Evidence map›Paper›PMID 36790221›Full record

ArticleGenes, chromosomes & cancer2023

Germline variation in RASAL2 may predict survival in patients with RAS-activated colorectal cancer.

Christopher Wills, Katie Watts, Timothy S Maughan, David Fisher, Nada A Al-Tassan, Richard S Houlston, Valentina Escott-Price, Jeremy P Cheadle

Open access · hybridAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 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

8 authors at 5 institutions in 2 countries.

Christopher WillsDivision of Cancer and Genetics, School of Medicine, Cardiff University, Cardiff, UK.ORCID 0000-0002-3178-8924
Katie WattsDivision of Cancer and Genetics, School of Medicine, Cardiff University, Cardiff, UK.ORCID 0000-0002-0267-3984
Timothy S MaughanCRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford, UK.ORCID 0000-0002-0580-5065
David FisherMRC Clinical Trials Unit, University College of London, London, UK.ORCID 0000-0002-2512-2296
Nada A Al-TassanDepartment of Genetics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia.ORCID 0000-0001-9076-0334
Richard S HoulstonDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.ORCID 0000-0002-5268-0242
Valentina Escott-PriceInstitute of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK.ORCID 0000-0003-1784-5483
Jeremy P CheadleDivision of Cancer and Genetics, School of Medicine, Cardiff University, Cardiff, UK.ORCID 0000-0001-9453-8458
Cardiff University · GBInstitute of Cancer Research · GBKing Faisal Specialist Hospital & Research Centre · SAMRC Clinical Trials Unit at UCL · GBUniversity of Oxford · GB

Funding

Cancer Research UK 25514Cancer Research UK C1298/A8362Medical Research Council MC_UU_00004/06Medical Research Council MC_UU_12023/20Medical Research Council MR/L010305/1
6 · The paper itself

Abstract

backgroundTherapeutic agents that specifically target patients with RAS mutant colorectal cancer (CRC) are needed. We sought potential drug targets by relating genome-wide association study and survival data in patients with advanced CRC profiled for mitogen-activated protein kinase (MAPK) pathway mutations.

methodsIn total, 694 patients from the clinical trials COIN and COIN-B had MAPK-activated CRCs (assigned as KRAS, NRAS, or BRAF mutant). Genome-wide single nucleotide polymorphism (SNP), gene, and gene-set analyses were performed to identify determinants of survival. For rs12028023 in RAS protein activator-like 2 (RASAL2), we studied its effect by MAPK pathway activation status (by comparing to 760 patients without MAPK-activated CRCs), MAPK gene mutation status, surface area of the primary tumor (as a marker of proliferation), and expression on RASAL2.

resultsIn MAGMA genome-wide analyses, RASAL2 was the most significant gene associated with survival (p = 2.0 × 10

conclusionOur data demonstrate a prognostic role for RASAL2 in patients with MAPK-activated CRCs, with potential as a therapeutic target.

Indexed as

Colorectal NeoplasmsGenome-Wide Association StudyGerm CellsGTPase-Activating ProteinsHumansMitogen-Activated Protein KinasesMutationProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)GTPase-Activating ProteinsMitogen-Activated Protein KinasesProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)RASAL2 protein, humancolorectal cancerMAPK-activationRASRASAL2survival

Identifiers

PMID36790221
PMCPMC10805173
OpenAlexW4320857934

What OpenQuestion holds

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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.