Deleted in 10–15% of all human cancers
The deletion you need to see.
Homozygous MTAP deletion may represent a clinically meaningful signal across solid tumors.
Understanding MTAP today and coordinating care can prepare for tomorrow's treatment landscape.
Why this biomarker, why now
A genetic vulnerability hiding in plain sight.
Homozygous deletion of the MTAP gene on chromosome 9p21 occurs in roughly 15% of all solid tumors — including non-small cell lung cancer, pancreatic ductal adenocarcinoma, glioblastoma, mesothelioma, bladder, and esophageal cancers.
When MTAP is lost, tumor cells become uniquely dependent on the PRMT5 methylation pathway — a synthetic lethal vulnerability that a new generation of investigational therapies is designed to exploit.
For pathologists and oncologists, the question is no longer whether to look for MTAP loss, but when.
~15%
of all solid tumors carry homozygous MTAP deletion
9p21.3
the chromosomal locus where MTAP and CDKN2A are co-deleted
PRMT5
the synthetic lethal target enabled by MTAP loss
Where to start
Four steps to operationalize MTAP testing.
Understand the biology
What MTAP does, why its loss creates PRMT5 dependency, and which tumor types are most often affected.
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Choose the right test
IHC, FISH, and NGS — how each detects homozygous loss, with guidance on interpretation pitfalls.
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Plan the clinical pathway
When to test, how to report, and how to coordinate molecular tumor boards around MTAP findings.
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Connect patients to trials
Investigational PRMT5 inhibitors are recruiting now. Identify candidates before progression narrows options.
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Clinical trials
When testing reveals an MTAP deletion, a trial may be the next conversation.
Investigational PRMT5 inhibitors are being studied in patients whose tumors carry homozygous MTAP loss. Refer eligible patients early — site activation, screening, and consent take time.
Search the trial directory