Evidence map›Paper›PMID 39993799›Full record

ArticleCancer genomics & proteomics

Accumulating Genetic Mutations from Primary to Secondary Biliary Tract Cancers: Analysis of Four Patients With Metachronous Biliary Tract Cancer Using Comprehensive Genomic Profiling.

Toshio Kokuryo, Yoshio Koike, Junpei Yamaguchi, Masaki Sunagawa, Taisuke Baba, Nobuyuki Watanabe, Shunsuke Onoe, Takashi Mizuno, Tomoki Ebata

Abstract read
In one paragraph

Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

9 authors.

Toshio KokuryoDivision of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan kokuryo.toshio.f8@f.mail.nagoya-u.ac.jp.
Yoshio KoikeDivision of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Junpei YamaguchiDivision of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masaki SunagawaDivision of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Taisuke BabaDivision of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Nobuyuki WatanabeDivision of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shunsuke OnoeDivision of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Takashi MizunoDivision of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Tomoki EbataDivision of Surgical Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimMetachronous biliary tract cancer (BTC) is a rare occurrence after curative resection of primary BTC. The genetic alterations and pathogenesis associated with metachronous BTC remain poorly understood. PATIENTS AND

methodsWe analyzed four patients with metachronous BTC who underwent resection at the Nagoya University Hospital between 2010 and 2024. Gene panel examination was performed on both primary and secondary tumors using next-generation sequencing.

resultsThe median interval between resection of the primary tumor and diagnosis of metachronous BTC was 24 months. Genetic alterations were observed in all paired primary and metachronous carcinomas. The number of genetic mutations was higher in metachronous lesions than in primary lesions.

conclusionThis study demonstrated that characteristic genetic alterations and their accumulation play important roles in metachronous BTC. This suggests that the increasing burden of gene mutations may play a crucial role in the carcinogenesis of metachronous BTC. Further investigation is required to validate these findings and elucidate the underlying molecular mechanisms.

Indexed as

Biliary Tract NeoplasmsMutationNeoplasms, Second PrimaryAgedFemaleGenomicsHigh-Throughput Nucleotide SequencingHumansMaleMiddle AgedSmad4 ProteinSmad4 ProteincarcinogenesisCDKN2Aclonal origincomprehensive genomic profilingfield cancerizationgenetic mutation accumulationgenetic predispositionMetachronous biliary tract cancernext-generation sequencingSMAD4

Identifiers

PMID39993799
PMCPMC11880928

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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.