Evidence map›Paper›PMID 42113041›Full record

ArticleCancer immunology, immunotherapy : CII2026

Broader gene representation by whole-exome sequencing improves accuracy of tumor mutational burden assessment for selection of pembrolizumab immunotherapy.

Milan Radovich, James Wacker, Jeffrey Solzak, Hongseok Tae, Jennifer R Ribeiro, Todd Maney, Bradley Hancock, James Hamrick, George W Sledge, Manmeet S Ahluwalia and 6 more

Abstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Milan RadovichCaris Life Sciences, Phoenix, AZ, USA. mradovich@carisls.com.
James WackerCaris Life Sciences, Phoenix, AZ, USA.
Jeffrey SolzakCaris Life Sciences, Phoenix, AZ, USA.
Hongseok TaeCaris Life Sciences, Phoenix, AZ, USA.
Jennifer R RibeiroCaris Life Sciences, Phoenix, AZ, USA.
Todd ManeyCaris Life Sciences, Phoenix, AZ, USA.
Bradley HancockCaris Life Sciences, Phoenix, AZ, USA.
James HamrickCaris Life Sciences, Phoenix, AZ, USA.
George W SledgeCaris Life Sciences, Phoenix, AZ, USA.
Manmeet S AhluwaliaMiami Cancer Institute, Miami, FL, USA.
Stephen V LiuGeorgetown Lombardi Comprehensive Cancer Center, Washington, DC, USA.
Emil LouUniversity of Minnesota, Minneapolis, MN, USA.
Vivek SubbiahSarah Cannon Research Institute, Nashville, TN, USA.
Balazs HalmosAlbert Einstein College of Medicine, Bronx, NY, USA.
Daniel MageeCaris Life Sciences, Phoenix, AZ, USA.
David B SpetzlerCaris Life Sciences, Phoenix, AZ, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the tissue-agnostic FDA approval of pembrolizumab for tumor mutational burden (TMB)-high tumors has provided meaningful clinical benefit to patients, there remains a need to optimize TMB assessment. In this cohort study, we investigated the discordance between whole-exome sequencing (WES) and panel-based methods and evaluated their relative clinical utility in identifying patients likely to benefit from pembrolizumab. Molecularly-profiled tumors from patients treated with pembrolizumab were analyzed (N = 26,756). TMB was calculated using WES data or panels of genes (324, 523, and 648) from commercially available assays (TMB-High ≥ 10 mutations/Mb). Pembrolizumab-specific overall survival (OS) was calculated from insurance claims data (treatment start to last contact). Targeted gene panels tended to overestimate TMB and demonstrated ~ 10-15% discordance in binary TMB calls from WES, which was most pronounced for the smallest panel. Discordant cases for all three panels clustered near the TMB clinical calling threshold. WES offered improved stratification of patients for pembrolizumab treatment: in a subset of "TMB-reliant" tumor types lacking disease-specific immune checkpoint inhibitor (ICI) indications (n = 3,981), median OS was approximately 5 months longer for cases identified as WES-TMB-High but panel-TMB-Low compared to those identified as WES-TMB-Low but panel-TMB-High (p < 0.05 for 324-gene and 648-gene panels). Approximately, 10-11% of patients were potentially misclassified by panels. These findings emphasize the importance of broader gene representation for accurate TMB determination near the clinical threshold-especially in tumor types lacking disease-specific ICI indications, where tissue-agnostic MSI-High/dMMR or TMB-High labeling represents the principal on-label route to ICI therapy.

Indexed as

Antibodies, Monoclonal, HumanizedAntineoplastic Agents, ImmunologicalBiomarkers, TumorExome SequencingImmunotherapyMutationNeoplasmsAgedFemaleHumansMaleMiddle AgedAntibodies, Monoclonal, HumanizedAntineoplastic Agents, ImmunologicalBiomarkers, TumorpembrolizumabImmune checkpoint inhibitorImmunotherapyLung cancerNext-generation sequencing-NGSTumor mutation burden-TMB

Identifiers

PMID42113041
PMCPMC13161441

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.