Evidence synthesis for the modern tumor board.

Galen helps oncology teams prepare more thorough cases in less time — surfacing relevant evidence from across the biomedical literature, organized by strength and relevance.

Deeper preparation, less time.

Synthesizes evidence from peer-reviewed databases so you’re not reading abstracts at midnight.

Organized by evidence strength.

Every finding tagged by source tier: clinical trials, experimental research, computational inference.

Fits your workflow.

Designed for the way tumor boards already work — case-by-case, focused, time-boxed.

See what evidence synthesis looks like.

A de-identified case showing how Galen prepares evidence for review.

Example case — de-identified

Stage IIIB NSCLC — multi-mutation profile

Genomic profile

BRAF V600ETP53 R175HCDKN2A deletion

Causal traces surfaced

BRAF V600E constitutively activates MAPK pathway → Dabrafenib + trametinib targets this cascade

Clinical · COMBI-d Trial, NEJM 2014

TP53 R175H loss of tumor suppression + gain-of-function activity → Associated with resistance to single-agent BRAF inhibition

Research · Walerych et al., Nature Cell Biology 2012

CDKN2A deletion loss of p16/CDK4 cell-cycle checkpoint → CDK4/6 inhibitor (palbociclib) under investigation

Research · NCT03454919, Phase II

Resistance mechanisms flagged

MAPK pathway reactivation via MEK2 C125S — documented in BRAF V600E patients on combination therapy.

Research · Long et al., Cancer Discovery 2014

TP53 gain-of-function may stabilize BRAF-mutant signaling under therapeutic pressure.

Computational · Galen causal model

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