Evidence map›Paper›PMID 30524909›Full record

ArticleOncoimmunology

Integrated analysis of the immunological and genetic status in and across cancer types: impact of mutational signatures beyond tumor mutational burden.

Jan Budczies, Anja Seidel, Petros Christopoulos, Volker Endris, Matthias Kloor, Balázs Győrffy, Barbara Seliger, Peter Schirmacher, Albrecht Stenzinger, Carsten Denkert

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 3% of its field
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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

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  8. Interferon Epsilon Loss Is Elusive 9p21 Link to Immune-Cold Tumors, Resistant to Immune Checkpoint Therapy, and Endogenous CXCL9/10 Induction.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2025
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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

10 authors at 6 institutions in 2 countries.

Jan BudcziesInstitute of Pathology, Charité University Hospital, Berlin, Germany.
Anja SeidelInstitute of Pathology, Charité University Hospital, Berlin, Germany.
Petros ChristopoulosDepartment of Thoracic Oncology, Thoraxklinik at University Hospital Heidelberg, Heidelberg, Germany.
Volker EndrisInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Matthias KloorInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Balázs Győrffy2nd Department of Pediatrics, Semmelweis University, Budapest, Hungary.
Barbara SeligerInstitute of Medical Immunology, Martin-Luther-University Halle-Wittenberg, Halle, Germany.
Peter SchirmacherInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Albrecht StenzingerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Carsten DenkertInstitute of Pathology, Charité University Hospital, Berlin, Germany.
German Cancer Research Center · DEUniversity Hospital Heidelberg · DECharité - Universitätsmedizin Berlin · DEDeutschen Konsortium für Translationale Krebsforschung · DEHUN-REN Research Centre for Natural Sciences · HUMartin Luther University Halle-Wittenberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Harnessing the immune system by checkpoint blockade has greatly expanded the therapeutic options for advanced cancer. Since the efficacy of immunotherapies is influenced by the molecular make-up of the tumor and its crosstalk with the immune system, comprehensive analysis of genetic and immunologic tumor characteristics is essential to gain insight into mechanisms of therapy response and resistance. We investigated the association of immune cell contexture and tumor genetics including tumor mutational burden (TMB), copy number alteration (CNA) load, mutant allele heterogeneity (MATH) and specific mutational signatures (MutSigs) using TCGA data of 5722 tumor samples from 21 cancer types. Among all genetic variables, MutSigs associated with DNA repair deficiency and AID/APOBEC gene activity showed the strongest positive correlations with immune parameters. For smoking-related and UV-light-exposure associated MutSigs a few positive correlations were identified, while MutSig 1 (clock-like process) correlated non-significantly or negatively with the major immune parameters in most cancer types. High TMB was associated with high immune cell infiltrates in some but not all cancer types, in contrast, high CNA load and high MATH were mostly associated with low immune cell infiltrates. While a bi- or multimodal distribution of TMB was observed in colorectal, stomach and endometrial cancer where its levels were associated with

Indexed as

immune checkpointsImmuno-oncologymutational signaturesPD-L1tumor mutational burden

Identifiers

PMID30524909
PMCPMC6279340
OpenAlexW2896640994

What OpenQuestion holds

Textmetadata
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.