ReviewCell proliferation2011
Wnt and SHH in prostate cancer: trouble mongers occupy the TRAIL towards apoptosis.
Review in Cell proliferation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Clonal evolution and transcriptional plasticity shape metastatic dissemination routes in prostate cancer.Nature communications · 2025Article
- Effects of an inhibitor of the SHH signaling pathway on endometrial cells of patients with endometriosis.BMC molecular and cell biology · 2022Article
- Long non-coding RNA regulation of TRAIL in breast cancer: A tangle of non-coding threads.Oncology letters · 2020Review
- Restoring TRAIL Induced Apoptosis Using Naturopathy. Hercules Joins Hand with Nature to Triumph Over Lernaean Hydra.Current genomics · 2017Review
- Diagnostic value of SFRP1 as a favorable predictive and prognostic biomarker in patients with prostate cancer.PloS one · 2015Article
- Activation of the transcription factor GLI1 by WNT signaling underlies the role of SULFATASE 2 as a regulator of tissue regeneration.The Journal of biological chemistry · 2013Article
- Hedgehog signaling inhibitor cyclopamine induces apoptosis by decreasing Gli2 and Bcl2 expression in human salivary pleomorphic adenoma cells.Biomedical reports · 2013Article
- Algae extracts and methyl jasmonate anti-cancer activities in prostate cancer: choreographers of 'the dance macabre'.Cancer cell international · 2012Article
- TRAIL and vitamins: opting for keys to castle of cancer proteome instead of open sesame.Cancer cell international · 2012Article
- Gene expression by simian virus 40 large T antigen-induced medulloblastomas in mice.Neural regeneration research · 2012Article
- NutriTRAILomics in prostate cancer: time to have two strings to one's bow.Molecular biology reports · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer is a serious molecular disorder that arises because of reduction in tumour suppressors and overexpression of oncogenes. The malignant cells survive within the context of a three-dimensional microenvironment in which they are exposed to mechanical and physical cues. These signals are, nonetheless, deregulated through perturbations to mechanotransduction, from the nanoscale level to the tissue level. Increasingly sophisticated interpretations have uncovered significant contributions of signal transduction cascades in governing prostate cancer progression. To dismantle the major determinants that lie beneath disruption of spatiotemporal patterns of activity, crosstalk between various signalling cascades and their opposing and promoting effects on TRAIL-mediated activities cannot be ruled out. It is important to focus on that molecular multiplicity of cancer cells, various phenotypes reflecting expression of a variety of target oncogenes, reversible to irreversible, exclusive, overlapping or linked, coexist and compete with each other. Comprehensive investigations into TRAIL-mediated mitochondrial dynamics will remain a worthwhile area for underlining causes of tumourigenesis and for unravelling interference options.
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.