Mutation-Driven Signals of ARID1A and PI3K Pathways in Ovarian Carcinomas: Alteration Is An Opportunity.
ARID1A
PI3K pathway
cellular signaling
ovarian cancers
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
15 Nov 2019
15 Nov 2019
Historique:
received:
14
10
2019
revised:
08
11
2019
accepted:
13
11
2019
entrez:
17
11
2019
pubmed:
17
11
2019
medline:
9
4
2020
Statut:
epublish
Résumé
The chromosome is a functionally dynamic structure. The dynamic nature of chromosome functionally connects it to almost every event within a cell, in health and sickness. Chromatin remodeling system acts in unison with the cell survival pathway in mediating a variety of cellular functions, including mitosis, differentiation, DNA damage repair, and apoptosis. In humans, the 16 SWI/SNF complexes are a class of nucleosome remodelers, and ARID1A, an epigenetic tumor suppressor, is a member of mammalian 17 chromatin remodeling complex, SWI/SNF. Alterations of chromatin remodeling system contribute to tumorigenic events in various cancers, including ovarian cancers. Oncogenic changes of genes of the PI3K pathway are one of the potential genetic determinants of ovarian carcinomas. In this review, we present the data demonstrating the co-occurrence of mutations of ARID1A and the PI3K pathway in our cohort of ovarian cancers from the Avera Cancer Institute (SD, USA). Taking into account data from our cohort and the cBioPortal, we interrogate the opportunity provided by this co-occurrence in the context of mutation-driven signals in the life cycle of a tumor cell and its response to the targeted anti-tumor drugs.
Identifiants
pubmed: 31731647
pii: ijms20225732
doi: 10.3390/ijms20225732
pmc: PMC6888220
pii:
doi:
Substances chimiques
ARID1A protein, human
0
DNA-Binding Proteins
0
Transcription Factors
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
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