ArticleOncogene2004
Wild-type p53 gene transfer is not detrimental to normal cells in vivo: implications for tumor gene therapy.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 29 citations in OpenAlex.
- p53 mitotic centrosome localization preserves centrosome integrity and works as sensor for the mitotic surveillance pathway.Cell death & disease · 2019Article
- The beneficial effect of Zinc(II) on low-dose chemotherapeutic sensitivity involves p53 activation in wild-type p53-carrying colorectal cancer cells.Journal of experimental & clinical cancer research : CR · 2015Article
- Article
- Therapeutic strategies for head and neck cancer based on p53 status.Experimental and therapeutic medicine · 2012Article
- HIPK2 is involved in cell proliferation and its suppression promotes growth arrest independently of DNA damage.Cell proliferation · 2009Article
- Endothelial NOS, estrogen receptor beta, and HIFs cooperate in the activation of a prognostic transcriptional pattern in aggressive human prostate cancer.The Journal of clinical investigation · 2009Article
- Silencing of stathmin induces tumor-suppressor function in breast cancer cell lines harboring mutant p53.Oncogene · 2007Article
- Trials of gene therapy for pancreatic carcinoma.Current gastroenterology reports · 2005Review
- Gene therapy in animal models of rheumatoid arthritis: are we ready for the patients?Arthritis research & therapy · 2004Review
- [The use of p53 as a tool for human cancer therapy].Molekuliarnaia biologiiaReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The p53 oncosuppressor is strictly maintained in an inactive form under normal conditions, while it is post-translationally activated by a variety of stresses, enacting different protective biological functions. Since one critical issue in cancer gene therapy is tumor specificity, we asked whether the tight p53 regulation applies also to exogenously transferred p53. In principle, this type of regulation could allow p53 gene transfer in both normal and tumor cells to produce detrimental effects only in the latter ones. Here, we report that primary bone marrow cells infected with a p53 recombinant retrovirus and transplanted into irradiated mice reconstitute the hematopoietic system, with no detectable alterations in any of its compartments. Furthermore, simultaneous infection of leukemia and bone marrow cells depleted the neoplastic contamination, allowing lifelong, disease-free survival of 65% of the transplanted animals. These results show that exogenous p53 is controlled as tightly as the endogenous one, and opens the way to p53 gene therapy, without requiring tumor targeting.
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.