Evidence map›Paper›PMID 36115838›Full record

ArticleNature communications2022

Spatio-temporal analysis of prostate tumors in situ suggests pre-existence of treatment-resistant clones.

Maja Marklund, Niklas Schultz, Stefanie Friedrich, Emelie Berglund, Firas Tarish, Anna Tanoglidi, Yao Liu, Ludvig Bergenstråhle, Andrew Erickson, Thomas Helleday and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Spatial landscapes of cancers: insights and opportunities.Nature reviews. Clinical oncology · 2024
    Review
  11. Review
  12. 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

13 authors at 4 institutions in 3 countries.

Maja Marklund *Department of Gene Technology, KTH Royal Institute of Technology, Science for Life Laboratory, Solna, Sweden.ORCID 0000-0003-2627-2437
Niklas Schultz *Division of Translational Medicine & Chemical Biology, Karolinska Institute, Science for Life Laboratory, Solna, Sweden.
Stefanie Friedrich *Department of Biochemistry and Biophysics, Stockholm University, Science for Laboratory, Solna, Sweden.ORCID 0000-0002-3889-5589
Emelie BerglundDepartment of Gene Technology, KTH Royal Institute of Technology, Science for Life Laboratory, Solna, Sweden.ORCID 0000-0003-1857-307X
Firas TarishDivision of Translational Medicine & Chemical Biology, Karolinska Institute, Science for Life Laboratory, Solna, Sweden.
Anna TanoglidiDepartment of Pathology, Evangelismos General Hospital, 45-47 Ipsilantou str, Athens, Greece.
Yao LiuDivision of Translational Medicine & Chemical Biology, Karolinska Institute, Science for Life Laboratory, Solna, Sweden.ORCID 0000-0001-5572-723X
Ludvig BergenstråhleDepartment of Gene Technology, KTH Royal Institute of Technology, Science for Life Laboratory, Solna, Sweden.ORCID 0000-0002-5108-4481
Andrew EricksonNuffield Department of Surgical Sciences, University of Oxford, Oxford, UK.
Thomas HelledayDivision of Translational Medicine & Chemical Biology, Karolinska Institute, Science for Life Laboratory, Solna, Sweden.ORCID 0000-0002-7384-092X
Alastair D LambNuffield Department of Surgical Sciences, University of Oxford, Oxford, UK.ORCID 0000-0002-2968-7155
Erik SonnhammerDepartment of Biochemistry and Biophysics, Stockholm University, Science for Laboratory, Solna, Sweden. erik.sonnhammer@scilifelab.se.ORCID 0000-0002-9015-5588
Joakim LundebergDepartment of Gene Technology, KTH Royal Institute of Technology, Science for Life Laboratory, Solna, Sweden. joakim.lundeberg@scilifelab.se.ORCID 0000-0003-4313-1601
Science for Life Laboratory · SEStockholm University · SEUniversity of Oxford · GBEvangelismos Hospital · GR

Funding

Cancer Research UK 25812Prostate Cancer UK PA14-022
6 · The paper itself

Abstract

The molecular mechanisms underlying lethal castration-resistant prostate cancer remain poorly understood, with intratumoral heterogeneity a likely contributing factor. To examine the temporal aspects of resistance, we analyze tumor heterogeneity in needle biopsies collected before and after treatment with androgen deprivation therapy. By doing so, we are able to couple clinical responsiveness and morphological information such as Gleason score to transcriptome-wide data. Our data-driven analysis of transcriptomes identifies several distinct intratumoral cell populations, characterized by their unique gene expression profiles. Certain cell populations present before treatment exhibit gene expression profiles that match those of resistant tumor cell clusters, present after treatment. We confirm that these clusters are resistant by the localization of active androgen receptors to the nuclei in cancer cells post-treatment. Our data also demonstrates that most stromal cells adjacent to resistant clusters do not express the androgen receptor, and we identify differentially expressed genes for these cells. Altogether, this study shows the potential to increase the power in predicting resistant tumors.

Indexed as

Prostatic NeoplasmsReceptors, AndrogenAndrogen AntagonistsAndrogensClone CellsHumansMaleSpatio-Temporal AnalysisAndrogen AntagonistsAndrogensReceptors, Androgen

Identifiers

PMID36115838
PMCPMC9482614
OpenAlexW4296187574

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.