ArticleJournal of translational medicine2018
Coexisting YAP expression and TP53 missense mutations delineates a molecular scenario unexpectedly associated with better survival outcomes in advanced gastric cancer.
Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Mutant TP53 switches therapeutic vulnerability during gastric cancer progression within interleukin-6 family cytokines.Cell reports · 2024Article
- Hippo pathway dysregulation in gastric cancer: from Helicobacter pylori infection to tumor promotion and progression.Cell death & disease · 2023Review
- Systematic Review and Meta-analysis of TP53, HER2/ERBB2, KRAS, APC, and PIK3CA Genes Expression Pattern in Gastric Cancer.Middle East journal of digestive diseases · 2022Review
- Isoforms of the p53 Family and Gastric Cancer: A Ménage à Trois for an Unfinished Affair.Cancers · 2021Review
- Article
- Hippo-YAP signaling in digestive system tumors.American journal of cancer research · 2021Review
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Authors and funding
21 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously reported that nuclear expression of the Hippo transducer TAZ in association with Wnt pathway mutations negatively impacts survival outcomes in advanced gastric cancer (GC) patients. Here, we extended these previous findings by investigating another oncogenic cooperation, namely, the interplay between YAP, the TAZ paralogue, and p53. The molecular output of the YAP-p53 cooperation is dependent on TP53 mutational status. In the absence of mutations, the YAP-p53 crosstalk elicits a pro-apoptotic response, whereas in the presence of TP53 mutations it activates a pro-proliferative transcriptional program. In order to study this phenomenon, we re-analyzed data from 83 advanced GC patients treated with chemotherapy whose tissue samples had been characterized for YAP expression (immunohistochemistry, IHC) and TP53 mutations (deep sequencing). In doing so, we generated a molecular model combining nuclear YAP expression in association with TP53 missense variants (YAP+/TP53
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