PMID- 26722235
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1792-1074 (Print)
IS  - 1792-1082 (Electronic)
IS  - 1792-1074 (Linking)
VI  - 10
IP  - 5
DP  - 2015 Nov
TI  - Improved survival associated with somatic PIK3CA mutations in copy-number low 
      endometrioid endometrial adenocarcinoma.
PG  - 2743-2748
AB  - The phosphoinositide-3-kinase (PI3K) signaling pathway has been implicated in the 
      development of endometrioid endometrial adenocarcinoma (EEC). Recently, The 
      Cancer Genome Atlas (TCGA) project stratified EEC into four molecular subgroups, 
      with the majority of tumors falling into the copy-number low-EEC (CNL-EEC) 
      molecular subgroup. The aim of the present study was to investigate whether 
      alterations of the PI3K pathway are associated with specific survival outcomes in 
      patients with EEC. The clinical and genomic data of 307 patients with 
      endometrioid-type tumors were obtained from TCGA project, including 90 patients 
      in the CNL-EEC subgroup. Patients were evaluated in terms of survival and 
      clinicopathological characteristics, as well as mutations in the PI3K catalytic 
      subunit alpha (PIK3CA) gene and their effect on PIK3CA function. In CNL-EEC 
      subgroup patients, somatic PIK3CA mutations (48/90 cases) were associated with 
      significantly improved overall survival compared with that of wild-type PIK3CA 
      (P=0.018). Furthermore, this improved survival was specific to the CNL-EEC 
      subgroup and was not observed in other TCGA molecular subgroups. The majority of 
      CNL-EEC cases were low-stage (stage I) and low-to-intermediate grade (grades 1-2) 
      endometrioid tumors. There were no significant differences in age, stage, 
      histology or International Federation of Gynecology and Obstetrics grade between 
      PIK3CA-mutated and non-mutated patient groups (P>0.05). In addition, the majority 
      of cases contained activating PIK3CA mutations. Overall, in the TCGA cohort, 
      PIK3CA mutations had a favorable effect on the survival of patients with EEC, and 
      this effect was dependent on tumoral molecular sub-stratification. Future studies 
      on larger independent cohorts with long term follow-up are warranted to further 
      analyze this association.
FAU - Lin, Douglas I
AU  - Lin DI
AD  - Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA 02215, 
      USA.
LA  - eng
PT  - Journal Article
DEP - 20150915
PL  - Greece
TA  - Oncol Lett
JT  - Oncology letters
JID - 101531236
PMC - PMC4665731
OTO - NOTNLM
OT  - PIK3CA mutation
OT  - The Cancer Genome Atlas
OT  - endometrial adenocarcinoma
OT  - phosphoinositide-3-kinase pathway
EDAT- 2016/01/02 06:00
MHDA- 2016/01/02 06:01
PMCR- 2015/09/15
CRDT- 2016/01/02 06:00
PHST- 2014/11/05 00:00 [received]
PHST- 2015/07/21 00:00 [accepted]
PHST- 2016/01/02 06:00 [entrez]
PHST- 2016/01/02 06:00 [pubmed]
PHST- 2016/01/02 06:01 [medline]
PHST- 2015/09/15 00:00 [pmc-release]
AID - OL-0-0-3702 [pii]
AID - 10.3892/ol.2015.3702 [doi]
PST - ppublish
SO  - Oncol Lett. 2015 Nov;10(5):2743-2748. doi: 10.3892/ol.2015.3702. Epub 2015 Sep 
      15.