Evidence map›Paper›PMID 26446945›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2016

Germline Variants in Asporin Vary by Race, Modulate the Tumor Microenvironment, and Are Differentially Associated with Metastatic Prostate Cancer.

Paula J Hurley, Debasish Sundi, Brian Shinder, Brian W Simons, Robert M Hughes, Rebecca M Miller, Benjamin Benzon, Sheila F Faraj, George J Netto, Ismael A Vergara and 17 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. ASPORIN: A root of the matter in tumors and their host environment.Biochimica et biophysica acta. Reviews on cancer · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Observational
  20. 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

27 authors at 1 institution in 1 country.

Paula J HurleyBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland. Department of Oncology, Johns Hopkins University, Baltimore, Maryland. Sidney Kimmel Comprehensive Cancer Institute, Johns Hopkins University, Baltimore, Maryland. phurley2@jhmi.edu.
Debasish SundiBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland.
Brian ShinderBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland.
Brian W SimonsBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland. Department of Molecular and Comparative Pathobiology, Johns Hopkins University, Baltimore, Maryland.
Robert M HughesBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland.
Rebecca M MillerBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland.
Benjamin BenzonBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland.
Sheila F FarajDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland.
George J NettoDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland.
Ismael A VergaraGenome Dx Biosciences Inc., Vancouver, British Columbia, Canada.
Nicholas ErhoGenome Dx Biosciences Inc., Vancouver, British Columbia, Canada.
Elai DavicioniGenome Dx Biosciences Inc., Vancouver, British Columbia, Canada.
R Jeffrey KarnesDepartment of Urology, Mayo Clinic, Rochester, Minnesota.
Guifang YanBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland.
Charles EwingBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland.
Sarah D IsaacsBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland.
David M BermanDepartment of Pathology and Molecular Medicine and Cancer Research Institute, Queens University, Kingston, Ontario, Canada.
Jennifer R RiderDepartment of Epidemiology, Harvard University, T.H. Chan School of Public Health, Boston, Massachusetts.
Kristina M JordahlDepartment of Epidemiology, Harvard University, T.H. Chan School of Public Health, Boston, Massachusetts.
Lorelei A MucciDepartment of Epidemiology, Harvard University, T.H. Chan School of Public Health, Boston, Massachusetts.
Jessie HuangThe Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
Steven S AnThe Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. The Department of Chemical and Biomolecular Engineering, The Johns Hopkins University, Baltimore, Maryland. Physical Sciences-Oncology Center, Johns Hopkins University, Baltimore, Maryland.
Ben H ParkDepartment of Oncology, Johns Hopkins University, Baltimore, Maryland. Sidney Kimmel Comprehensive Cancer Institute, Johns Hopkins University, Baltimore, Maryland.
William B IsaacsBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland.
Luigi MarchionniDepartment of Oncology, Johns Hopkins University, Baltimore, Maryland.
Ashley E RossBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland. Department of Oncology, Johns Hopkins University, Baltimore, Maryland. Sidney Kimmel Comprehensive Cancer Institute, Johns Hopkins University, Baltimore, Maryland. Department of Pathology, Johns Hopkins University, Baltimore, Maryland.
Edward M SchaefferBrady Urological Institute, Department of Urology, Johns Hopkins University, Baltimore, Maryland. Department of Oncology, Johns Hopkins University, Baltimore, Maryland. Sidney Kimmel Comprehensive Cancer Institute, Johns Hopkins University, Baltimore, Maryland.
Johns Hopkins University · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007309 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI COX, ANDREA L · 1985 to 2019
$43.2M
UCLA SPORE IN PROSTATE CANCERP50CA092131 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FREEMAN, MICHAEL R · 2002 to 2023
$42.6M
Training Program in Cellular and Molecular MedicineT32GM008752 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI RAO, RAJINI · 2000 to 2019
$11.7M
Urology Research Training GrantT32DK007552 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI COFFEY, DONALD STRALEY · 1987 to 2012
$2.9M
NCI NIH HHS P30 CA006973NCI NIH HHS P30CA006973NCI NIH HHS P50 CA092131NIDDK NIH HHS T32 DK007552NIDDK NIH HHS T32DK007552NIGMS NIH HHS T32 GM007309NIGMS NIH HHS T32 GM008752
6 · The paper itself

Abstract

purposeProstate cancers incite tremendous morbidity upon metastatic growth. We previously identified Asporin (ASPN) as a potential mediator of metastatic progression found within the tumor microenvironment. ASPN contains an aspartic acid (D)-repeat domain and germline polymorphisms in D-repeat-length have been associated with degenerative diseases. Associations of germline ASPN D polymorphisms with risk of prostate cancer progression to metastatic disease have not been assessed. EXPERIMENTAL

designGermline ASPN D-repeat-length was retrospectively analyzed in 1,600 men who underwent radical prostatectomy for clinically localized prostate cancer and in 548 noncancer controls. Multivariable Cox proportional hazards models were used to test the associations of ASPN variations with risk of subsequent oncologic outcomes, including metastasis. Orthotopic xenografts were used to establish allele- and stroma-specific roles for ASPN D variants in metastatic prostate cancer.

resultsVariation at the ASPN D locus was differentially associated with poorer oncologic outcomes. ASPN D14 [HR, 1.72; 95% confidence interval (CI), 1.05-2.81, P = 0.032] and heterozygosity for ASPN D13/14 (HR, 1.86; 95% CI, 1.03-3.35, P = 0.040) were significantly associated with metastatic recurrence, while homozygosity for the ASPN D13 variant was significantly associated with a reduced risk of metastatic recurrence (HR, 0.44; 95% CI, 0.21-0.94, P = 0.035) in multivariable analyses. Orthotopic xenografts established biologic roles for ASPN D14 and ASPN D13 variants in metastatic prostate cancer progression that were consistent with patient-based data.

conclusionsWe observed associations between ASPN D variants and oncologic outcomes, including metastasis. Our data suggest that ASPN expressed in the tumor microenvironment is a heritable modulator of metastatic progression.

Indexed as

AllelesAnimalsDisease ProgressionExtracellular Matrix ProteinsGenetic Predisposition to DiseaseGerm CellsHumansMaleMice, Inbred NODMice, SCIDNeoplasm MetastasisPolymorphism, GeneticProstatectomyProstatic NeoplasmsRacial GroupsRetrospective StudiesASPN protein, humanExtracellular Matrix Proteins

Identifiers

PMID26446945
PMCPMC4715968
OpenAlexW2181264562

What OpenQuestion holds

Textmetadata
LicenceTDM
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.