Indication
Colorectal cancer with KRAS G12C mutation
Colorectal cancer with a KRAS G12C mutation is a biologically distinct subset of gastrointestinal malignancy arising from the epithelial lining of the colon or rectum. Read more about Colorectal cancer with KRAS G12C mutation
2 drugs 1 manufacturers
Drugs that treat it
Common Colorectal cancer with KRAS G12C mutation therapies.
LUMAKRAS (sotorasib)
News & literature
Coming soonRelated codes
Coming soonRelated conditions & guidelines
Coming soonColorectal cancer with a KRAS G12C mutation is a biologically distinct subset of gastrointestinal malignancy arising from the epithelial lining of the colon or rectum.
It is defined by a specific somatic point mutation in the *KRAS* oncogene, where a glycine residue is substituted by cysteine at codon 12.
This alteration impairs GTP hydrolysis, locking the KRAS GTPase in a constitutively active state that drives unregulated signaling through the downstream MAPK/ERK pathway, promoting malignant cellular proliferation, survival, and therapeutic resistance.
Present in approximately 3% to 4% of metastatic colorectal cancer cases, this biomarker identifies an aggressive disease phenotype characterized by poor prognosis, reduced sensitivity to standard chemotherapy, and intrinsic resistance to anti-EGFR monotherapy.
- nih.gov
Colorectal cancer with a KRAS G12C mutation is a biologically distinct subset of gastrointestinal malignancy arising from the epithelial lining of the colon or rectum This alteration impairs GTP hydrolysis, locking the KRAS GTPase in a constitutively active state that drives unregulated signaling through the downstream MAPK/ERK pathway, promoting malignant cellular proliferation, survival, and therapeutic resistance
- colorectalcancer.org
Colorectal cancer with a KRAS G12C mutation is a biologically distinct subset of gastrointestinal malignancy arising from the epithelial lining of the colon or rectum
- nih.gov
It is defined by a specific somatic point mutation in the *KRAS* oncogene, where a glycine residue is substituted by cysteine at codon 12 This alteration impairs GTP hydrolysis, locking the KRAS GTPase in a constitutively active state that drives unregulated signaling through the downstream MAPK/ERK pathway, promoting malignant cellular proliferation, survival, and therapeutic resistance Present in approximately 3% to 4% of metastatic colorectal cancer cases, this biomarker identifies an aggress...
- nih.gov
It is defined by a specific somatic point mutation in the *KRAS* oncogene, where a glycine residue is substituted by cysteine at codon 12
- nih.gov
Present in approximately 3% to 4% of metastatic colorectal cancer cases, this biomarker identifies an aggressive disease phenotype characterized by poor prognosis, reduced sensitivity to standard chemotherapy, and intrinsic resistance to anti-EGFR monotherapy
Personalize your experience
Follow Colorectal cancer with KRAS G12C mutation and get updates as they land.
Already a member? Sign in
Follow an indication and get alerts when its drugs, labels, or guidelines change
Save any drug on this page to your favorites, synced across devices
AI-curated peer-reviewed research, summarized for your specialty
A morning digest of indication-relevant updates, when you want it
Sign in to follow this indication
Following an indication requires a free Physicians Office Resource account.