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Diagnostic & Clinical · Somatic

Match the
tumor
to its therapy

Comprehensive somatic tumor profiling on the OncoMine platform — coverage of the actionable cancer gene landscape with biomarkers (MSI, TMB, PD-L1) for immunotherapy eligibility. Built for FFPE specimens.

500+
Genes (Comprehensive)
MSI/TMB
Reported
10d
SLA from accession
DNA double helix annotated with five clinically actionable somatic variantsB-form DNA double helix shown in side view with major and minor grooves, base-pair rungs colored by purine/pyrimidine pair, and five clinically annotated somatic variant flags showing HGVS nomenclature, AMP/ASCO/CAP tier classification, and variant allele frequency for EGFR L858R, KRAS G12C, BRAF V600E, TP53 R175H, and PIK3CA E545K.majorgrooveminorgrooveTIER IEGFRp.L858RVAF 38%TIER IKRASp.G12CVAF 24%TIER IBRAFp.V600EVAF 41%TIER IITP53p.R175HVAF 52%TIER IIIPIK3CAp.E545KVAF 11%
NCCN-aligned
Ion Torrent S5
FFPE compatible
Why somatic profiling

Different question, different test

A germline cancer panel asks “what risk did I inherit?” Somatic tumor profiling asks “what is driving this tumor right now, and which targeted or immune therapy fits?” Both have a place — but they answer different clinical questions.

Treatment selection

Identify FDA-approved targeted therapies and trial-eligible alterations for the patient in front of you.

Immunotherapy biomarkers

MSI, TMB, and PD-L1 (when paired with IHC) are reported together to inform checkpoint-inhibitor eligibility.

FFPE-ready

Optimized for archived FFPE blocks, validated to operate at low tumor content with strong analytical sensitivity.

Biomarkers reported

Genomic signal, in one report

Variants and biomarkers are co-reported with tier classification (AMP/ASCO/CAP) and database annotation (OncoKB, ClinVar).

SNV / INDEL

Hotspot mutations

Activating and loss-of-function variants across the actionable cancer gene set.

CNV

Copy number alterations

Amplifications and deletions called from sequencing depth.

FUSION

Gene fusions

RNA-based detection of clinically relevant fusion partners.

MSI

Microsatellite instability

Reported as MSI-High or MSS using sequence-based scoring.

TMB

Tumor mutational burden

Mutations per megabase, calibrated against reference material.

PD-L1

PD-L1 (paired)

Reported alongside referring-center IHC when provided.

HRD

Homologous recombination

HRD-related variants flagged for PARP-inhibitor eligibility review.

FFPE QC

Specimen QC

DNA quality, tumor content, and minimum coverage thresholds reported.

Inside the report

Sample report excerpt

A redacted view of the variants and biomarker section. Tier classification follows AMP/ASCO/CAP guidelines; therapeutic relevance is annotated through OncoKB.

Specimen ID — IMC-ON-2026-04-2841  ·  Block — FFPE A1 (2024-11)
Diagnosis — NSCLC, adenocarcinoma · stage IIIB
Assay — OncoMine Comprehensive Plus v3 · Ion Torrent S5
Tumor purity — 60%  ·  Mean depth — 750×  ·  DOR — 2026-04-15
REDACTED PHI   REDACTED MRN
MSSTMB 14.2 mut/Mb · highPD-L1 TPS 65%HRD 28 · low
Gene / variantHGVSVAFTierTherapeutic relevance
EGFR L858R
Exon 21 missense, activating
NM_005228.5:c.2573T>G38.4%TIER IFDA-approved EGFR TKIs (osimertinib first line in NSCLC). Sensitizing mutation.
TP53 R175H
DNA-binding domain hotspot
NM_000546.6:c.524G>A41.2%TIER IIPrognostic. Co-occurring with EGFR drivers in NSCLC. Clinical trial eligibility may apply.
CDKN2A deletion
Homozygous loss, exons 1–3
CNV: 0.05 (homozygous)TIER IICDK4/6 inhibitor sensitivity in select tumor types. Trial eligibility.
MET amplification
Focal high-level CN gain · 7q31.2
CNV: 8.4 copiesTIER IICapmatinib / tepotinib activity in MET-amplified NSCLC. Trial eligibility (NCT04606771).
KRAS WT
Codons 12, 13, 61, 117, 146 negative
< 1%REFWild-type. Confirms EGFR-driven biology; consistent with EGFR TKI candidacy.
PIK3CA E545K
Helical domain hotspot
NM_006218.4:c.1633G>A11.8%TIER IIIVariant of uncertain clinical significance in this tumor type. No established targeted therapy.
STK11 Q37*
Truncating, exon 1
NM_000455.5:c.109C>T33.7%TIER IIIResistance signal: associated with reduced ICI benefit in NSCLC. Co-occurring with KEAP1 to be ruled out.
EML4–ALK fusion
Not detected · RNA fusion panel
REFNot detected. ROS1, RET, NTRK1/2/3 also negative.
Biomarker summary panel: MSI, TMB histogram, PD-L1 TPS, HRD scoreFour-tile biomarker panel showing microsatellite instability status as MSS, tumor mutational burden of 14.2 mutations per megabase positioned high relative to a histogram of cohort distribution, PD-L1 tumor proportion score of 65 percent, and homologous recombination deficiency score of 28.MSI STATUSMSSstable · 0/95 markersMSSMSI-LMSI-HTMB14.2mut/Mb▲ HIGH (≥10)010≥30PD-L1 (22C3)65%TPS · high expression050% cutoff100HRD SCORE28below 42 threshold · lowLOWHIGH 42+
Variants annotated: OncoKB v4.21 · ClinVar 2026-03 · COSMIC v100
Reported by IMC Genomics · Tashkent · ISO 15189
Therapy matching

From variant to clinical decision

Each Tier I and Tier II finding is paired with FDA-approved targeted therapies, NCCN-listed regimens, and active clinical-trial options drawn from a curated knowledge base.

EGFR L858R
Osimertinib (1L NSCLC)
KRAS G12C
Sotorasib · Adagrasib
BRAF V600E
Dabrafenib + Trametinib
ALK fusion
Alectinib · Lorlatinib
MSI-High / TMB-High
Pembrolizumab (tissue-agnostic)
HRD / BRCA1/2 somatic
PARP inhibitor (where indicated)

Speak with the oncology team

Submit a tumor block, request a sample report, or talk through assay selection between the Standard, Comprehensive, and Liquid Biopsy options.