Evidence map›Paper›PMID 32240795›Full record

ReviewAnnals of oncology : official journal of the European Society for Medical Oncology2020

Germline and sporadic cancers driven by the RAS pathway: parallels and contrasts.

V Dunnett-Kane, E Burkitt-Wright, F H Blackhall, A Malliri, D G Evans, C R Lindsay

Open access · bronzeAbstract readReview
In one paragraph

Review in Annals of oncology : official journal of the European Society for Medical Oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 70 citations in OpenAlex.

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  14. Single nucleotide variants in lung cancer.Chinese medical journal pulmonary and critical care medicine · 2024
    Review
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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

6 authors at 4 institutions in 1 country.

V Dunnett-KaneManchester University NHS Foundation Trust, Manchester, UK.
E Burkitt-WrightManchester Centre for Genomic Medicine, Manchester University NHS Foundation Trust, Manchester, UK.
F H BlackhallDepartment of Medical Oncology, the Christie NHS Foundation Trust, Manchester, UK; Cancer Research UK Lung Cancer Centre of Excellence, London and Manchester, UK; Division of Molecular and Clinical Cancer Sciences, University of Manchester, Manchester, UK.
A MalliriCancer Research UK Manchester Institute, University of Manchester, Manchester, UK.
D G EvansManchester Centre for Genomic Medicine, Manchester University NHS Foundation Trust, Manchester, UK; Division of Evolution and Genomic Medicine, Faculty of Biology and Health, University of Manchester, Manchester, UK.
C R LindsayDepartment of Medical Oncology, the Christie NHS Foundation Trust, Manchester, UK; Cancer Research UK Lung Cancer Centre of Excellence, London and Manchester, UK; Division of Molecular and Clinical Cancer Sciences, University of Manchester, Manchester, UK. Electronic address: colin.lindsay@manchester.ac.uk.
Manchester University NHS Foundation Trust · GBUniversity of Manchester · GBCancer Research UK · GBThe Christie NHS Foundation Trust · GB

Funding

Cancer Research UK 20410
6 · The paper itself

Abstract

Somatic mutations in RAS and related pathway genes such as NF1 have been strongly implicated in the development of cancer while also being implicated in a diverse group of developmental disorders named the 'RASopathies', including neurofibromatosis type 1 (NF1), Noonan syndrome (NS), Noonan syndrome with multiple lentigines (NSML), Costello syndrome (CS), cardiofaciocutaneous syndrome (CFC), and capillary malformation-arteriovenous syndrome (CM-AVM). It remains unclear why (i) there is little overlap in mutational subtype between Ras-driven malignancies associated with sporadic disease and those associated with the RASopathy syndromes, and (ii) RASopathy-associated cancers are usually of different histological origin to those seen with sporadic mutations of the same genes. For instance, germline variants in KRAS and NRAS are rarely found at codons 12, 13 or 61, the most common sites for somatic mutations in sporadic cancers. An exception is CS, where germline variants in codons 12 and 13 of HRAS occur relatively frequently. Given recent renewed drug interest following early clinical success of RAS G12C and farnesyl transferase inhibitors, an improved understanding of this relationship could help guide targeted therapies for both sporadic and germline cancers associated with the Ras pathway.

Indexed as

Costello SyndromeNeoplasmsNoonan SyndromeGerm CellsHumansMutationras Proteinsras ProteinsCostello syndromeneurofibromatosis type 1Noonan syndromeRASRASopathy

Identifiers

PMID32240795
PMCPMC7322396
OpenAlexW3013963303

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.