Evidence map›Paper›PMID 38637546›Full record

ArticleScientific reports2024

Disruption of the pro-oncogenic c-RAF-PDE8A complex represents a differentiated approach to treating KRAS-c-RAF dependent PDAC.

Sean F Cooke, Thomas A Wright, Yuan Yan Sin, Jiayue Ling, Elka Kyurkchieva, Nattaporn Phanthaphol, Thomas Mcskimming, Katharine Herbert, Selma Rebus, Andrew V Biankin and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2024. 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
0.5field-weighted citation impact, top 38% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

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

13 authors at 2 institutions in 2 countries.

Sean F CookeCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, Scotland, UK.
Thomas A WrightCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, Scotland, UK.
Yuan Yan SinCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, Scotland, UK.
Jiayue LingCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, Scotland, UK.
Elka KyurkchievaCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, Scotland, UK.
Nattaporn PhanthapholSiriraj Centre of Research Excellence for Cancer Immunotherapy, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Thomas McskimmingCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, Scotland, UK.
Katharine HerbertWolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, UK.
Selma RebusWolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, UK.
Andrew V BiankinWolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, UK.
David K ChangWolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, Scotland, UK.
George S BaillieCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, Scotland, UK.
Connor M BlairCollege of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, Scotland, UK. connor.blair@glasgow.ac.uk.
University of Glasgow · GBSiriraj Hospital · TH

Funding

Medical Research Council MC_PC_19039Wellcome TrustWellcome Trust 204820/Z/16/Z
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is considered the third leading cause of cancer mortality in the western world, offering advanced stage patients with few viable treatment options. Consequently, there remains an urgent unmet need to develop novel therapeutic strategies that can effectively inhibit pro-oncogenic molecular targets underpinning PDACs pathogenesis and progression. One such target is c-RAF, a downstream effector of RAS that is considered essential for the oncogenic growth and survival of mutant RAS-driven cancers (including KRAS

Indexed as

Carcinoma, Pancreatic DuctalPancreatic Neoplasms3',5'-Cyclic-AMP PhosphodiesterasesCell Line, TumorCell ProliferationHumansProto-Oncogene Proteins p21(ras)Signal Transduction3',5'-Cyclic-AMP PhosphodiesterasesKRAS protein, humanPDE8A protein, humanProto-Oncogene Proteins p21(ras)c-RAF-PDE8ADisruptor peptideKRASPancreatic ductal adenocarcinomaProtein–protein interaction

Identifiers

PMID38637546
PMCPMC11026450
OpenAlexW4394908245

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.