- Design
- Retrospective diagnostic concordance study
- Population
- 24 peritoneal and 25 pleural mesotheliomas, 10 reactive mesothelial proliferations
- Primary outcome
- Concordance of MTAP IHC and FISH with CDKN2A homozygous deletion by FISH
- Effect
- Peritoneal: kappa 0.21 (MTAP IHC vs CDKN2A FISH); pleural: 100% specificity, 68.8% sensitivity
An Italian group tested 24 peritoneal mesotheliomas with MTAP immunohistochemistry, MTAP FISH and CDKN2A FISH, with 25 pleural mesotheliomas and 10 reactive proliferations as controls.
In pleural mesothelioma the tests agreed as expected: MTAP IHC matched MTAP FISH perfectly (kappa 1.00), with 100% specificity for CDKN2A homozygous deletion. In peritoneal mesothelioma, MTAP IHC still matched MTAP FISH (kappa 0.83), but agreement with CDKN2A deletion was poor (kappa 0.21), with 50% sensitivity and 75% specificity. The two genes appear to be co-deleted less often in the peritoneum.
The practical reading is that the pleural shortcut does not transfer. MTAP loss in a peritoneal lesion may still support mesothelioma, but it does not tell you CDKN2A status. The sample is small and was selected by molecular status.
- Do not report MTAP loss as implying CDKN2A deletion in peritoneal mesothelioma.
- Request CDKN2A FISH when CDKN2A status matters to the diagnosis in peritoneal disease.
- Use BAP1 and MTAP together as supporting markers, not as a single test.
- State the site explicitly when interpreting surrogate markers.
Why it matters
A surrogate validated at one anatomical site is being used at another where it behaves differently.
Don't overread it
A small, molecularly selected series; it shows the surrogate is unreliable in the peritoneum, not how often each gene is lost there.
The statistics, in plain English
Kappa measures agreement beyond chance: 1.0 is perfect, 0.21 is slight. With only 24 peritoneal cases chosen by their molecular status, the sensitivity and specificity figures are imprecise and may not match an unselected series.
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