Evidence map›Paper›PMID 37029223›Full record

ArticleJournal of gastroenterology2023

Genomic landscape and clinical features of rare subtypes of pancreatic cancer: analysis with the national database of Japan.

Tomoki Sakakida, Takeshi Ishikawa, Toshifumi Doi, Ryuichi Morita, Seita Kataoka, Hayato Miyake, Kanji Yamaguchi, Michihisa Moriguchi, Yoshio Sogame, Hiroaki Yasuda and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of gastroenterology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

28 citing papers in PubMed, 32 citations in OpenAlex.

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  6. Progress and challenges in the development of advanced pancreatic cancer organoids.Journal of experimental & clinical cancer research : CR · 2026
    Review
  7. [Research progress in clinical pathology and molecular mechanisms of pancreatic adenosquamous carcinoma].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Tomoki SakakidaDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji Agaru, Kawaramachi Street, Kamigyoku, Kyoto City, Kyoto, 602-8566, Japan.ORCID 0000-0003-1913-7923
Takeshi IshikawaDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji Agaru, Kawaramachi Street, Kamigyoku, Kyoto City, Kyoto, 602-8566, Japan. iskw-t@koto.kpu-m.ac.jp.
Toshifumi DoiDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji Agaru, Kawaramachi Street, Kamigyoku, Kyoto City, Kyoto, 602-8566, Japan.
Ryuichi MoritaDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji Agaru, Kawaramachi Street, Kamigyoku, Kyoto City, Kyoto, 602-8566, Japan.
Seita KataokaDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji Agaru, Kawaramachi Street, Kamigyoku, Kyoto City, Kyoto, 602-8566, Japan.
Hayato MiyakeDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji Agaru, Kawaramachi Street, Kamigyoku, Kyoto City, Kyoto, 602-8566, Japan.
Kanji YamaguchiDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji Agaru, Kawaramachi Street, Kamigyoku, Kyoto City, Kyoto, 602-8566, Japan.
Michihisa MoriguchiDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji Agaru, Kawaramachi Street, Kamigyoku, Kyoto City, Kyoto, 602-8566, Japan.
Yoshio SogameDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji Agaru, Kawaramachi Street, Kamigyoku, Kyoto City, Kyoto, 602-8566, Japan.
Hiroaki YasudaDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji Agaru, Kawaramachi Street, Kamigyoku, Kyoto City, Kyoto, 602-8566, Japan.
Masahiro IwasakuDepartment of Cancer Genome Medical Center, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Hideyuki KonishiDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji Agaru, Kawaramachi Street, Kamigyoku, Kyoto City, Kyoto, 602-8566, Japan.
Koichi TakayamaDepartment of Cancer Genome Medical Center, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Yoshito ItohDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji Agaru, Kawaramachi Street, Kamigyoku, Kyoto City, Kyoto, 602-8566, Japan.
Kyoto Prefectural University of Medicine · JPKyoto Prefectural University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSpecial subtypes of pancreatic cancer, such as acinar cell carcinoma (ACC), adenosquamous carcinoma (ASC), and anaplastic carcinoma of the pancreas (ACP), are rare, and so data on them are limited. Using the C-CAT database, we analyzed clinical and genomic characteristics of patients with these and evaluated differences on comparison with pancreatic ductal adenocarcinoma (PDAC) patients.

methodsWe retrospectively reviewed data on 2691 patients with unresectable pancreatic cancer: ACC, ASC, ACP, and PDAC, entered into C-CAT from June 2019 to December 2021. The clinical features, MSI/TMB status, genomic alterations, overall response rate (ORR), disease control rate (DCR), and time to treatment failure (TTF) on receiving FOLFIRINOX (FFX) or GEM + nab-PTX (GnP) therapy as first-line treatment were evaluated.

resultsNumbers of patients with ACC, ASC, ACP, and PDAC were 44 (1.6%), 54 (2.0%), 25 (0.9%), and 2,568 (95.4%), respectively. KRAS and TP53 mutations were prevalent in ASC, ACP, and PDAC (90.7/85.2, 76.0/68.0, and 85.1/69.1%, respectively), while their rates were both significantly lower in ACC (13.6/15.9%, respectively). Conversely, the rate of homologous recombination-related (HRR) genes, including ATM and BRCA1/2, was significantly higher in ACC (11.4/15.9%) than PDAC (2.5/3.7%). In ASC and ACP, no significant differences in ORR, DCR, or TTF between FFX and GnP were noted, while ACC patients showed a trend toward higher ORR with FFX than GnP (61.5 vs. 23.5%, p = 0.06) and significantly more favorable TTF (median 42.3 vs. 21.0 weeks, respectively, p = 0.004).

conclusionsACC clearly harbors different genomics compared with PDAC, possibly accounting for differences in treatment efficacy.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsAntineoplastic Combined Chemotherapy ProtocolsBRCA1 ProteinBRCA2 ProteinGenomicsHumansJapanRetrospective StudiesBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanAcinar cell carcinomaAdenosquamous carcinomaAnaplastic carcinoma of the pancreasGenome analysisPancreatic ductal adenocarcinoma

Identifiers

PMID37029223
PMCPMC10199859
OpenAlexW4362705680

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.