann Oncol. 2008;19(5):915-8.
  4. Meta-Analysis Group In Cancer. Toxicity of fluorouracil in patients with advanced colorectal cancer: effect of administration schedule and prognostic factors. J Clin Oncol.1998;16(11):3537-41.
  5. van Kuilenburg AB, et al. Genotype and phenotype in patients with dihydropyrimidine dehydrogenase deficiency. Hum Genet. 1999;104(1):1-9.
  6. van Kuilenburg AB, et al. Lethal outcome of a patient with a complete dihydropyrimidine dehydrogenase (DPD) deficiency after administration of 5-fluorouracil: frequency of the common IVS14+1G>A mutation causing DPD deficiency. Clin Cancer Res. 2001;7(5):1149-53.
  7. Morel A, et al. Clinical relevance of different dihydropyrimidine dehydrogenase gene single nucleotide polymorphisms on 5-fluorouracil tolerance. Mol Cancer Ther.2006;5(11):2895-904.
  8. Sargent DJ, et al. Confirmation of deficient mismatch repair (dMMR) as a predictive marker for lack of benefit from 5-FU based chemotherapy in stage II and III colon cancer (CC):a pooled molecular reanalysis of randomized chemotherapy trials. J Clin Oncol. 2008;26(15 Suppl):4008.
  9. Popat S, et al. Systematic review of microsatellite instability and colorectal cancer prognosis. J Clin Oncol. 2005;23(3):609-18.
  10. Des Guetz G, et al. Does microsatellite instability predict the efficacy of adjuvant chemotherapy in colorectal cancer? A systematic review with meta-analysis. Eur J Cancer.2009;45(10):1890-6.
  11. Rouits E, et al. Pharmacokinetic and pharmagenetic determinants of the activity and toxicity of irinotecan in metastatic colorectal cancer. Br J Cancer. 2008;99(8):1239-45.
  12. Lièvre, A, et al. KRAS mutations as an independent prognostic factor in patients with advanced colorectal cancer treated with cetuximab. J Clin Oncol. 2008;26(3):374-9.
  13. Amado RG, et al. Wild-type (WT) KRAS is required for panitumumab efficacy in patient-with metastatic colorectal cancer. J Clin Oncol. 2008;26(10):1626-34.
  14. Di Nicolantonio F, et al. Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer. J Clin Oncol. 2008;26(35):5705-12.
  15. Cohen SJ, et al. Relationship of circulating tumor cells to tumor response, progression-free survival, and overall survival in patients with metastatic colorectal cancer. J Clin Oncol.2008;26(19):3213-21.

Genoptix® and NexCourse® are registered trademarks of Genoptix, Inc.