Evidence map›Paper›PMID 32552802›Full record

ArticleBMC cancer2020

Immune landscape of human prostate cancer: immune evasion mechanisms and biomarkers for personalized immunotherapy.

Mayassa J Bou-Dargham, Linlin Sha, Qing-Xiang Amy Sang, Jinfeng Zhang

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
2.6field-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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

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  4. CTLA-4: a promising immunosuppressive immune checkpoint in prostate cancer therapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

4 authors at 1 institution in 1 country.

Mayassa J Bou-DarghamDepartment of Chemistry and Biochemistry, Florida State University, Tallahassee, Florida, USA. mdargham@chem.fsu.edu.ORCID http://orcid.org/0000-0002-1551-8887
Linlin ShaDepartment of Statistics, Florida State University, Tallahassee, Florida, USA.
Qing-Xiang Amy SangDepartment of Chemistry and Biochemistry, Florida State University, Tallahassee, Florida, USA. qxsang@chem.fsu.edu.
Jinfeng ZhangDepartment of Statistics, Florida State University, Tallahassee, Florida, USA. jinfeng@stat.fsu.edu.
Florida State University · US

Funding

Collaborative Research: Mathematical Framework for Biomolecules: From Protein to RNA to ChromosomesR01GM126558 · NIGMS · FLORIDA STATE UNIVERSITY · PI ZHANG, JINFENG · 2017 to 2021
$1.5M
National Institute of General Medical Sciences of the National Institute of Health R01GM126558NIGMS NIH HHS R01 GM126558
6 · The paper itself

Abstract

backgroundDespite recent advances in cancer immunotherapy, the efficacy of these therapies for the treatment of human prostate cancer patients is low due to the complex immune evasion mechanisms (IEMs) of prostate cancer and the lack of predictive biomarkers for patient responses.

methodsTo understand the IEMs in prostate cancer and apply such understanding to the design of personalized immunotherapies, we analyzed the RNA-seq data for prostate adenocarcinoma from The Cancer Genome Atlas (TCGA) using a combination of biclustering, differential expression analysis, immune cell typing, and machine learning methods.

resultsThe integrative analysis identified eight clusters with different IEM combinations and predictive biomarkers for each immune evasion cluster. Prostate tumors employ different combinations of IEMs. The majority of prostate cancer patients were identified with immunological ignorance (89.8%), upregulated cytotoxic T lymphocyte-associated protein 4 (CTLA4) (58.8%), and upregulated decoy receptor 3 (DcR3) (51.6%). Among patients with immunologic ignorance, 41.4% displayed upregulated DcR3 expression, 43.26% had upregulated CTLA4, and 11.4% had a combination of all three mechanisms. Since upregulated programmed cell death 1 (PD-1) and/or CTLA4 often co-occur with other IEMs, these results provide a plausible explanation for the failure of immune checkpoint inhibitor monotherapy for prostate cancer.

conclusionThese findings indicate that human prostate cancer specimens are mostly immunologically cold tumors that do not respond well to mono-immunotherapy. With such identified biomarkers, more precise treatment strategies can be developed to improve therapeutic efficacy through a greater understanding of a patient's immune evasion mechanisms.

Indexed as

Biomarkers, TumorCTLA-4 AntigenDatasets as TopicGene Expression Regulation, NeoplasticHumansImmune EvasionImmunotherapyMalePrecision MedicineProstatic NeoplasmsReceptors, Tumor Necrosis Factor, Member 6bRNA-SeqBiomarkers, TumorCTLA-4 AntigenCTLA4 protein, humanReceptors, Tumor Necrosis Factor, Member 6bTNFRSF6B protein, humanBiomarkersCombination therapyImmune evasionImmunotherapyProstate cancer

Identifiers

PMID32552802
PMCPMC7302357
OpenAlexW3035824467

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.