ArticleEJIFCC2014
Mechanisms of Androgen-Independent Prostate Cancer.
Article in EJIFCC, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- The Role of the Metzincin Superfamily in Prostate Cancer Progression: A Systematic-Like Review.International journal of molecular sciences · 2021Pooled it
- Ciprofloxacin beyond antibacterial therapy: pharmacological mechanisms, anticancer activity, and translational limitations.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- The Transcription Axes ERK-Elk1, JNK-cJun, and JAK-STAT Promote Autophagy Activation and Proteasome Inhibitor Resistance in Prostate Cancer Cells.Current issues in molecular biology · 2025Article
- Prostate Cancer-Targeting Liposome Loaded with Zinc Ion-Coordinated Photosensitizer for Enhanced Chemo-Photodynamic Therapy.Pharmaceutics · 2025Article
- Molecular pathways in reproductive cancers: a focus on prostate and ovarian cancer.Cancer cell international · 2025Review
- Anticancer Properties of Phenylboronic Acid in Androgen-Dependent (LNCaP) and Androgen-Independent (PC3) Prostate Cancer CellsAnti-cancer agents in medicinal chemistry · 2025Article
- Cellular dynamics as a marker of normal-to-cancer transition in human cells.Scientific reports · 2023Article
- Castration-Resistant Prostate Cancer: From Uncovered Resistance Mechanisms to Current Treatments.Cancers · 2023Review
- Redefining serological diagnostics with immunoaffinity proteomics.Clinical proteomics · 2023Review
- Megakaryocyte-Derived IL-8 Acts as a Paracrine Factor for Prostate Cancer Aggressiveness through CXCR2 Activation and Antagonistic AR Downregulation.Biomolecules & therapeutics · 2023Article
- Hormone-Glutamine Metabolism: A Critical Regulatory Axis in Endocrine-Related Cancers.International journal of molecular sciences · 2022Review
- Interplay of Developmental Hippo-Notch Signaling Pathways with the DNA Damage Response in Prostate Cancer.Cells · 2022Review
- Raloxifene Suppresses Tumor Growth and Metastasis in an Orthotopic Model of Castration-Resistant Prostate Cancer.Biomedicines · 2022Article
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- Combination therapy for mCRPC with immune checkpoint inhibitors, ADT and vaccine: A mathematical model.PloS one · 2022Article
- Therapeutic Applications of Physalins: Powerful Natural Weapons.Frontiers in pharmacology · 2022Review
- Effects of orlistat combined with enzalutamide and castration through inhibition of fatty acid synthase in a PC3 tumor-bearing mouse model.Bioscience reports · 2021Article
- Current Status and Future Perspectives of Androgen Receptor Inhibition Therapy for Prostate Cancer: A Comprehensive Review.Biomolecules · 2021Review
- The use of zebrafish model in prostate cancer therapeutic development and discovery.Cancer chemotherapy and pharmacology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer is the second leading cause of cancer-related deaths among men in North America. Almost all prostate cancers begin in an androgen-dependent state, so androgen deprivation therapy is administered and results in improved clinical outcomes. However, over time, some cancerous cells are able to survive and grow during this treatment, resulting in androgen-independent prostate cancer. At this point, the disease is fatal, as there are no effective targeted therapies available. Most prostate cancer tumors require androgen receptor (AR) signalling for survival. During the progression to androgen-independence, this signalling cascade has been found to be altered at many levels within prostate cancers. Mechanisms that enhance AR signalling during androgen deprivation include: AR gene amplifications, AR gene mutations, changes in expression of AR co-regulatory proteins, changes in expression of steroid-generating enzymes, ligand-independent activation of AR via 'outlaw' pathways, and AR-independent pathways that become activated, termed 'bypass' pathways. One or more of these aforementioned changes can lead to prostate cancer cells to gain androgen-independent properties. Understanding the molecular alterations that occur during this process will allow for improved therapeutic strategies to target key molecules and pathways important for this progression.
Indexed as
Identifiers
27683456PMC4975190W2551193472What 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.