Evidence map›Paper›PMID 25131421›Full record

ArticleThe American journal of pathology2014

Single-cell genetic analysis reveals insights into clonal development of prostate cancers and indicates loss of PTEN as a marker of poor prognosis.

Kerstin M Heselmeyer-Haddad, Lissa Y Berroa Garcia, Amanda Bradley, Leanora Hernandez, Yue Hu, Jens K Habermann, Christoph Dumke, Christoph Thorns, Sven Perner, Ekaterina Pestova and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Single-cell Technology in Stem Cell Research.Current stem cell research & therapy · 2025
    Review
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  17. TBL1XR1 in physiological and pathological states.American journal of clinical and experimental urology · 2015
    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

16 authors at 8 institutions in 2 countries.

Kerstin M Heselmeyer-HaddadGenetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Electronic address: heselmek@mail.nih.gov.
Lissa Y Berroa GarciaGenetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Amanda BradleyGenetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Leanora HernandezGenetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Yue HuGenetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Jens K HabermannSection for Translational Surgical Oncology and Biobanking, Department of Surgery, University of Lübeck and University Medical Center Schleswig-Holstein, Campus University of Lübeck, Lübeck, Germany.
Christoph DumkeSection for Translational Surgical Oncology and Biobanking, Department of Surgery, University of Lübeck and University Medical Center Schleswig-Holstein, Campus University of Lübeck, Lübeck, Germany.
Christoph ThornsInstitute of Pathology, University of Lübeck and University Medical Center Schleswig-Holstein, Campus University of Lübeck, Lübeck, Germany.
Sven PernerDepartment of Prostate Cancer Research, Institute of Pathology, University Hospital of Bonn, Bonn, Germany.
Ekaterina PestovaAbbott Molecular, Des Plaines, Illinois.
Catherine BurkeDepartment of Urology, Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California.
Salim A ChowdhuryJoint Carnegie Mellon/University of Pittsburgh Ph.D. Program in Computational Biology, Carnegie Mellon University, Pittsburgh, Pennsylvania; Lane Center for Computational Biology, Carnegie Mellon University, Pittsburgh, Pennsylvania.
Russell SchwartzLane Center for Computational Biology, Carnegie Mellon University, Pittsburgh, Pennsylvania; Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania.
Alejandro A SchäfferComputational Biology Branch, National Center for Biotechnology Information, the National Institutes of Health, Bethesda, Maryland.
Pamela L ParisDepartment of Urology, Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California.
Thomas RiedGenetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Center for Cancer Research · USUniversity of Lübeck · DENational Cancer Institute · USUCSF Helen Diller Family Comprehensive Cancer Center · USAbbott (United States) · USCarnegie Mellon University · USNational Institutes of Health · USUniversity of Pittsburgh · US

Funding

Intratumor heterogeneity and tumor evolutionZIABC010834 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RIED, THOMAS · 2009 to 2023
$12.2M
Case Studies In GeneticsZIALM000097 · NLM · NATIONAL LIBRARY OF MEDICINE · PI SCHAFFER, ALEJANDRO A · 2009 to 2019
$4.6M
CaP Metastasis Biomarkers: Validation/Genomics/BiologyR01CA115484 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PARIS, PAMELA L · 2005 to 2009
$1.4M
Heterogeneous Cancer Progression from Microarray DataR01CA140214 · NCI · CARNEGIE-MELLON UNIVERSITY · PI SCHWARTZ, RUSSELL S · 2009 to 2013
$1.4M
Inferring in vivo Capsid Assembly Kinetics from in vitro by Stochastic SimulationR01AI076318 · NIAID · CARNEGIE-MELLON UNIVERSITY · PI SCHWARTZ, RUSSELL S · 2009 to 2012
$1.1M
Intramural NIH HHSNCI NIH HHS R01 CA115484NCI NIH HHS R01 CA140214NIAID NIH HHS R01 AI076318
6 · The paper itself

Abstract

Gauging the risk of developing progressive disease is a major challenge in prostate cancer patient management. We used genetic markers to understand genomic alteration dynamics during disease progression. By using a novel, advanced, multicolor fluorescence in situ hybridization approach, we enumerated copy numbers of six genes previously identified by array comparative genomic hybridization to be involved in aggressive prostate cancer [TBL1XR1, CTTNBP2, MYC (alias c-myc), PTEN, MEN1, and PDGFB] in six nonrecurrent and seven recurrent radical prostatectomy cases. An ERG break-apart probe to detect TMPRSS2-ERG fusions was included. Subsequent hybridization of probe panels and cell relocation resulted in signal counts for all probes in each individual cell analyzed. Differences in the degree of chromosomal and genomic instability (ie, tumor heterogeneity) or the percentage of cells with TMPRSS2-ERG fusion between samples with or without progression were not observed. Tumors from patients that progressed had more chromosomal gains and losses, and showed a higher degree of selection for a predominant clonal pattern. PTEN loss was the most frequent aberration in progressers (57%), followed by TBL1XR1 gain (29%). MYC gain was observed in one progresser, which was the only lesion with an ERG gain, but no TMPRSS2-ERG fusion. According to our results, a probe set consisting of PTEN, MYC, and TBL1XR1 would detect progressers with 86% sensitivity and 100% specificity. This will be evaluated further in larger studies.

Indexed as

AdenocarcinomaAgedBiomarkers, TumorChromosomal InstabilityComparative Genomic HybridizationDisease ProgressionHumansIn Situ Hybridization, FluorescenceMaleMiddle AgedOncogene Proteins, FusionPloidiesPrognosisProstateProstatectomyProstatic NeoplasmsBiomarkers, TumorOncogene Proteins, FusionPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID25131421
PMCPMC4188868
OpenAlexW2116978640

What OpenQuestion holds

Textmetadata
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.