Evidence map›Paper›PMID 32593694›Full record

ArticleClinics and research in hepatology and gastroenterology2021

The type of KRAS mutation drives PI3Kα/γ signalling dependency: Implication for the choice of targeted therapy in pancreatic adenocarcinoma patients.

Coralie Cayron, Julie Guillermet-Guibert

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In one paragraph

Article in Clinics and research in hepatology and gastroenterology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
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  4. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Coralie CayronInserm U1037, CRCT, Université Toulouse III Paul Sabatier, 2 av Hubert Curien, 31037 Toulouse, France; Laboratoire d'Excellence ANR-Toucan, Toulouse, France.
Julie Guillermet-GuibertInserm U1037, CRCT, Université Toulouse III Paul Sabatier, 2 av Hubert Curien, 31037 Toulouse, France; Laboratoire d'Excellence ANR-Toucan, Toulouse, France. Electronic address: julie.guillermet@inserm.fr.
Université Toulouse III - Paul Sabatier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma PDAC is a complex disease with an important diversity of genetic alterations found between patients. KRAS mutation is considered as a major oncogenic driver in this cancer (around 90% of the patients), but there exists different KRAS mutation types. The type of KRAS mutation was recently shown to be of importance to detect signalling vulnerabilities in a subset of PDAC patients. We comment on these innovative results and discuss their importance when designing clinical trials with PI3K targeted therapies in this cancer.

Indexed as

AdenocarcinomaCarcinoma, Pancreatic DuctalPancreatic NeoplasmsHumansMutationPhosphatidylinositol 3-KinasesProto-Oncogene Proteins p21(ras)KRAS protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins p21(ras)KRAS mutationMacropinocytosisPancreatic adenocarcinomaPancreatic cancerPDACPI3K

Identifiers

PMID32593694
OpenAlexW3037903677

What OpenQuestion holds

Textmetadata
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.