KRAS G12C

The most prevalent emerging biomarker in advanced non-small cell lung cancer (NSCLC)1–3

Targeting driver mutations enables personalized medicine.

KRAS mutations are common oncogenic drivers in NSCLC and generally exclusive of other driver mutations in genes such as EGFR, ALK, and ROS1.4 KRAS mutations are often early truncal mutations that can persist during disease progression.5

Although no KRAS-targeted therapies are approved for NSCLC, the KRAS G12C mutation is an emerging biomarker.

Prevalence of driver alterations in lung adenocarcinoma2

Detected in ~13% of NSCLC cases, KRAS G12C is nearly as frequent as all EGFR mutations combined.6

*Infrequent Alterations: ALK, BRAF, HER2, MEK1, NTRK1, PIK3CA, RET and ROS1

KRAS G12C is the single most prevalent emerging biomarker in NSCLC2

~1/8 patients

in the US with NSCLC have the KRAS G12C driver mutation5

Guidelines support testing KRAS as an emerging biomarker

Discovery of driver mutations through biomarker testing is key to creating personalized approaches to patient management. Upfront testing for KRAS mutations may be helpful in patients with advanced NSCLC.7 † ‡

KRAS Testing at Diagnosis


  • National Comprehensive Cancer Network® (NCCN®)

Expanded panel testing may be useful


  • CAP / IASLC / AMP and ASCO

Expanded panel recommended

  • † NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for NSCLC provide recommendations for individual biomarkers that should be tested and recommend testing techniques but do not endorse any specific commercially available biomarker assays.
  • ‡ Upfront testing for KRAS mutations may identify patients who are unlikely to benefit from further molecular testing because of the low probability of overlapping targetable alterations.

Biomarker testing reveals activated KRAS

KRAS is a membrane-associated GTPase that regulates cell proliferation and differentiation. KRAS G12C is a point mutation in codon 12 causing a glycine-to-cysteine substitution near a narrow pocket in the KRAS protein.8,9 Advances in understanding the protein structure have led to the investigation of inhibitors that target the pocket, potentially locking the KRAS G12C mutant protein in the inactive state.


KRAS G12C mutation drives oncogenic signaling10

The KRAS G12C mutation favors the active form of KRAS mutant protein.8

Amgen is committed to investigating strategies and understanding the role of the KRAS G12C mutation in cancer development and maintenance.

How to test for the KRAS G12C mutation in tissue and plasma

*KRAS educational content provided by Amgen Inc. for use by NeoGenomics.

For more information on specimen requirements and other test details please visit:
neogenomics.com /test-menu

References:

  1. Arbour KC, et al. Clin Cancer Research. 2018;24;334-340.
  2. Pakkala S, et al. JCI Insight. 2018;3 e120858.
  3. Graham RP, et al. Arch Path Lab Med. 2018 Feb ;142(2):163-167.
  4. Shea M, et al. Ther Adv Respir Dis. 2016;10:113-129.
  5. Villaflor V, et al. Oncotarget. 2016;7:66880-66891.
  6. Data on file, Amgen; 2020.
  7. Referenced with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Non-Small Cell Lung Cancer. V8.2020. © National Comprehensive Cancer Network, Inc. 2020. All rights reserved. Accessed September 22, 2020. To view the most recent and complete version of the guideline, go online to NCCN.org.
  8. Ryan MB, et al. Nat Rev Clin Oncol. 2018; 15:709-720.
  9. Cox AD, et al. Nat Rev Drug Discovery. 2014; 13:828-851.
  10. Gimple RC, et al. Front. Oncol. 2019: https://doi.org/10.3389/fonc.2019.00965.
  11. Neel N, et al. Genes Cancer. 2011;2(3):275-287.
  12. Ferrer I, et al. Lung Cancer. 2018;124;53-64.

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