PMID- 28789352
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220318
IS  - 1792-1074 (Print)
IS  - 1792-1082 (Electronic)
IS  - 1792-1074 (Linking)
VI  - 14
IP  - 2
DP  - 2017 Aug
TI  - PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours.
PG  - 1373-1378
LID - 10.3892/ol.2017.6331 [doi]
AB  - The present study examined the expression of mammalian target of rapamycin (mTOR) 
      and mutations in the phosphoinositide 3-kinase (PI3K)/AKT/mTOR pathway in 54 
      patients with typical carcinoid tumours (TC) or atypical carcinoid tumours (AC). 
      In total, 54 bronchopulmonary neuroendocrine tumour (NET) surgical specimens, 
      consisting of 17 TC, 8 AC, 17 large-cell neuroendocrine carcinoma (LCNEC), and 12 
      small-cell lung carcinoma (SCLC) samples, were tested for mTOR by 
      immunohistochemistry, and 104 exon sites were tested in the PI3K/AKT/mTOR pathway 
      by nested polymerase chain reaction. It was found that the positive rates for 
      mTOR expression in TC/AC and LCNEC/SCLC were 60 (15/25) and 55.2% (16/29), 
      respectively. In total, 4 missense mutations were found in 3 patients with TC/AC, 
      including mutations in exon 48 of mTOR (c.6667C>T), exon 21 of tuberous sclerosis 
      complex (TSC) 1 (c.2765G>A), and exons 12 (c.1265C>T) and 19 (c.2148C>T) of TSC2. 
      To the best of our knowledge, mutations in exon 48 of mTOR and exon 21 of TSC1 
      have not been previously reported. Tissues from patients with single mutations 
      exhibited strong positive mTOR immunohistochemical staining, and tissues from 
      patients with double mutations were weakly positive. The same mutations were not 
      observed in SCLC or LCNEC. In conclusion, gene mutations were observed and an 
      association between the gene mutations and mTOR expression were indicated in the 
      PI3K/AKT/mTOR pathway in TC/AC tumours. Those mutations may be driver genes and 
      treatment targets.
FAU - Zhang, Zixuan
AU  - Zhang Z
AD  - Division of Respiratory Medicine, Peking Union Medical College Hospital, Peking 
      Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, P.R. 
      China.
FAU - Wang, Mengzhao
AU  - Wang M
AD  - Division of Respiratory Medicine, Peking Union Medical College Hospital, Peking 
      Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, P.R. 
      China.
LA  - eng
PT  - Journal Article
DEP - 20170607
PL  - Greece
TA  - Oncol Lett
JT  - Oncology letters
JID - 101531236
PMC - PMC5529984
OTO - NOTNLM
OT  - gene mutation
OT  - immunohistochemistry
OT  - mTOR inhibition
OT  - pulmonary carcinoid tumours
OT  - therapeutic target
EDAT- 2017/08/10 06:00
MHDA- 2017/08/10 06:01
PMCR- 2017/06/07
CRDT- 2017/08/10 06:00
PHST- 2015/10/19 00:00 [received]
PHST- 2017/03/17 00:00 [accepted]
PHST- 2017/08/10 06:00 [entrez]
PHST- 2017/08/10 06:00 [pubmed]
PHST- 2017/08/10 06:01 [medline]
PHST- 2017/06/07 00:00 [pmc-release]
AID - OL-0-0-6331 [pii]
AID - 10.3892/ol.2017.6331 [doi]
PST - ppublish
SO  - Oncol Lett. 2017 Aug;14(2):1373-1378. doi: 10.3892/ol.2017.6331. Epub 2017 Jun 7.