ReviewBioMed research international2015
Beyond the Immune Suppression: The Immunotherapy in Prostate Cancer.
Review in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06471673 (A Study of BRIA-OTS Cellular Immunotherapy in Metastatic Recurrent Breast Cancer), which is not on this map. Cited by 12 papers.
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.
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.
A Study of BRIA-OTS Cellular Immunotherapy in Metastatic Recurrent Breast Cancer
Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- The Potential Role for Immunotherapy in Biochemically Recurrent Prostate Cancer.The Urologic clinics of North America · 2020Review
- Prostate cancer cell-intrinsic interferon signaling regulates dormancy and metastatic outgrowth in bone.EMBO reports · 2020Article
- Targeting Prostate Cancer Using Intratumoral Cytotopically Modified Interleukin-15 Immunotherapy in a Syngeneic Murine Model.ImmunoTargets and therapy · 2020Article
- miR-615 Inhibits Prostate Cancer Cell Proliferation and Invasion by Directly Targeting Cyclin D2.Oncology research · 2019Article
- Prostate Cancer Screening and Management in Solid Organ Transplant Candidates and Recipients.Reviews in urology · 2019Article
- Dendritic cell trafficking in tumor-bearing mice.Cancer immunology, immunotherapy : CII · 2018Article
- SV-BR-1-GM, a Clinically Effective GM-CSF-Secreting Breast Cancer Cell Line, Expresses an Immune Signature and Directly Activates CD4Frontiers in immunology · 2018Article
- miR-20b promotes cellular proliferation and migration by directly regulating phosphatase and tensin homolog in prostate cancer.Oncology letters · 2017Article
- Human Prostate Cancer Hallmarks Map.Scientific reports · 2016Article
- Immune Regulation and Antitumor Effect of TIM-1.Journal of immunology research · 2016Review
- MicroRNA-125a-5p regulates cancer cell proliferation and migration through NAIF1 in prostate carcinoma.OncoTargets and therapy · 2015Article
- Tumor-targeted IL-12 combined with local irradiation leads to systemic tumor control via abscopal effectsOncoimmunologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer (PCa) is the second most common cancer in men. As well in many other human cancers, inflammation and immune suppression have an important role in their development. We briefly describe the host components that interact with the tumor to generate an immune suppressive environment involved in PCa promotion and progression. Different tools provide to overcome the mechanisms of immunosuppression including vaccines and immune checkpoint blockades. With regard to this, we report results of most recent clinical trials investigating immunotherapy in metastatic PCa (Sipuleucel-T, ipilimumab, tasquinimod, Prostvac-VF, and GVAX) and provide possible future perspectives combining the immunotherapy to the traditional therapies.
Indexed as
Identifiers
What OpenQuestion holds
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.