Evidence map›Paper›PMID 41736133›Full record

ArticleGenome medicine2026

Cancer evolution and multi-omic profile of relapsed colorectal liver metastases after treatment.

Laura Tomás, Nathanael Raschzok, Eric Blanc, María Gallardo-Gómez, Andrea Menne, Kathy Astrahantseff, Loretta De Chiara, Dominik Geisel, Johann Pratschke, Dominik P Modest and 5 more

Abstract read
In one paragraph

Article in Genome medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

15 authors.

Laura Tomás *CINBIO, Universidade de Vigo, Vigo, 36310, Spain.ORCID 0000-0001-9848-002X
Nathanael Raschzok *Department of Surgery, Campus Charité Mitte | Campus Virchow-Klinikum, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID 0000-0001-5074-7063
Eric BlancCore Unit Bioinformatics (CUBI), Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany.
María Gallardo-GómezTranslational Oncology Group, Galicia Sur Health Research Institute (IIS Galicia Sur), SERGAS-UVIGO, Vigo, Spain.
Andrea MenneDepartment of Pediatric Surgery, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, Berlin, 13353, Germany.
Kathy AstrahantseffDepartment of Pediatric Oncology and Hematology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Loretta De ChiaraCINBIO, Universidade de Vigo, Vigo, 36310, Spain.
Dominik GeiselDepartment of Radiology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Johann PratschkeDepartment of Surgery, Campus Charité Mitte | Campus Virchow-Klinikum, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Dominik P ModestGerman Cancer Consortium (DKTK), partner site Berlin, a partnership between DKFZ and Charité-Universitätsmedizin Berlin, Berlin, Germany.
Angelika EggertDepartment of Pediatric Oncology and Hematology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Dieter BeuleCore Unit Bioinformatics (CUBI), Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany.
David PosadaCINBIO, Universidade de Vigo, Vigo, 36310, Spain.
Christine SersGerman Cancer Consortium (DKTK), partner site Berlin, a partnership between DKFZ and Charité-Universitätsmedizin Berlin, Berlin, Germany.
Soulafa MamloukDepartment of Pediatric Surgery, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, Berlin, 13353, Germany. soulafa.mamlouk@charite.de.ORCID 0000-0001-7285-1320

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecurrence following resection of colorectal cancer liver metastases remains a major obstacle to prolonged patient survival, often resulting in treatment-refractory disease with limited understanding of the underlying evolutionary drivers. To investigate these mechanisms, we performed an in-depth, patient-specific study of genomic and microenvironmental alterations in relapsed colorectal cancer liver metastases from nine individuals.

methodsClonal deconvolution and phylogenetic analysis was conducted on DNA sequencing data from multiregion liver metastasis and relapse samples from the same patient. Archived primary tumor specimens were included to trace the clonal lineages responsible for relapse. In parallel, transcriptomic data from the liver metastasis and relapse samples were analyzed to characterize tumor-infiltrating immune cell populations.

resultsPhylogenetic analyses of relapsed metastases revealed two distinct patterns: (1) relapses that retain a clone already present in ancestral liver metastasis, and (2) relapses with no evident clonal link to the original metastasis. Relapses in the first group carried a chemotherapy-associated mutational signature, which then appeared across all relapse samples. In one patient, the relapsing clone had already diversified within the primary tumor. Tumor microenvironment analyses exposed heterogeneous responses followwing relapse, ranging from decreased to markedly increased infiltration by multiple immune cell types, accompanied by shifts in consensus molecular subtypes and altered neoantigen profiles.

conclusionsOur study reveals patient-specific evolutionary trajectories underlying relapse in colorectal cancer, highlighting diverse routes to recurrence, including chemotherapy-driven clonal expansion and early divergence from the primary tumor. Our findings reveal a landscape of patient-specific evolutionary trajectories in relapsed colorectal cancer, underscoring the potential value of personalized approaches for understanding and monitoring recurrent disease.

Indexed as

Colorectal NeoplasmsLiver NeoplasmsAgedClonal EvolutionEvolution, MolecularFemaleGene Expression ProfilingHumansMaleMiddle AgedMultiomicsMutationNeoplasm Recurrence, LocalPhylogenyRecurrenceTumor MicroenvironmentImmune-cell infiltrationNeoantigensResistanceSubclone

Identifiers

PMID41736133
PMCPMC12980905

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Registered trials

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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.