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Genetic analysis and phosphoinositide 3‑kinase/protein kinase B signaling pathway status in ovarian endometrioid borderline tumor samples

  • Authors:
    • Kohei Nakamura
    • Kentaro Nakayama
    • Masako Ishikawa
    • Toshiko Minamoto
    • Tomoka Ishibashi
    • Emi Sato
    • Kaori Sanuki
    • Hitomi Yamashita
    • Ruriko Ono
    • Kouji Iida
    • Razia Sultana
    • Mohammad Mahmud Hossain
    • Noriyoshi Ishikawa
    • Satoru Kyo
  • View Affiliations / Copyright

    Affiliations: Department of Obstetrics and Gynecology, Shimane University School of Medicine, Izumo, Shimane 693‑8501, Japan, Department of Organ Pathology, Shimane University School of Medicine, Izumo, Shimane 693‑8501, Japan
    Copyright: © Nakamura et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 189-194
    |
    Published online on: May 3, 2018
       https://doi.org/10.3892/ol.2018.8626
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Abstract

Ovarian endometrioid borderline tumors (EBTs) are extremely rare, and are thought to be precursors of endometrioid carcinoma, beginning as adenofibroma or endometriosis and progressing in a slow, stepwise manner. In endometrioid carcinomas, a high frequency of activating mutations in phosphatase and tensin homolog (PTEN), β‑catenin or AT‑rich interaction domain 1A (ARID1A) genes, and the activation of the phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling pathway have been observed. However, the frequency of these alterations in EBTs and how they contribute to tumor progression remain unclear. To the best of our knowledge, this is the first study to assess the status of the PI3K/AKT signaling pathway in EBTs, in association with PTEN and ARID1A mutations. PTEN mutations were observed in EBTs and also in the area of endometriosis without atypia. However, the PI3K/AKT signaling pathway was revealed to be activated only in EBTs. The observations of the present study suggest that the PTEN mutation represents an early event in EBT tumorigenesis, while additional genetic alterations may be necessary to activate the PI3K/AKT signaling pathway and induce the development of the invasive carcinoma.
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Copy and paste a formatted citation
Spandidos Publications style
Nakamura K, Nakayama K, Ishikawa M, Minamoto T, Ishibashi T, Sato E, Sanuki K, Yamashita H, Ono R, Iida K, Iida K, et al: Genetic analysis and phosphoinositide 3‑kinase/protein kinase B signaling pathway status in ovarian endometrioid borderline tumor samples. Oncol Lett 16: 189-194, 2018.
APA
Nakamura, K., Nakayama, K., Ishikawa, M., Minamoto, T., Ishibashi, T., Sato, E. ... Kyo, S. (2018). Genetic analysis and phosphoinositide 3‑kinase/protein kinase B signaling pathway status in ovarian endometrioid borderline tumor samples. Oncology Letters, 16, 189-194. https://doi.org/10.3892/ol.2018.8626
MLA
Nakamura, K., Nakayama, K., Ishikawa, M., Minamoto, T., Ishibashi, T., Sato, E., Sanuki, K., Yamashita, H., Ono, R., Iida, K., Sultana, R., Hossain, M. M., Ishikawa, N., Kyo, S."Genetic analysis and phosphoinositide 3‑kinase/protein kinase B signaling pathway status in ovarian endometrioid borderline tumor samples". Oncology Letters 16.1 (2018): 189-194.
Chicago
Nakamura, K., Nakayama, K., Ishikawa, M., Minamoto, T., Ishibashi, T., Sato, E., Sanuki, K., Yamashita, H., Ono, R., Iida, K., Sultana, R., Hossain, M. M., Ishikawa, N., Kyo, S."Genetic analysis and phosphoinositide 3‑kinase/protein kinase B signaling pathway status in ovarian endometrioid borderline tumor samples". Oncology Letters 16, no. 1 (2018): 189-194. https://doi.org/10.3892/ol.2018.8626
Copy and paste a formatted citation
x
Spandidos Publications style
Nakamura K, Nakayama K, Ishikawa M, Minamoto T, Ishibashi T, Sato E, Sanuki K, Yamashita H, Ono R, Iida K, Iida K, et al: Genetic analysis and phosphoinositide 3‑kinase/protein kinase B signaling pathway status in ovarian endometrioid borderline tumor samples. Oncol Lett 16: 189-194, 2018.
APA
Nakamura, K., Nakayama, K., Ishikawa, M., Minamoto, T., Ishibashi, T., Sato, E. ... Kyo, S. (2018). Genetic analysis and phosphoinositide 3‑kinase/protein kinase B signaling pathway status in ovarian endometrioid borderline tumor samples. Oncology Letters, 16, 189-194. https://doi.org/10.3892/ol.2018.8626
MLA
Nakamura, K., Nakayama, K., Ishikawa, M., Minamoto, T., Ishibashi, T., Sato, E., Sanuki, K., Yamashita, H., Ono, R., Iida, K., Sultana, R., Hossain, M. M., Ishikawa, N., Kyo, S."Genetic analysis and phosphoinositide 3‑kinase/protein kinase B signaling pathway status in ovarian endometrioid borderline tumor samples". Oncology Letters 16.1 (2018): 189-194.
Chicago
Nakamura, K., Nakayama, K., Ishikawa, M., Minamoto, T., Ishibashi, T., Sato, E., Sanuki, K., Yamashita, H., Ono, R., Iida, K., Sultana, R., Hossain, M. M., Ishikawa, N., Kyo, S."Genetic analysis and phosphoinositide 3‑kinase/protein kinase B signaling pathway status in ovarian endometrioid borderline tumor samples". Oncology Letters 16, no. 1 (2018): 189-194. https://doi.org/10.3892/ol.2018.8626
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