Evidence map›Paper›PMID 31899823›Full record

Trial reportThe Prostate2020

Association between immunosuppressive cytokines and PSA progression in biochemically recurrent prostate cancer treated with intermittent hormonal therapy.

Jessica E Hawley, Samuel Pan, William D Figg, Zoila A Lopez-Bujanda, Jonathan D Strope, David H Aggen, Matthew C Dallos, Emerson A Lim, Mark N Stein, Jianhua Hu and 1 more

Registry-linked trialOpen access · greenAbstract readClinical Trial, Phase IIIRandomized Controlled Trial
In one paragraph

Trial report in The Prostate, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00020085, which is not on this map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 32% 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.

NCT00020085 no registry record found
3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
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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

11 authors at 3 institutions in 1 country.

Jessica E HawleyDivision of Hematology and Oncology, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York.ORCID 0000-0003-1720-5654
Samuel PanDivision of Hematology and Oncology, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York.
William D FiggMolecular Pharmacology Section, Genitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
Zoila A Lopez-BujandaColumbia Center for Translational Immunology, Columbia University Medical Center, New York, New York.
Jonathan D StropeMolecular Pharmacology Section, Genitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
David H AggenDivision of Hematology and Oncology, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York.
Matthew C DallosDivision of Hematology and Oncology, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York.
Emerson A LimDivision of Hematology and Oncology, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York.
Mark N SteinDivision of Hematology and Oncology, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York.
Jianhua HuDivision of Hematology and Oncology, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York.
Charles G DrakeDivision of Hematology and Oncology, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York.ORCID 0000-0001-9610-3677
Columbia University Irving Medical Center · USNational Institutes of Health · USJohns Hopkins University · US

Funding

Tumor Biology and Microenvironment ProgramP30CA013696 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Parisa Tehranifar · 1985 to 2026
$115.3M
Identify SNPs and Polymorphisms Involved in the Development of Prostate CancerZIABC010453 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI FIGG, WILLIAM DOUGLAS · 2009 to 2025
$10.4M
Drug Development for Prostate Cancer and other Metastatic ProcessesZIABC010547 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI FIGG, WILLIAM DOUGLAS · 2009 to 2025
$10.2M
Molecular Oncology Training ProgramT32CA203703 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Katherine D Crew, DAWN HERSHMAN · 2016 to 2026
$4.1M
NCI NIH HHS P30 CA013696NCI NIH HHS P30CA013696NCI NIH HHS T32 CA203703NIH HHS T32CA203703
6 · The paper itself

Abstract

backgroundImmunosuppressive cytokines have the potential to promote prostate cancer progression. Assessing their longitudinal changes may implicate mechanisms of progression, treatment resistance, and suggest new therapeutic targets.

methodsThirty-seven men with biochemically recurrent (BCR) prostate cancer who received 6 months of androgen deprivation therapy (ADT) and were monitored until the time to prostate-specific antigen progression (TTPP) were identified from a completed phase III trial (NCT00020085). Serum samples were archived at baseline, 3 months after ADT, and at TTPP. Cytokine concentrations were quantified using a 36-parameter electrochemiluminescence assay. The Wilcoxon signed-rank sum test was used to compare observations between time points. Kaplan-Meier analysis was used to calculate TTPP dichotomized by cytokine values above or below the median. Pearson's rank correlation coefficient was used to compare continuous variables.

resultsMedian TTPP was 399 days (range, 114-1641). Median prostate-specific antigen (PSA) at baseline and progression were 8.5 and 5.3 ng/mL, respectively. Twenty-three patients (62%) achieved undetectable PSA with ADT. Castrate levels of testosterone (<50 ng/dL) after 3 months of ADT occurred in 35 patients (95%). TNF-α (P = .002), IL-23 (P = .002), and CXCL10 (P = .001) significantly increased from baseline to post ADT. Certain cytokines correlated longitudinally: TNF-α correlated with IL-23 (r = .72; P < .001) and IL-8 (r = .59; P < .001) from baseline to post ADT and to PSA progression. Neutrophil-to-lymphocyte ratio correlated with IL-27 (r = .57; P < .001) and MIP-3α (r = .56; P < .001). Patients with a detectable PSA after ADT had elevated levels of IL-6 (P = .049) and IL-8 (P = .013) at PSA progression as compared with those with an undetectable PSA. There was a trend toward shorter TTPP in patients with TNF-α levels above the median (P = .042).

conclusionsSeveral innate cytokines were associated with biochemically recurrent prostate cancer.

Indexed as

AgedAntineoplastic Agents, HormonalBiomarkers, TumorCohort StudiesCytokinesDisease ProgressionDouble-Blind MethodGoserelinHumansImmune ToleranceImmunity, InnateImmunosuppressive AgentsKallikreinsLeuprolideLongitudinal StudiesMaleAntineoplastic Agents, HormonalBiomarkers, TumorCytokinesGoserelinImmunosuppressive AgentsKallikreinsKLK3 protein, humanLeuprolideProstate-Specific AntigenThalidomidebiochemical recurrenceIL-23IL-8TNF-α

Identifiers

PMID31899823
PMCPMC6980998
OpenAlexW2997072492

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.