Evidence map›Paper›PMID 38006445›Full record

ArticleJournal of gastroenterology2024

Genomic profile and clinical features of MSI-H and TMB-high pancreatic cancers: real-world data from C-CAT database.

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

Abstract read
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In one paragraph

Article in Journal of gastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

19 citing papers in PubMed, 19 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

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, Kyoto, 602-8566, Japan.
Takeshi IshikawaDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji agaru, Kawaramachi Street, Kamigyoku, Kyoto, Kyoto, 602-8566, Japan. iskw-t@koto.kpu-m.ac.jp.ORCID 0000-0002-5770-9710
Toshifumi DoiDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji agaru, Kawaramachi Street, Kamigyoku, Kyoto, Kyoto, 602-8566, Japan.
Ryuichi MoritaDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji agaru, Kawaramachi Street, Kamigyoku, Kyoto, Kyoto, 602-8566, Japan.
Seita KataokaDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji agaru, Kawaramachi Street, Kamigyoku, Kyoto, Kyoto, 602-8566, Japan.
Hayato MiyakeDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji agaru, Kawaramachi Street, Kamigyoku, Kyoto, Kyoto, 602-8566, Japan.
Kanji YamaguchiDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji agaru, Kawaramachi Street, Kamigyoku, Kyoto, Kyoto, 602-8566, Japan.
Michihisa MoriguchiDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji agaru, Kawaramachi Street, Kamigyoku, Kyoto, Kyoto, 602-8566, Japan.
Yoshio SogameDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji agaru, Kawaramachi Street, Kamigyoku, Kyoto, Kyoto, 602-8566, Japan.
Hiroaki YasudaDepartment of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Hirokoji agaru, Kawaramachi Street, Kamigyoku, Kyoto, 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, 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, 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

backgroundMicrosatellite instability high (MSI-H) and tumor mutational burden high (TMB-high) pancreatic cancer are rare, and information is lacking. Based on the C-CAT database, we analyzed the clinical and genomic characteristics of patients with these subtypes.

methodsWe retrospectively reviewed data on 2206 patients with unresectable pancreatic adenocarcinoma enrolled in C-CAT between July 2019 and January 2022. The clinical features, proportion of genomic variants classified as oncogenic/pathogenic in C-CAT, overall response rate (ORR), disease control rate (DCR), and time to treatment failure (TTF) of chemotherapy as first-line treatment were evaluated.

resultsNumbers of patients with MSI-H and TMB-high were 7 (0.3%) and 39 (1.8%), respectively. All MSI-H patients were TMB-high. MSI-H and TMB-high patients harbored more mismatch repair genes, such as MSH2, homologous recombination-related genes, such as ATR and BRCA2, and other genes including BRAF, KMT2D, and SMARCA4. None of the 6 MSI-H patients who received chemotherapy achieved a clinical response, including 4 patients treated with gemcitabine plus nab-paclitaxel (GnP) therapy, whose DCR was significantly lower than that of microsatellite stable (MSS) patients (0 vs. 67.0%, respectively, p = 0.01). Among the TMB-high and TMB-low groups, no significant differences were shown in ORR, DCR (17.1 vs. 23.1% and 57.1 vs. 63.1%, respectively), or median TTF (25.9 vs. 28.0 weeks, respectively) of overall first-line chemotherapy.

conclusionsMSI-H and TMB-high pancreatic cancers showed some distinct genomic and clinical features from our real-world data. These results suggest the importance of adapting optimal treatment strategies according to the genomic alterations.

Indexed as

AdenocarcinomaPancreatic NeoplasmsBiomarkers, TumorDNA HelicasesHumansMicrosatellite InstabilityMutationNuclear ProteinsRetrospective StudiesTranscription FactorsBiomarkers, TumorDNA HelicasesNuclear ProteinsSMARCA4 protein, humanTranscription FactorsChemotherapyGene mutationMicrosatellite instabilityPancreatic cancerTumor mutational burden

Identifiers

PMID38006445
OpenAlexW4388998972

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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.