ArticleCancer biology & therapy2013
Non-canonical p53 signaling to promote invasion.
Article in Cancer biology & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Heterogeneity Analysis of Esophageal Squamous Cell Carcinoma in Cell Lines, Tumor Tissues and Patient-Derived Xenografts.Journal of Cancer · 2021Article
- NEDD4 over-expression regulates the afatinib resistant phenotype of NSCLC cells.Oncology signaling · 2018Article
- Gene expression profile of human esophageal squamous carcinoma cell line TE-1.International journal of clinical and experimental medicine · 2015Article
- The other side of the coin: the tumor-suppressive aspect of oncogenes and the oncogenic aspect of tumor-suppressive genes, such as those along the CCND-CDK4/6-RB axis.Cell cycle (Georgetown, Tex.) · 2014Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
It has been known for a number of years that mutated "inactive" p53 proteins still capable of binding to DNA per se, can bind to DNA sequences that are non-canonical for p53, with for example, a resultant increase in the transcription and expression of growth factor receptors such as ERBB1, (1)(,) (2) i.e., mutation of p53 not merely results in "no p53 function" but in fact results in "oncogenic p53 function". And in agreement with this postulate transduction of p53 null cells with mutant p53 can cause transformation. (3) In prior studies the authors of the present manuscript had demonstrated that expression of p53 (R175H) and ERBB1 could transform immortalized primary esophageal cells, in parallel with increased migratory ability. (4) These present studies have defined why those transformed cells became invasive: increased c-Met activity. (5.)
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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 OpenQuestion graph.