ReviewCancer biology & therapy2007
Radiosensitization of prostate cancer by priming the wild-type p53-dependent cellular senescence pathway.
Review in Cancer biology & therapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 17 citations in OpenAlex.
- Radiosensitization Effect of PARP Inhibitor Talazoparib Involves Decreasing Mitochondrial Membrane Potential and Induction of Cellular Senescence.Current issues in molecular biology · 2025Article
- Distinct mechanisms mediating therapy-induced cellular senescence in prostate cancer.Cell & bioscience · 2022Review
- Article
- Duocarmycin SA, a potent antitumor antibiotic, sensitizes glioblastoma cells to proton radiation.Bioorganic & medicinal chemistry letters · 2018Article
- Extracellular Vesicles in Prostate Cancer Carcinogenesis, Diagnosis, and Management.Frontiers in oncology · 2018Review
- Targeting signaling and apoptotic pathways involved in chemotherapeutic drug-resistance of hematopoietic cells.Oncotarget · 2017Article
- Hedgehog signaling in prostate cancer and its therapeutic implication.International journal of molecular sciences · 2013Review
- Enhancement of radiosensitivity in human glioblastoma cells by the DNA N-mustard alkylating agent BO-1051 through augmented and sustained DNA damage response.Radiation oncology (London, England) · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A dramatic stage-migration in diagnosis of prostate cancer has led to earlier detection of clinically localized carcinoma and an increased use of radiation therapy. The p53 protein responds to irradiation-induced DNA damage by removing critically damaged cells from the proliferative pool. This review will focus on the dominant role that p53-dependent cellular senescence, rather than cell death, plays in determining the radiosensitivity of human prostate cancer cells in vitro. The finding that senescence is a primary mechanism of tumor regression indicates that p53 activators or downstream effectors may prove effective in radiosensitizing some carcinoma of the prostate.
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.