Biomarker & Genomic Mutation Library
A precision-oncology resource connecting biomarkers to targeted therapies, clinical trials, global research breakthroughs, and the world's leading specialists.
Cancer biology is driven by genetic mutations and molecular alterations that shape diagnosis, treatment, and prognosis. This Biomarker Library provides a comprehensive, curated, and continuously updated reference for the biomarkers that matter most in modern oncology.
Each biomarker includes associated therapies, related clinical trials, key research insights, and specialists with expertise in that specific mutation.
Most Searched Biomarkers
EGFR
EGFR Mutation
KRAS
KRAS Mutation
BRCA1/BRCA2
BRCA1/BRCA2 Mutation
PD-L1
PD-L1 Expression
BRAF
BRAF V600E Mutation
TP53
TP53 Mutation
NTRK
NTRK Fusions
HER2
HER2 Amplification
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All Biomarkers
EGFR Mutation
Chromosome: 7p11.2
EGFR mutations lead to uncontrolled cell growth via aberrant signaling in the EGFR pathway. They are among the most important biomarkers in lung cancer, guiding targeted therapy decisions and predicting response to EGFR inhibitors.
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KRAS Mutation
Chromosome: 12p12.1
KRAS mutations drive tumor growth through the RAS-MAPK pathway. Historically considered 'undruggable,' KRAS has recently become targetable, especially in the G12C variant.
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BRCA1/BRCA2 Mutation
Chromosome: 17q21 / 13q13
BRCA1/2 mutations impair DNA repair via homologous recombination, increasing risk for breast, ovarian, pancreatic, and prostate cancers.
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PD-L1 Expression
Chromosome: 9p24.1
PD-L1 levels predict benefit from certain immunotherapies.
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BRAF V600E Mutation
Chromosome: 7q34
BRAF V600E mutation leads to constitutive activation of the MAPK pathway, driving uncontrolled cell proliferation.
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TP53 Mutation
Chromosome: 17p13.1
The most commonly mutated tumor suppressor gene. TP53 mutations disrupt cell cycle regulation and apoptosis.
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NTRK Fusions
Chromosome: 1q23.1
NTRK gene fusions result in constitutive activation of TRK proteins, driving cancer growth.
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HER2 Amplification
Chromosome: 17q12
HER2 amplification leads to overexpression of HER2 protein, promoting aggressive tumor growth.
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