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Molecular profile
Multi-omic data from your tumour sample.
Interpretation engine
Integrates the real biological signal, not a proxy, to model whether the pathway is driving the tumour.
Per-patient roadmap
A ranked, evidence-graded list of research-described treatment options, structured to support the clinician's prescribing decision.
Astron interpretation engine
Our platform integrates the real biological signal, not a proxy, to model whether a pathway is actually driving the tumour. We score every drug-gene pair against the patient's individual molecular context, not against a generic tumour-type playbook.
The most evidenced option, for this patient.
We don't just surface treatments, we weigh each one across the factors that matter for this specific patient, from pathway dependency to clinical-trial maturity, to identify the option with the strongest evidence behind it. Every rank is fully decomposed, so theconsultant oncologist can see exactly what drives it.
An excerpt from an Astron molecular report.
Every Astron report follows the same structure: key findings, the pathways and hallmarks affected, a clinician synthesis, and a plain-language explanation you can use directly with your patient.
About this document
This sample is for information only. It is not medical advice, does not diagnose or treat disease, and must be interpreted by a qualified treating clinician.
Sample report excerpt · Astron
Colorectal cancer
Comprehensive genomic profile · 47 y female · sample report
Report ID RPT-eb764478-0c2a-4d88-b4b0-811712ee83c6 · Released 29 Jun 2026 · Authorizing consultant X. Orion
1
Drivers
6
Alterations
3
FDA-matched treatments
1
High confidence trial matched
Bottom line
Start with checkpoint immunotherapy — pembrolizumab (or dostarlimab as an equivalent anti-PD-1 alternative): this tumour is dMMR/MSI-H, the strongest predictor of response, making it the board's preferred first-line option.
Hold KRAS G12C-directed therapy (adagrasib + cetuximab) in reserve for later lines, with FOLFIRI available as a cytotoxic backbone once DPYD/UGT1A1 genotyping is complete.
Underlying biology: KRAS G12C drives oncogenic MAPK signaling, while concurrent MSH2 and BRCA2 loss-of-function compounds the genomic instability that makes immunotherapy effective.
Reviewed and prioritised by the board for the treating clinician · metastatic dMMR/MSI-H colorectal adenocarcinoma
Do first · standard of care
Checkpoint immunotherapy — Pembrolizumab
dMMR/MSI-H is the strongest treatment marker present. Pembrolizumab is the board's preferred first-line agent (Phase III KEYNOTE-177 in MSI-H mCRC); dostarlimab is an equivalent anti-PD-1 alternative. Offer first unless the patient has already progressed on a checkpoint inhibitor.
Backbone · test first
Cytotoxic chemotherapy — FOLFIRI
Available as chemotherapy or a bridge. Complete DPYD and UGT1A1 genotyping (Testing section) before starting.
Reserve · later-line
KRAS G12C-directed — Adagrasib + Cetuximab
The board's retained KRAS G12C option, labeled for use after prior therapy. Targets the expanding KRAS G12C clone — bring forward if immunotherapy is unsuitable or exhausted. (Sotorasib + panitumumab, a co-equal alternative, was not carried forward.)
Monitor · surveillance
Track emerging resistance clones
Serial ctDNA shows KRAS G12C and PIK3CA H1047R expanding alongside emergent ERBB2 amplification. HER2-directed therapy is not an option in this RAS-mutant tumour, so HER2 confirmation by IHC/FISH is not required — track these clones for resistance instead. The cleared TP53 R175H should not be relied on as a current target.
Options to weigh up for this patient · check the conditions and drug interactions before prescribing
An immunotherapy (anti-PD-1) that helps the patient's own immune system attack the cancer. It works well in MSI-H/dMMR colorectal cancer because these tumours carry many mutations, which makes them easier for the immune system to recognise.
Full dosing & evidence · §2
Another anti-PD-1 immunotherapy. It targets the same weakness — faulty DNA repair (dMMR) that leaves the tumour with many mutations the immune system can spot.
Full dosing & evidence · §2
Dose · Adagrasib — 600 mg orally twice daily
Adagrasib switches off the KRAS G12C protein and cetuximab blocks EGFR. Used together, they shut down the KRAS-driven growth signal in this metastatic colorectal cancer.
After prior therapy.
Full dosing & evidence · §2
Standard chemotherapy for metastatic colorectal cancer (first- or second-line): folinic acid + fluorouracil + irinotecan. It is chosen based on the cancer type, treatment line and patient fitness — not on a specific gene change.
