Evidence map›Paper›PMID 32314446›Full record

ArticleCancer science2020

Combination of KRAS and SMAD4 mutations in formalin-fixed paraffin-embedded tissues as a biomarker for pancreatic cancer.

Takahiro Yokose, Minoru Kitago, Sachiko Matsuda, Yasushi Sasaki, Yohei Masugi, Yuki Nakamura, Masahiro Shinoda, Hiroshi Yagi, Yuta Abe, Go Oshima and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

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  14. The Role ofCancers · 2022
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  16. Cancers · 2022
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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

17 authors at 2 institutions in 1 country.

Takahiro YokoseDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.ORCID https://orcid.org/0000-0001-6946-280X
Minoru KitagoDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Sachiko MatsudaDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Yasushi SasakiDepartment of Medical Genome Sciences, Research Institute for Frontier Medicine, Sapporo Medical University, Sapporo, Japan.ORCID https://orcid.org/0000-0002-3500-8059
Yohei MasugiDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Yuki NakamuraDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Masahiro ShinodaDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Hiroshi YagiDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Yuta AbeDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Go OshimaDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Shutaro HoriDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Fujita YusukeDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Yutaka NakanoDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Yutaka EndoDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Kodai AbeDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Takashi TokinoDepartment of Medical Genome Sciences, Research Institute for Frontier Medicine, Sapporo Medical University, Sapporo, Japan.
Yuko KitagawaDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Keio University · JPSapporo Medical University · JP

Funding

Japan Society for the Promotion of Science 16H06279
6 · The paper itself

Abstract

Formalin-fixed paraffin-embedded (FFPE) tissues used for routine pathological diagnosis are valuable for cancer genomic analysis; however, the association between mutation status derived from these specimens and prognosis in pancreatic ductal adenocarcinoma (PDAC) remains unclear. We analyzed 50 cancer-related gene mutations including driver genes in PDAC, using next-generation sequencing (NGS) to clarify the association between gene mutations and prognosis. DNA was extracted from FFPE tissues obtained from 74 patients with untreated resectable PDAC who underwent surgery at our institution between 2013 and 2018. Fifty of the 74 patients with DNA extracts from FFPE samples suitable for NGS were analyzed. The prevalence of driver gene mutations was as follows: 84% for KRAS, 62% for TP53, 32% for SMAD4, and 18% for CDKN2A. There were no cases of single SMAD4 mutations; its rate of coincidence with KRAS or TP53 mutations was 30% and 2%, respectively. The combination of KRAS and SMAD4 mutations resulted in significantly shorter relapse-free survival (RFS; median survival time [MST], 12.3 vs. 28.9 months, P = .014) and overall survival (OS; MST, 22.3 months vs. not reached, P = .048). On multivariate analysis, the combination of KRAS and SMAD4 mutations was an independent prognostic factor for RFS (hazard ratio [HR] 4.218; 95% confidence interval [CI], 1.77-10.08; P = .001) and OS (HR 6.730; 95% CI, 1.93-23.43; P = .003). The combination of KRAS and SMAD4 mutations in DNA obtained from FFPE tissues is an independent poor prognostic factor in PDAC.

Indexed as

AdultAgedAged, 80 and overBiomarkers, TumorCarcinoma, Pancreatic DuctalDNA Mutational AnalysisFemaleFormaldehydeHigh-Throughput Nucleotide SequencingHumansMaleMiddle AgedMutationPancreatic NeoplasmsParaffin EmbeddingPrognosisBiomarkers, TumorFormaldehydeKRAS protein, humanProto-Oncogene Proteins p21(ras)Smad4 ProteinSMAD4 protein, humanKRASnext-generation sequencingpancreatic ductal adenocarcinomaprognosisSMAD4

Identifiers

PMID32314446
PMCPMC7293095
OpenAlexW3016582508

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.