Evidence map›Paper›PMID 36124727›Full record

ArticleThe oncologist2022

KRAS Mutation Variants and Co-occurring PI3K Pathway Alterations Impact Survival for Patients with Pancreatic Ductal Adenocarcinomas.

Adam C Diehl, Lindsay M Hannan, David B Zhen, Andrew L Coveler, Gentry King, Stacey A Cohen, William P Harris, Veena Shankaran, Kit M Wong, Steven Green and 10 more

Open access · goldAbstract read
In one paragraph

Article in The oncologist, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.8field-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

25 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  5. Review
  6. Prognostic Implications of Codon-SpecificJCO precision oncology · 2026
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  7. Review
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  10. Evaluating the Effect ofJCO precision oncology · 2025
    Article
  11. Review
  12. Distinct Molecular and Clinical Features of Specific Variants of KRAS Codon 12 in Pancreatic Adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Anticancer drugs: How to select small molecule combinations?Trends in pharmacological sciences · 2024
    Review
  18. Review
  19. Article
  20. Article
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

20 authors at 3 institutions in 1 country.

Adam C DiehlDivision of Medical Oncology, Department of Medicine, University of Washington, Seattle, WA, USA.ORCID 0000-0003-4984-8128
Lindsay M HannanDivision of Medical Oncology, Department of Medicine, University of Washington, Seattle, WA, USA.
David B ZhenDivision of Medical Oncology, Department of Medicine, University of Washington, Seattle, WA, USA.
Andrew L CovelerDivision of Medical Oncology, Department of Medicine, University of Washington, Seattle, WA, USA.
Gentry KingDivision of Medical Oncology, Department of Medicine, University of Washington, Seattle, WA, USA.
Stacey A CohenDivision of Medical Oncology, Department of Medicine, University of Washington, Seattle, WA, USA.
William P HarrisDivision of Medical Oncology, Department of Medicine, University of Washington, Seattle, WA, USA.
Veena ShankaranDivision of Medical Oncology, Department of Medicine, University of Washington, Seattle, WA, USA.ORCID 0000-0001-8136-6140
Kit M WongDivision of Medical Oncology, Department of Medicine, University of Washington, Seattle, WA, USA.
Steven GreenFred Hutchinson Cancer Center, Seattle, WA, USA.
Natasha NgFred Hutchinson Cancer Center, Seattle, WA, USA.
Venu G PillarisettyDepartment of Surgery, University of Washington, Seattle, WA, USA.
Jonathan G ShamDepartment of Surgery, University of Washington, Seattle, WA, USA.
James O ParkDepartment of Surgery, University of Washington, Seattle, WA, USA.
Deepti ReddiDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Eric Q KonnickDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Colin C PritchardDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Kelsey BakerFred Hutchinson Cancer Center, Seattle, WA, USA.
Mary RedmanFred Hutchinson Cancer Center, Seattle, WA, USA.
E Gabriela ChioreanDivision of Medical Oncology, Department of Medicine, University of Washington, Seattle, WA, USA.
University of Washington Medical Center · USUniversity of Washington · USFred Hutch Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKRAS variant alleles may have differential biological properties which impact prognosis and therapeutic options in pancreatic ductal adenocarcinomas (PDA). MATERIALS AND

methodsWe retrospectively identified patients with advanced PDA who received first-line therapy and underwent blood and/or tumor genomic sequencing at the University of Washington between 2013 and 2020. We examined the incidence of KRAS mutation variants with and without co-occurring PI3K or other genomic alterations and evaluated the association of these mutations with clinicopathological characteristics and survival using a Cox proportional hazards model.

resultsOne hundred twenty-six patients had genomic sequencing data; KRAS mutations were identified in 111 PDA and included the following variants: G12D (43)/G12V (35)/G12R (23)/other (10). PI3K pathway mutations (26% vs. 8%) and homologous recombination DNA repair (HRR) defects (35% vs. 12.5%) were more common among KRAS G12R vs. non-G12R mutated cancers. Patients with KRAS G12R vs. non-G12R cancers had significantly longer overall survival (OS) (HR 0.55) and progression-free survival (PFS) (HR 0.58), adjusted for HRR pathway co-mutations among other covariates. Within the KRAS G12R group, co-occurring PI3K pathway mutations were associated with numerically shorter OS (HR 1.58), while no effect was observed on PFS.

conclusionsPatients with PDA harboring KRAS G12R vs. non-G12R mutations have longer survival, but this advantage was offset by co-occurring PI3K alterations. The KRAS/PI3K genomic profile could inform therapeutic vulnerabilities in patients with PDA.

Indexed as

NeoplasmsPhosphatidylinositol 3-KinasesGenomicsHumansMutationProto-Oncogene Proteins p21(ras)Retrospective StudiesKRAS protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins p21(ras)KRASpancreatic cancerPI3K

Identifiers

PMID36124727
PMCPMC10249424
OpenAlexW4296782025

What OpenQuestion holds

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LicenceCC BY
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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.