Requires DPYD and UGT1A1 genotyping before use — see Testing.
Full dosing & evidence · §2
Follow-up testing
Order now — each result would change the plan
People with low DPYD activity can have severe, even life-threatening, side effects from fluoropyrimidine chemotherapy (part of FOLFIRI). Test before treatment (EMA-required; ESMO III,A). Carriers need at least a 50% lower dose.
People with the UGT1A1*28/*28 result clear irinotecan slowly, which raises the risk of severe low white-cell counts and diarrhoea. Consider starting about 30% lower.
Clinical trials
Worth considering once the standard options have run out
A phase II basket study pairing molecular findings with off-label, FDA-approved precision drugs. This patient's ERBB2 amplification opens a curated, biomarker-matched arm. Recruiting now at Windham Hospital (47 mi).
Full detail · Appendix E
Consider trial enrolment — 25 matched trials for this molecular profile if disease progresses.
Trial list · Appendix E
Molecular rationale
Supporting evidence for the actions above — the variants driving each recommendation
Actionable alterations
Locks the KRAS protein in its "on" state, so the RAS-MAPK growth signal stays switched on and the cancer cells keep multiplying. It also stops anti-EGFR drugs from working.
Targetable — eligible for sotorasib or adagrasib (KRAS G12C inhibitors, FDA-approved in CRC).
This inherited (Lynch) change breaks the MSH2/MSH6 "spell-check" that fixes DNA copying errors. Mistakes build up (microsatellite instability), so the tumour carries many mutations — making it easier for the immune system to spot.
MSI-H/dMMR status supports evaluation for pembrolizumab or dostarlimab-gxly.
Alterations under investigation
Switches off the BRCA2 gene, so the cell loses a key way of repairing broken DNA. That adds to the genetic instability and may make the tumour sensitive to PARP-inhibitor drugs.
HRR deficiency; PARP-inhibitor eligibility investigational in CRC — consider trial enrolment.
This common "hotspot" change keeps the PI3K/AKT pathway switched on, helping the cancer cells survive, grow, and change how they use energy.
PI3K/AKT co-activation; no approved PI3K inhibitor in CRC — consider clinical trial.
Extra copies of ERBB2 (HER2) make too much HER2 protein, switching on growth pathways. But because this tumour also carries a KRAS mutation, HER2-targeted drugs should not be used.
HER2-directed therapy contraindicated in RAS-mutant CRC — not appropriate despite amplification.
Other changes of biological interest
Cuts the APC protein short and removes the brake on the WNT/β-catenin pathway, which then stays on and pushes the cells to grow and change.
Canonical CRC tumour-suppressor loss; no approved targeted therapy — defines tumour biology.
KRAS
G12C · VAF 34%
MAPK signaling · activating missense
MSH2
A636P · VAF 46%
DNA repair · Lynch-associated
PIK3CA
H1047R · VAF 29%
PI3K/AKT signaling · hotspot
BRCA2
S1982Rfs*22 · VAF 45%
DNA repair · loss-of-function
ERBB2
amplification
RTK signaling · focal amplification
APC
R1450* · VAF 78%
WNT signaling · truncating
RTK → MAPK / PI3K signaling
Receptor tyrosine kinase activation drives proliferative and survival signals via the RAS-MAPK and PI3K-AKT cascades.
p53 / DNA damage response
Checkpoint activation and DNA-repair maintenance in response to genotoxic stress; loss here compounds genomic instability.
Bypass / resistance signaling
Convergent activation of downstream effectors may drive bypass of RTK-targeted therapy under selective pressure.
Sustaining proliferative signaling is the most convergently active process: KRAS G12C locks RAS in its active state, ERBB2 amplification floods the cell with receptor tyrosine kinase activity, PIK3CA H1047R sustains PI3K-AKT survival signaling, and APC truncation releases the WNT brake. Genome instability is the second major feature: BRCA2 frameshift loss disables homologous-recombination repair while MSH2 loss disrupts mismatch repair in a Lynch-associated pattern — generating the hypermutated, microsatellite-unstable landscape that underpins immunotherapy response.
TMB
High
41.0 mut/Mb
MSI / MMR
MSI-H
Mismatch-repair deficient
HRD
Not assessed
Data unavailable from assay
PD-L1
CPS 8
Indeterminate · 22C3
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