Evidence map›Paper›PMID 39623053›Full record

ArticleNPJ precision oncology2024

Intratumoral heterogeneity drives acquired therapy resistance in a patient with metastatic prostate cancer.

Dena P Rhinehart, Jiaying Lai, David E Sanin, Varsha Vakkala, Adrianna Mendes, Christopher Bailey, Emmanuel S Antonarakis, Channing J Paller, Xiaojun Wu, Tamara L Lotan and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in NPJ precision oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. Advances in spatial omics for the analysis of prostate cancer.Analytical and bioanalytical chemistry · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. 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

12 authors.

Dena P Rhinehart *The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD, USA.
Jiaying Lai *Institute for Computational Medicine at Johns Hopkins University, Baltimore, MD, USA.ORCID http://orcid.org/0000-0003-3652-1070
David E SaninThe Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD, USA.ORCID http://orcid.org/0000-0003-0188-7267
Varsha VakkalaThe Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD, USA.
Adrianna MendesThe Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD, USA.
Christopher BaileyThe Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD, USA.
Emmanuel S AntonarakisUniversity of Minnesota Masonic Cancer Center, Minneapolis, MN, USA.
Channing J PallerThe Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD, USA.
Xiaojun WuThe Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD, USA.
Tamara L LotanThe Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD, USA.ORCID http://orcid.org/0000-0002-0494-9067
Rachel KarchinInstitute for Computational Medicine at Johns Hopkins University, Baltimore, MD, USA. karchin@jhu.edu.
Laura A SenaThe Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD, USA. laura.sena@jhmi.edu.ORCID http://orcid.org/0000-0001-6724-9546

Funding

Synthetic lethal metabolic drug combinations for castration-resistant prostate cancerK08CA273167 · NCI · JOHNS HOPKINS UNIVERSITY · PI Laura A. Sena · 2023 to 2026
$877k
NCI NIH HHS K08 CA273167U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) K08CA273167
6 · The paper itself

Abstract

Metastatic prostate cancer (PCa) is not curable due to its ability to acquire therapy resistance. Theoretically, acquired therapy resistance can be driven by changes to previously sensitive cancer cells or their environment and/or by outgrowth of a subpopulation of cancer cells with primary resistance. Direct demonstration of the latter mechanism in patients with PCa is lacking. Here we present a case report as proof-of-principle that outgrowth of a subpopulation of cancer cells lacking the genomic target and present prior to therapy initiation can drive acquired resistance to targeted therapy and threaten survival in patients with PCa.

Identifiers

PMID39623053
PMCPMC11612198

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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.