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PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours

  • Authors:
    • Zixuan Zhang
    • Mengzhao Wang
  • View Affiliations / Copyright

    Affiliations: Division of Respiratory Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, P.R. China
    Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1373-1378
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    Published online on: June 7, 2017
       https://doi.org/10.3892/ol.2017.6331
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Abstract

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.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang Z and Wang M: PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours. Oncol Lett 14: 1373-1378, 2017.
APA
Zhang, Z., & Wang, M. (2017). PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours. Oncology Letters, 14, 1373-1378. https://doi.org/10.3892/ol.2017.6331
MLA
Zhang, Z., Wang, M."PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours". Oncology Letters 14.2 (2017): 1373-1378.
Chicago
Zhang, Z., Wang, M."PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours". Oncology Letters 14, no. 2 (2017): 1373-1378. https://doi.org/10.3892/ol.2017.6331
Copy and paste a formatted citation
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Spandidos Publications style
Zhang Z and Wang M: PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours. Oncol Lett 14: 1373-1378, 2017.
APA
Zhang, Z., & Wang, M. (2017). PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours. Oncology Letters, 14, 1373-1378. https://doi.org/10.3892/ol.2017.6331
MLA
Zhang, Z., Wang, M."PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours". Oncology Letters 14.2 (2017): 1373-1378.
Chicago
Zhang, Z., Wang, M."PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours". Oncology Letters 14, no. 2 (2017): 1373-1378. https://doi.org/10.3892/ol.2017.6331
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