Evidence map›Paper›PMID 35567350›Full record

ArticleCancer science2022

KRAS variant allele frequency, but not mutation positivity, associates with survival of patients with pancreatic cancer.

Tatsunori Suzuki, Yohei Masugi, Yosuke Inoue, Tsuyoshi Hamada, Mariko Tanaka, Manabu Takamatsu, Junichi Arita, Tomotaka Kato, Yoshikuni Kawaguchi, Akiko Kunita and 16 more

Abstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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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

26 authors.

Tatsunori SuzukiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yohei MasugiDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.ORCID https://orcid.org/0000-0002-6952-4043
Yosuke InoueDepartment of Hepatobiliary and Pancreatic Surgery, The Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Tsuyoshi HamadaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0002-3937-2755
Mariko TanakaDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Manabu TakamatsuDivision of Pathology, The Cancer Institute of Japanese Foundation for Cancer Research, Tokyo, Japan.
Junichi AritaHepato-Biliary-Pancreatic Surgery Division, Department of Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Tomotaka KatoDepartment of Hepatobiliary and Pancreatic Surgery, The Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Yoshikuni KawaguchiHepato-Biliary-Pancreatic Surgery Division, Department of Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Akiko KunitaNext-Generation Precision Medicine Development Laboratory, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yousuke NakaiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yutaka NakanoDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Yoshihiro OnoDepartment of Hepatobiliary and Pancreatic Surgery, The Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Naoki SasahiraDepartment of Hepato-Biliary-Pancreatic Medicine, The Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Tsuyoshi TakedaDepartment of Hepato-Biliary-Pancreatic Medicine, The Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Keisuke TateishiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Sho UemuraDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Kazuhiko KoikeDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Tetsuo UshikuDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kengo TakeuchiDivision of Pathology, The Cancer Institute of Japanese Foundation for Cancer Research, Tokyo, Japan.
Michiie SakamotoDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Kiyoshi HasegawaHepato-Biliary-Pancreatic Surgery Division, Department of Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0001-8734-740X
Minoru KitagoDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Yu TakahashiDepartment of Hepatobiliary and Pancreatic Surgery, The Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan.
Mitsuhiro FujishiroDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0002-4074-1140
GTK Pancreatic Cancer Study Group in Japan

Funding

Daiwa Securities Health FoundationJapan Agency for Medical Research and Development JP21ck0106557Japan Society for the Promotion of Science JP19K08362Japan Society for the Promotion of Science JP20K07414Japan Society for the Promotion of Science JP21K15368Japan Society for the Promotion of Science JP21K15393Takeda Science Foundation
6 · The paper itself

Abstract

KRAS mutation is a major driver of pancreatic carcinogenesis and will likely be a therapeutic target. Due to lack of sensitive assays for clinical samples of pancreatic cancer with low cellularity, KRAS mutations and their prognostic association have not been fully examined in large populations. In a multi-institutional cohort of 1162 pancreatic cancer patients with formalin-fixed paraffin-embedded tumor samples, we undertook droplet digital PCR (ddPCR) for KRAS codons 12/13/61. We examined detection rates of KRAS mutations by clinicopathological parameters and survival associations of KRAS mutation status. Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) for disease-free survival (DFS) and overall survival (OS) were computed using the Cox regression model with adjustment for potential confounders. KRAS mutations were detected in 1139 (98%) patients. The detection rate did not differ by age of tissue blocks, tumor cellularity, or receipt of neoadjuvant chemotherapy. KRAS mutations were not associated with DFS or OS (multivariable HR comparing KRAS-mutant to KRAS-wild-type tumors, 1.04 [95% CI, 0.62-1.75] and 1.05 [95% CI, 0.60-1.84], respectively). Among KRAS-mutant tumors, KRAS variant allele frequency (VAF) was inversely associated with DFS and OS with HRs per 20% VAF increase of 1.27 (95% CI, 1.13-1.42; p

Indexed as

Pancreatic NeoplasmsProto-Oncogene Proteins p21(ras)Biomarkers, TumorGene FrequencyHumansMutationPrognosisBiomarkers, TumorKRAS protein, humanProto-Oncogene Proteins p21(ras)cohort studyoncogenepancreatectomypancreatic neoplasmsequence analysis

Identifiers

PMID35567350
PMCPMC9459293

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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.