Evidence map›Paper›PMID 31446281›Full record

ArticleNeoplasia (New York, N.Y.)2019

Pseudogene Associated Recurrent Gene Fusion in Prostate Cancer.

Balabhadrapatruni Vsk Chakravarthi, Pavithra Dedigama-Arachchige, Shannon Carskadon, Shanker Kalyana Sundaram, Jia Li, Kuan-Han Hank Wu, Darshan Shimoga Chandrashekar, James O Peabody, Hans Stricker, Clara Hwang and 8 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. KLK4T2 Is a Hormonally Regulated Transcript from theInternational journal of molecular sciences · 2021
    Article
  10. Androgen-Driven Fusion Genes and Chimeric Transcripts in Prostate Cancer.Frontiers in cell and developmental biology · 2021
    Review
  11. Strategies to Study the Functions of Pseudogenes in Mouse Models of Cancer.Methods in molecular biology (Clifton, N.J.) · 2021
    Review
  12. Pseudogenes as Biomarkers and Therapeutic Targets in Human Cancers.Methods in molecular biology (Clifton, N.J.) · 2021
    Review
  13. Clonal evaluation of prostate cancer molecular heterogeneity in biopsy samples by dual immunohistochemistry and dual RNA in situ hybridization.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020
    Article
  14. 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

18 authors at 4 institutions in 1 country.

Balabhadrapatruni Vsk ChakravarthiDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL.
Pavithra Dedigama-ArachchigeVattikuti Urology Institute, Department of Urology, Henry Ford Health System, Detroit, MI.
Shannon CarskadonVattikuti Urology Institute, Department of Urology, Henry Ford Health System, Detroit, MI.
Shanker Kalyana SundaramMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI.
Jia LiDepartment of Public Health Sciences, Henry Ford Health System, Detroit, MI.
Kuan-Han Hank WuDepartment of Public Health Sciences, Henry Ford Health System, Detroit, MI.
Darshan Shimoga ChandrashekarDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL.
James O PeabodyVattikuti Urology Institute, Department of Urology, Henry Ford Health System, Detroit, MI.
Hans StrickerVattikuti Urology Institute, Department of Urology, Henry Ford Health System, Detroit, MI.
Clara HwangDepartment of Hematology and Oncology, Henry Ford Health System, Detroit, MI.
Dhananjay A ChitaleDepartment of Pathology, Henry Ford Health System, Detroit, MI.
Sean R WilliamsonDepartment of Pathology, Henry Ford Health System, Detroit, MI.
Nilesh S GuptaDepartment of Pathology, Henry Ford Health System, Detroit, MI.
Nora M NavoneDepartment of Genitourinary Medical Oncology-The University of Texas, M D, Anderson Cancer Center, TX.
Craig RogersVattikuti Urology Institute, Department of Urology, Henry Ford Health System, Detroit, MI.
Mani MenonVattikuti Urology Institute, Department of Urology, Henry Ford Health System, Detroit, MI.
Sooryanarayana VaramballyDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL; O'Neal Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL.
Nallasivam PalanisamyVattikuti Urology Institute, Department of Urology, Henry Ford Health System, Detroit, MI. Electronic address: npalani1@hfhs.org.
Henry Ford Health System · USUniversity of Alabama at Birmingham · USMichigan Center for Translational Pathology · USThe University of Texas MD Anderson Cancer Center · US

Funding

Targeting Tumor Microenvironment-Induced Therapy Resistance in Prostate Cancer Bone MetastasisP50CA140388 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOGOTHETIS, CHRISTOPHER J., THOMPSON, TIMOTHY CHARLES · 2009 to 2022
$23.4M
FUNCTIONAL CHARACTERIZATION OF PSEUDOGENES AS NEW BIOMARKER IN PROSTATE CANCERR21CA176330 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PALANISAMY, NALLASIVAM · 2014 to 2015
$364k
NCI NIH HHS P50 CA140388NCI NIH HHS R21 CA176330
6 · The paper itself

Abstract

We present the functional characterization of a pseudogene associated recurrent gene fusion in prostate cancer. The fusion gene KLK4-KLKP1 is formed by the fusion of the protein coding gene KLK4 with the noncoding pseudogene KLKP1. Screening of a cohort of 659 patients (380 Caucasian American; 250 African American, and 29 patients from other races) revealed that the KLK4-KLKP1 is expressed in about 32% of prostate cancer patients. Correlative analysis with other ETS gene fusions and SPINK1 revealed a concomitant expression pattern of KLK4-KLKP1 with ERG and a mutually exclusive expression pattern with SPINK1, ETV1, ETV4, and ETV5. Development of an antibody specific to KLK4-KLKP1 fusion protein confirmed the expression of the full-length KLK4-KLKP1 protein in prostate tissues. The in vitro and in vivo functional assays to study the oncogenic properties of KLK4-KLKP1 confirmed its role in cell proliferation, cell invasion, intravasation, and tumor formation. Presence of strong ERG and AR binding sites located at the fusion junction in KLK4-KLKP1 suggests that the fusion gene is regulated by ERG and AR. Correlative analysis of clinical data showed an association of KLK4-KLKP1 with lower preoperative PSA values and in young men (<50 years) with prostate cancer. Screening of patient urine samples showed that KLK4-KLKP1 can be detected noninvasively in urine. Taken together, we present KLK4-KLKP1 as a class of pseudogene associated fusion transcript in cancer with potential applications as a biomarker for routine screening of prostate cancer.

Indexed as

Gene FusionPseudogenesAmino Acid SequenceAnimalsCell Line, TumorChick EmbryoGene Expression Regulation, NeoplasticGenetic LociHumansKallikreinsMaleNeoplasm GradingOncogene Proteins, FusionProstatic NeoplasmsTissue Kallikreinskallikrein 4KallikreinsKLKP1 protein, humanOncogene Proteins, FusionTissue Kallikreins

Identifiers

PMID31446281
PMCPMC6713813
OpenAlexW2969646901

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.