ReviewCurrent pharmaceutical design2011
p73 as a pharmaceutical target for cancer therapy.
Review in Current pharmaceutical design, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 37 citations in OpenAlex.
- Harnessing TP73‑targeted nintedanib: A novel strategy to halt triple‑negative breast cancer via p53‑PPARα/PI3K‑Akt pathway suppression.International journal of oncology · 2025Article
- The Robust Tumoricidal Effects of Combined BET/HDAC Inhibition in Cutaneous T-Cell Lymphoma Can Be Reproduced by ΔNp73 Depletion.The Journal of investigative dermatology · 2022Article
- Discovery of a potent cytotoxic agent that promotes GInternational journal of oncology · 2022Article
- Small-Molecule NSC59984 Induces Mutant p53 Degradation through a ROS-ERK2-MDM2 Axis in Cancer Cells.Molecular cancer research : MCR · 2022Article
- Use of signals of positive and negative selection to distinguish cancer genes and passenger genes.eLife · 2021Article
- Article
- DLC2 inhibits development of glioma through regulating the expression ratio of TAp73α/TAp73β.American journal of cancer research · 2018Article
- Markers of Oral Lichen Planus Malignant Transformation.Disease markers · 2018Review
- Benzyl Isothiocyanate potentiates p53 signaling and antitumor effects against breast cancer through activation of p53-LKB1 and p73-LKB1 axes.Scientific reports · 2017Article
- Signalling pathways in UHRF1-dependent regulation of tumor suppressor genes in cancer.Journal of experimental & clinical cancer research : CR · 2016Review
- Overexpression of CXCL3 can enhance the oncogenic potential of prostate cancer.International urology and nephrology · 2016Article
- Oncogenic Intra-p53 Family Member Interactions in Human Cancers.Frontiers in oncology · 2016Review
- Hypoxia-inducible TAp73 supports tumorigenesis by regulating the angiogenic transcriptome.Nature cell biology · 2015Article
- Hypoxia-induced DNp73 stabilization regulates Vegf-A expression and tumor angiogenesis similar to TAp73.Cell cycle (Georgetown, Tex.) · 2015Article
- AMPK couples p73 with p53 in cell fate decision.Cell death and differentiation · 2014Article
- Eradication of metastatic melanoma through cooperative expression of RNA-based HDAC1 inhibitor and p73 by oncolytic adenovirus.Oncotarget · 2014Article
- Prodigiosin rescues deficient p53 signaling and antitumor effects via upregulating p73 and disrupting its interaction with mutant p53.Cancer research · 2014Article
- p53 Family and Cellular Stress Responses in Cancer.Frontiers in oncology · 2014Review
- A phthalide derivative isolated from endophytic fungi Pestalotiopsis photiniae induces G1 cell cycle arrest and apoptosis in human HeLa cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2013Article
- Recent progress in genetics of aging, senescence and longevity: focusing on cancer-related genes.Oncotarget · 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
About half of all human tumors contain an inactivating mutation of p53, while in the remaining tumors, the p53 pathway is frequently abrogated by alterations of other components of its signaling pathway. In humans, the p53 tumor suppressor is part of a small gene family that includes two other members, p73 and p63, structurally and functionally related to p53. Accumulating evidences indicate that all p53-family proteins function as molecular hubs of a highly interconnected signaling network that coordinates cell proliferation, differentiation and death in response to physiological inputs and oncogenic stress. Therefore, not only the p53-pathway but the entire "p53-family pathway" is a primary target for cancer drug development. In particular, the p53-related protein p73 has a crucial role in determining cellular responses to chemotherapy, and can vicariate p53 functions in triggering cell death after DNA damage in multiple experimental models. The biology and regulation of p73 is complex, since the TP73 gene incorporates both tumor-suppressive and proto-oncogenic functions. However, the p73 gene is rarely mutated in tumors, so appropriate pharmacological manipulation of the p73 pathway is a very promising approach for cancer therapy. Here we provide an overview of the principal mechanism of p73 regulation, and describe several examples of pharmacological tools that can induce p73 accumulation and function by acting on upstream p73 modulators or displacing inhibitory p73 interactors. A better understanding of how the p73 pathway works is mandatory to discover additional players intervening in this pathway and has important implications for the improvement of cancer treatment with the development of new molecules or with the reposition of currently available drugs.
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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 Socratic graph.