Evidence map›Paper›PMID 36573306›Full record

ArticleCancer medicine2023

Genomic analysis of aggressive ductal adenocarcinoma of the prostate.

Hiroaki Kobayashi, Takeo Kosaka, Kohei Nakamura, Tokuhiro Kimura, Hiroshi Nishihara, Mototsugu Oya

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

7 citing papers in PubMed, 11 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

6 authors at 1 institution in 1 country.

Hiroaki KobayashiDepartment of Urology, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0003-1038-8793
Takeo KosakaDepartment of Urology, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0002-4371-4594
Kohei NakamuraGenomics Unit, Keio Cancer Center, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0002-5162-7132
Tokuhiro KimuraDivision of Diagnostic Pathology, Saiseikai Yokohamashi Tobu Hospital, Kanagawa, Japan.
Hiroshi NishiharaGenomics Unit, Keio Cancer Center, Keio University School of Medicine, Tokyo, Japan.
Mototsugu OyaDepartment of Urology, Keio University School of Medicine, Tokyo, Japan.
Keio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenomic profile analysis using next-generation sequencing can potentially elucidate the pathogenesis of rare cancers. Ductal adenocarcinoma, a rare subtype of prostate cancer, has an aggressive nature. This is the first study to analyze the genomic profile of ductal adenocarcinoma in an Asian population.

methodsWe identified 12 patients newly diagnosed with ductal adenocarcinoma of the prostate at two hospitals, and nine patients (75.0%) had the pure type. Genomic assessment was performed using either the PleSSision testing platform or FoundationOne CDx.

resultsAt least one genomic alteration occurred in 11 patients (91.7%), and the most frequently mutated gene was tumor suppressor protein p53 (TP53), which was found in six cases (50.0%). Alterations characteristic of this cohort were found in four cases (33.3%) of retinoblastoma transcriptional corepressor 1 (RB1), which was only observed in the pure type. Compared to previous study results, the frequency of genetic alterations in the phosphoinositide 3-kinase (PI3K) pathway (n = 3; 25.0%) and Wnt-β-catenin pathway (n = 5; 41.7%) was comparable, but no alterations in the DNA damage repair (DDR) pathway were observed. None of the patients presented high tumor mutation burden or microsatellite instability.

conclusionsWe found that the Asian cohort with ductal adenocarcinoma had actionable alterations, and a high frequency of alterations in TP53 and RB1 reflected the aggressive nature of the tumor. Genetic analysis using next-generation sequencing is expected to help elucidate the pathogenesis of ductal adenocarcinoma.

Indexed as

AdenocarcinomaProstateGenomicsHigh-Throughput Nucleotide SequencingHumansMaleMutationPhosphatidylinositol 3-KinasesTumor Suppressor Protein p53Phosphatidylinositol 3-KinasesTumor Suppressor Protein p53ductal adenocarcinomanext generation sequencingretinoblastoma transcriptional corepressor 1 (RB1)tumor suppressor protein p53 (TP53)

Identifiers

PMID36573306
PMCPMC10134333
OpenAlexW4312210601

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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.