Evidence map›Paper›PMID 38940126›Full record

ArticleBioinformatics (Oxford, England)2024

Modeling metastatic progression from cross-sectional cancer genomics data.

Kevin Rupp, Andreas Lösch, Yanren Linda Hu, Chenxi Nie, Rudolf Schill, Maren Klever, Simon Pfahler, Lars Grasedyck, Tilo Wettig, Niko Beerenwinkel and 1 more

Abstract read
In one paragraph

Article in Bioinformatics (Oxford, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Bioinformatics advances · 2026
    Article
  3. Article
  4. Review
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

11 authors.

Kevin RuppFaculty of Informatics and Data Science-Statistical Bioinformatics Group, University of Regensburg, Regensburg 93053, Germany.
Andreas LöschFaculty of Informatics and Data Science-Statistical Bioinformatics Group, University of Regensburg, Regensburg 93053, Germany.
Yanren Linda HuFaculty of Informatics and Data Science-Statistical Bioinformatics Group, University of Regensburg, Regensburg 93053, Germany.
Chenxi NieDepartment of Biosystems Science and Engineering, ETH Zurich, Basel 4056, Switzerland.
Rudolf SchillFaculty of Informatics and Data Science-Statistical Bioinformatics Group, University of Regensburg, Regensburg 93053, Germany.
Maren KleverInstitute for Geometry and Applied Mathematics, RWTH Aachen, Aachen 52062, Germany.
Simon PfahlerFaculty of Physics, University of Regensburg, Regensburg 93053, Germany.
Lars GrasedyckInstitute for Geometry and Applied Mathematics, RWTH Aachen, Aachen 52062, Germany.
Tilo WettigFaculty of Physics, University of Regensburg, Regensburg 93053, Germany.
Niko BeerenwinkelDepartment of Biosystems Science and Engineering, ETH Zurich, Basel 4056, Switzerland.ORCID 0000-0002-0573-6119
Rainer SpangFaculty of Informatics and Data Science-Statistical Bioinformatics Group, University of Regensburg, Regensburg 93053, Germany.

Funding

Deutsche Forschungsgemeinschaft TRR 305-A02Swiss Cancer League KFS-2977-08-2012Swiss National Science Foundation 179518
6 · The paper itself

Abstract

motivationMetastasis formation is a hallmark of cancer lethality. Yet, metastases are generally unobservable during their early stages of dissemination and spread to distant organs. Genomic datasets of matched primary tumors and metastases may offer insights into the underpinnings and the dynamics of metastasis formation.

resultsWe present metMHN, a cancer progression model designed to deduce the joint progression of primary tumors and metastases using cross-sectional cancer genomics data. The model elucidates the statistical dependencies among genomic events, the formation of metastasis, and the clinical emergence of both primary tumors and their metastatic counterparts. metMHN enables the chronological reconstruction of mutational sequences and facilitates estimation of the timing of metastatic seeding. In a study of nearly 5000 lung adenocarcinomas, metMHN pinpointed TP53 and EGFR as mediators of metastasis formation. Furthermore, the study revealed that post-seeding adaptation is predominantly influenced by frequent copy number alterations. AVAILABILITY AND IMPLEMENTATION: All datasets and code are available on GitHub at https://github.com/cbg-ethz/metMHN.

Indexed as

GenomicsNeoplasm MetastasisAdenocarcinoma of LungCross-Sectional StudiesDisease ProgressionErbB ReceptorsHumansLung NeoplasmsMutationNeoplasmsTumor Suppressor Protein p53ErbB ReceptorsTumor Suppressor Protein p53cancer genomicscancer progression modelslung cancerMarkov chainsmetastasisMutual Hazard Networks

Identifiers

PMID38940126
PMCPMC11245855

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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.