Identification of a Gene Panel for Endometrioid Endometrial Cancer: a Possible Prognostic Value? View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2020-01-06

AUTHORS

Francesca Malentacchi, Irene Turrini, Flavia Sorbi, Elisabetta Projetto, Francesca Castiglione, Federica Vergoni, Gianni Amunni, Massimiliano Fambrini, Felice Petraglia, Ivo Noci, Serena Pillozzi

ABSTRACT

The incidence of endometrial cancer (EC) is increasing in developed countries. The most frequent is the endometrioid subtype with usually good prognosis; nevertheless, some cases escape this paradigm and may have recurrence. A recent study from The Cancer Genome Atlas suggested to implement the EC analysis by molecular profile for improving diagnosis, prognosis, and therapeutic treatment. The present preliminary study was performed on 15 G3 endometrioid endometrial cancers (G3 EEC) for the identification of somatic mutations in a panel of specific exons in selected genes as ARID1A, CTNNB1, KRAS, PIK3CA, POLE, PTEN, and TP53. The combined procedure, based on the Sanger sequencing and PCR-high-resolution melting analysis, allowed the identification of variations of the selected gene panel in most of patients (93%) of our cohort. The overall evaluation of mutational load exhibited that the most frequent mutated genes were PTEN (93%), followed by PIK3CA (47%) suggesting a deep involvement of PI3K pathway alteration in G3 EEC. Mutations in TP53 (27%), ARID1A (27%), POLE (13%), and at the lower level in KRAS and CTNNB1 (7%) were also observed (exclusively in FIGO III stage patients). The evaluation of the mutations of our proposed panel (ARID1A, CTNNB1, KRAS, PIK3CA, POLE, PTEN, TP53) is suitable to improve the characterization of G3 EEC and could suggest targetable pathways for development of personalized treatments. More... »

PAGES

592-598

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s43032-019-00059-8

DOI

http://dx.doi.org/10.1007/s43032-019-00059-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1123852998

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/32046431


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95 somatic mutations
96 specific exons
97 study
98 subtypes
99 targetable pathways
100 therapeutic treatment
101 treatment
102 values
103 variation
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