Evidence map›Paper›PMID 35049068›Full record

ArticleThe Prostate2022

Ductal and acinar components of mixed prostatic adenocarcinoma frequently have a common clonal origin.

Claes Lindh, Hemamali Samaratunga, Brett Delahunt, Rebecka Bergström, Venkatesh Chellappa, John Yaxley, Johan Lindberg, Lars Egevad

Open access · hybridAbstract read
In one paragraph

Article in The Prostate, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
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

8 authors at 4 institutions in 3 countries.

Claes LindhDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-6176-1511
Hemamali SamaratungaAquesta Uropathology and University of Queensland, Brisbane, Queensland, Australia.ORCID 0000-0001-5796-1791
Brett DelahuntDepartment of Pathology and Molecular Medicine, Wellington School of Medicine and Health Sciences, University of Otago, Wellington, New Zealand.
Rebecka BergströmDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0001-7609-0733
Venkatesh ChellappaDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
John YaxleyWesley Urology Clinic, Brisbane, Queensland, Australia.
Johan LindbergDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0003-3610-6774
Lars EgevadDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0001-8531-222X
Karolinska Institutet · SEThe University of Queensland · AUUniversity of Otago · NZWesley Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDuctal adenocarcinoma (DA) is an aggressive subtype of prostate cancer. It is most commonly seen in mixed tumors together with conventional acinar adenocarcinoma (AA). The genetic profile of DA and its clonal origin is not fully characterized.

objectiveTo investigate whether DA represents a distinct genetic subtype and to investigate the somatic relationship between the ductal and acinar components of mixed cancers. DESIGN, SETTING, AND

participantsIn 17 radical prostatectomy specimens ductal and acinar tumor components from the same tumor foci were dissected. DNA was extracted and genomic sequencing performed. After exclusion of two cases with low cell yield, 15 paired samples remained for analysis.

resultsIn 12 of 15 cases a common somatic denominator was identified, while three cases had clonally separate components. In DA, TMPRSS2-ERG gene fusions were detected in 47% (7/15), clonal FOXA1 alterations in 33% (5/15) and SPOP alterations in 27% (4/15) of cases. In one case KIAA1549-BRAF fusion was identified. Genome doubling events, resulting in an increased ploidy, were identified in the DA in 53% (8/15) of cases, but not seen in any AA. PTEN and CTNNB1 alterations were enriched in DA (6/15) but not seen in any AA. No cancers showed microsatellite instability or high tumor mutation burden.

conclusionsDuctal and acinar prostate adenocarcinoma components of mixed tumors most often share the same origin and are clonally related. DA components in mixed tumor often exhibit genome doubling events resulting in aneuploidy, consistent with the aggressive nature of high grade prostate cancer.

Indexed as

Carcinoma, Acinar CellCarcinoma, DuctalProstatic NeoplasmsHumansMaleNuclear ProteinsProstateProstatectomyRepressor ProteinsNuclear ProteinsRepressor ProteinsSPOP protein, humanclonalityductal adenocarcinomageneticsprostate cancer

Identifiers

PMID35049068
PMCPMC9306900
OpenAlexW4206690439

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.