Publications by authors named "Yukiko Bono"

Circulating tumor cells (CTC) are newly discovered biomarkers of cancers. Although many systems detect CTC, a gold standard has not yet been established. We analyzed CTC in uterine cervical cancer patients using an advanced version of conditionally replicative adenovirus targeting telomerase-positive cells, which was enabled to infect coxsackievirus-adenovirus receptor-negative cells and to reduce false-positive signals in myeloid cells.

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Positron emission tomography (PET) with fluorodeoxyglucose F18 ( F-FDG) is useful for detecting malignancies, but benign lesions occasionally have false-positive F-FDG uptake. Here, we report the cases of five postmenopausal women with solid ovarian tumors suspected to be ovarian cancer on magnetic resonance imaging and F-FDG uptake. Mean age of the five patients was 57 years (range, 53-65 years).

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Article Synopsis
  • Tamoxifen is an anti-estrogen drug used to treat breast cancer, and its use in premenopausal women in Japan is increasing, prompting a study on its effects on ovarian function.
  • The study analyzed 11 women with high serum estradiol levels during tamoxifen therapy, focusing on their serum Follicular Stimulating Hormone (FSH) levels and follicular development.
  • Results showed that tamoxifen could stimulate ovarian function even after two years of treatment, with observed large follicles indicating potential adverse effects on the hormone regulation system.
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Dienogest (DNG) is a selective progesterone receptor (PR) agonist and oral administration of DNG is used for the treatment of endometriosis. DNG is considered to act on PR to down-regulate pathophysiological factors associated with endometriosis. PR exists as two major isoforms, PR-A and PR-B, and their physiological functions are mostly distinct.

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Objective: To investigate the impact of estrogen contained in oral contraceptives (OCs) on the action of progestin on ovarian endometrioma epithelial cells.

Design: Experimental in vitro study and immunohistochemical analysis.

Setting: University hospital.

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A small subset of cells with CD133 expression is thought to have increased chemoresistance and tumorigenicity, features of cancer stem cells (CSCs); the molecular mechanisms by which these properties arise remain unclear. We characterized CD133+ endometrial cancer cells based on microarray analyses of Ishikawa cells. Of the genes upregulated in CD133+ cells compared with CD133- cells, we noted several key factors involved in the aggressive behavior of cells, including ABCG2 and matrix metalloproteinase (MMP).

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The use of molecular target therapy has not been established for endometrial cancer. The present study investigated the potential therapeutic strategy of targeting CD117-positive cancer cells as a novel molecular target therapy. FACS-sorted CD117(+) cells isolated from endometrial cancer cell lines (Ishikawa or MFE280 cells) exhibited higher proliferative capacity in vitro and colony forming activity on soft agar, and decreased sensitivity to cisplatin, compared to CD117(-) cells.

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Article Synopsis
  • Progestin inhibits the growth of both normal and cancerous endometrial cells mainly through the progesterone receptor subtype PRB, rather than PRA.
  • *The study identified that the gene FOXO1 is up-regulated by progestin in a PRB-dependent way, and it acts as an upstream regulator of IGFBP-1, which is also induced by progestin.
  • *The findings suggest that the FOXO1/IGFBP-1 pathway is crucial for the growth-inhibitory effects of progestin in endometrial epithelial cells, highlighting potential therapeutic applications.*
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Purpose: Although the KRAS mutation is one of critical genetic alterations in endometrial carcinogenesis, the downstream targets are not known.

Experimental Design: In this study, we investigated the molecular targets of KRAS signals, using tumorigenic cells with oncogenic KRAS mutation established from telomerase reverse transcriptase (TERT)-immortalized endometrial epithelial cells.

Results: We first confirmed that the RAF-ERK pathway, but not the PI3K-Akt pathway, was activated in KRAS tumorigenic cells.

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