ArticleBMC medical genetics2018
The altered activity of P53 signaling pathway by STK11 gene mutations and its cancer phenotype in Peutz-Jeghers syndrome.
Article in BMC medical genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Strategy for early diagnosis of pancreatic cancer.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
- Comprehensively Testing the Function of Missense Variation in thebioRxiv : the preprint server for biology · 2025Article
- Serine/threonine kinase 11 (STK11) associated adnexal tumors: from biology to therapeutic impact.Human genomics · 2025Review
- Genetic Investigation and Transcriptome Profiling in a Nuclear Family With Peutz-Jeghers Syndrome.Human mutation · 2025Article
- Effect of genetic profiling on surgical decisions at hereditary colorectal cancer syndromes.Heliyon · 2024Review
- CD8/PD-L1 immunohistochemical reactivity and gene alterations in cutaneous squamous cell carcinoma.PloS one · 2023Article
- Review
- Functional assessment of somatic STK11 variants identified in primary human non-small cell lung cancers.Carcinogenesis · 2021Article
- Early screening the small bowel is key to protect Peutz-Jeghers syndrome patients from surgery: a novel mutation c.243delG in STK11 gene.BMC gastroenterology · 2019Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPeutz-Jeghers syndrome (PJS) is caused by mutations in serine/threonine kinase 11 (STK11) gene. The increased cancer risk has been connected to P53 pathway.
methodsPJS probands with STK11 mutation were included in the function analysis. P53 activity elevated by STK11 mutants was investigated using dual-luciferase reporter assay in vitro after constructing expression vectors of STK11 wild type and mutants generated by site-directed substitution. The association between the P53 activity and clinicopathological factors was analysis, especially the cancer history.
resultsThirteen probands with STK11 mutations were involved, and within the mutations, c.G924A was novel. P53 activity elevation caused by 6 truncating mutations were significantly lower than that of STK11 wild type (P < 0.05). Family history of cancer was observed in 5 families. Within them, P53 activity was reduced and cancer occurred before 40 in 2 families, while it was not significantly changed and cancers happened after 45 in the other 3 families.
conclusionsThe affected P53 activity caused by STK11 mutations in PJS patients is significantly associated with protein truncation, while cancer risk in PJS can be elevated through pathways rather than P53 pathway. P53 activity test is probably a useful supporting method to predict cancer risk in PJS, which could be helpful in clinical practice.
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