Evidence map›Paper›PMID 40585306›Full record

ArticleNAR genomics and bioinformatics2025

Novel treatment-specific causal biomarkers for colorectal cancer by omics integration.

Akram Yazdani, Azam Yazdani, Raul Mendez-Giraldez, Gianluigi Pillonetto, Esmat Samiei, Reza Hadi, Heinz-Josef Lenz, Alan P Venook, Ahmad Samiei, Andrew B Nixon and 4 more

Abstract read
In one paragraph

Article in NAR genomics and bioinformatics, 2025. 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

14 authors.

Akram YazdaniDivision of Pharmacotherapy and Experimental Therapeutics, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, NC 27599, United States.ORCID https://orcid.org/0000-0002-1243-6317
Azam YazdaniDivision of Preventive Medicine, Department of Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115, United States.
Raul Mendez-GiraldezBiostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, Durham, NC 27709, United States.
Gianluigi PillonettoDepartment of Information Engineering, University of Padova, Padova 35131, Italy.
Esmat SamieiGam Electronic, Tehran 45611, Iran.
Reza HadiSchool of Mathematics, University of Science and Technology of Iran, Tehran 13114, Iran.
Heinz-Josef LenzUSC Norris Comprehensive Cancer Center, Los Angeles, CA 90033, United States.
Alan P VenookUniversity of California at San Francisco, San Francisco, CA 94158, United States.
Ahmad SamieiDivision of Pulmonary Medicine, Boston Children's Hospital, Boston, MA 02115, United States.
Andrew B NixonDuke Center for Cancer Immunotherapy, Duke University, Durham, NC 27701, United States.
Joseph A LucciDepartment of Pharmacy, University of Texas Heath-Memorial Hermann Cancer Center, Houston, TX 77030, United States.
Scott KopetzDepartment of Gastrointestinal Medical Oncology, University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, United States.
Monica M BertagnolliDana-Farber/Partners Cancer Care, Harvard Medical School, Boston, MA 02215, United States.
Federico InnocentiDivision of Pharmacotherapy and Experimental Therapeutics, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, NC 27599, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While monoclonal antibody-based targeted therapies have substantially improved progression-free survival in cancer patients, the variability in individual responses poses a significant challenge in patient care. Therefore, identifying cancer subtypes and their associated biomarkers is required for assigning effective treatment. In this study, we integrated genotype and pre-treatment tissue RNA-seq data and identified biomarkers causally associated with the overall survival (OS) of colorectal cancer (CRC) patients treated with either cetuximab or bevacizumab. We performed enrichment analysis for specific consensus molecular subtypes (CMS) of CRC and evaluated differential expression of identified genes using paired tumor and normal tissue from an external cohort. In addition, we replicated the causal effect of these genes on OS using a validation cohort and assessed their association with The Cancer Genome Atlas Program data as an external cohort. One of the replicated findings was

Indexed as

Biomarkers, TumorColorectal NeoplasmsAntineoplastic Agents, ImmunologicalBevacizumabCetuximabFemaleGene Expression Regulation, NeoplasticHumansMaleAntineoplastic Agents, ImmunologicalBevacizumabBiomarkers, TumorCetuximab

Identifiers

PMID40585306
PMCPMC12204401

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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.