Evidence map›Paper›PMID 36968142›Full record

ArticleCancer research communications2023

A

Vigdis Nygaard, Anne Hansen Ree, Vegar Johansen Dagenborg, Anne-Lise Børresen-Dale, Bjørn Edwin, Åsmund Avdem Fretland, Krzysztof Grzyb, Mads H Haugen, Gunhild M Mælandsmo, Kjersti Flatmark

Open access · goldFull text read
In one paragraph

Article in Cancer research communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

7 citing papers in PubMed, 5 citations in OpenAlex.

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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 2 institutions in 1 country.

Vigdis NygaardDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.ORCID 0000-0001-8150-3731
Anne Hansen ReeInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.ORCID 0000-0002-8264-3223
Vegar Johansen DagenborgDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.ORCID 0000-0002-9851-1866
Anne-Lise Børresen-DaleDepartment of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.ORCID 0000-0001-9875-9602
Bjørn EdwinInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.ORCID 0000-0002-3137-6225
Åsmund Avdem FretlandDepartment of Hepato-Pancreato-Biliary Surgery, Oslo University Hospital, Oslo, Norway.ORCID 0000-0002-0945-5189
Krzysztof GrzybDepartment of Pathology, Oslo University Hospital, Oslo, Norway.ORCID 0000-0002-2718-8125
Mads H HaugenDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.ORCID 0000-0002-7143-2594
Gunhild M Mælandsmo *Department of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.ORCID 0000-0002-4797-1600
Kjersti Flatmark *Department of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.ORCID 0000-0001-7409-0780
Oslo University Hospital · NOUniversity of Oslo · NO

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Disease recurrence and drug resistance are major challenges in the clinical management of patients with colorectal cancer liver metastases (CLM), and because tumors are generally microsatellite stable (MSS), responses to immune therapies are poor. The mesenchymal phenotype is overrepresented in treatment-resistant cancers and is associated with an immunosuppressed microenvironment. The aim of this work was to molecularly identify and characterize a mesenchymal subgroup of MSS CLM to identify novel therapeutic approaches. We here generated a mesenchymal gene expression signature by analysis of resection specimens from 38 patients with CLM using ranked expression level of the epithelial-to-mesenchymal transition-related transcription factor Significance: CLM is an important cause of colorectal cancer mortality where the majority of patients have yet to benefit from immunotherapies. In this study of gene expression profiling analyses, we uncovered novel immune checkpoint targets in a subgroup of patients with MSS CLMs harboring a mesenchymal phenotype.

Indexed as

Colorectal NeoplasmsLiver NeoplasmsB7-H1 AntigenHepatitis A Virus Cellular Receptor 2Homeodomain ProteinsHumansMicrosatellite RepeatsNeoplasm Recurrence, LocalProgrammed Cell Death 1 ReceptorTumor MicroenvironmentB7-H1 AntigenHepatitis A Virus Cellular Receptor 2Homeodomain ProteinsProgrammed Cell Death 1 ReceptorPRRX1 protein, human

Identifiers

PMID36968142
PMCPMC10035516
OpenAlexW4318815873

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read37
identifiers read7
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.