Evidence map›Paper›PMID 37291757›Full record

ArticleThe journal of pathology. Clinical research2023

Post-operative mortality and recurrence patterns in pancreatic cancer according to KRAS mutation and CDKN2A, p53, and SMAD4 expression.

Yohei Masugi, Manabu Takamatsu, Mariko Tanaka, Kensuke Hara, Yosuke Inoue, Tsuyoshi Hamada, Tatsunori Suzuki, Junichi Arita, Yuki Hirose, Yoshikuni Kawaguchi and 15 more

Open access · goldAbstract read
In one paragraph

Article in The journal of pathology. Clinical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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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

25 authors at 5 institutions in 1 country.

Yohei Masugi *Department of Pathology, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0002-6952-4043
Manabu Takamatsu *Division of Pathology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Mariko Tanaka *Department of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kensuke HaraDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Yosuke InoueDepartment of Hepatobiliary and Pancreatic Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Tsuyoshi HamadaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-3937-2755
Tatsunori SuzukiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Junichi AritaHepato-Biliary-Pancreatic Surgery Division, Department of Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yuki HiroseDepartment of Hepatobiliary and Pancreatic Surgery, Cancer Institute Hospital, 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.
Yousuke NakaiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Atsushi ObaDepartment of Hepatobiliary and Pancreatic Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Naoki SasahiraDepartment of Hepato-Biliary-Pancreatic Medicine, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Gaku ShimaneDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Tsuyoshi TakedaDepartment of Hepato-Biliary-Pancreatic Medicine, Cancer Institute Hospital, 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.
Mitsuhiro FujishiroDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kiyoshi HasegawaHepato-Biliary-Pancreatic Surgery Division, Department of Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Minoru KitagoDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Yu TakahashiDepartment of Hepatobiliary and Pancreatic Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Tetsuo Ushiku *Department of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kengo Takeuchi *Division of Pathology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Michiie Sakamoto *Department of Pathology, Keio University School of Medicine, Tokyo, Japan.
GTK Pancreatic Cancer Study Group in Japan
Japanese Foundation For Cancer Research · JPThe University of Tokyo · JPKeio University · JPAkita University · JPUniversity of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alterations in KRAS, CDKN2A (p16), TP53, and SMAD4 genes have been major drivers of pancreatic carcinogenesis. The clinical course of patients with pancreatic cancer in relation to these driver alterations has not been fully characterised in large populations. We hypothesised that pancreatic carcinomas with different combinations of KRAS mutation and aberrant expression of CDKN2A, p53, and SMAD4 might show distinctive recurrence patterns and post-operative survival outcomes. To test this hypothesis, we utilised a multi-institutional cohort of 1,146 resected pancreatic carcinomas and assessed KRAS mutations by droplet digital polymerase chain reaction and CDKN2A, p53, and SMAD4 expression by immunohistochemistry. Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) for disease-free survival (DFS) and overall survival (OS) were computed according to each molecular alteration and the number of altered genes using the Cox regression models. Multivariable competing risks regression analyses were conducted to assess the associations of the number of altered genes with specific patterns of recurrence. Loss of SMAD4 expression was associated with short DFS (multivariable HR, 1.24; 95% CI, 1.09-1.43) and OS times (multivariable HR, 1.27; 95% CI, 1.10-1.46). Compared to cases with 0-2 altered genes, cases with three and four altered genes had multivariable HRs for OS of 1.28 (95% CI, 1.09-1.51) and 1.47 (95% CI, 1.22-1.78), respectively (p

Indexed as

CarcinomaPancreatic NeoplasmsCyclin-Dependent Kinase Inhibitor p16HumansMutationProto-Oncogene Proteins p21(ras)Smad4 ProteinTumor Suppressor Protein p53CDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16KRAS protein, humanProto-Oncogene Proteins p21(ras)Smad4 ProteinSMAD4 protein, humanTumor Suppressor Protein p53cohort studiesoncogenesoutcomepancreatectomypancreatic ductal adenocarcinoma

Identifiers

PMID37291757
PMCPMC10397380
OpenAlexW4379967327

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.