Keio University · Medicine
Professor Tatsuyuki Chiyoda's research lab focuses on the molecular mechanisms underlying aggressive gynecological cancers, particularly ovarian and uterine carcinomas, with an emphasis on epithelial-mesenchymal transition (EMT), chromosomal instability, and tumor suppressor pathways. The lab integrates genomics, phosphoproteomics, and functional studies to identify actionable biomarkers and therapeutic targets in high-grade serous and other malignant ovarian tumors. A key focus is understanding how genetic alterations—such as in *BRCA1* or LATS1—reprogram cellular metabolism and signaling to drive tumorigenesis. The lab also investigates rare and aggressive tumors, such as vulvar epithelioid sarcoma, to improve early diagnosis and treatment outcomes.
Figures are computed from collected data and may differ slightly.
Uterine carcinosarcoma (CS) is usually classified as uterine endometrial carcinoma (EC). However, CS is more aggressive even compared with high grade EC. CS is also reported to undergo epithelial to mesenchymal transition (EMT). In this study, we compared the gene expression profiles of CS, EC, and uterine sarcoma (US) and evaluated the role of EMT and chromosomal aberrations in CS tumor formation. Frozen tissues of 46 patients (14 CS, 24 EC, and 8 US) were included. The similarity was examined
In the mitotic exit network of budding yeast, Dbf2 kinase phosphorylates and regulates Cdc14 phosphatase. In contrast, no phosphatase substrates of LATS1/WARTS kinase, the mammalian equivalent of Dbf2, has been reported. To address this discrepancy, we performed phosphoproteomic screening using LATS1 kinase. Screening identified MYPT1 (myosin phosphatase-targeting subunit 1) as a new substrate for LATS1. LATS1 directly and preferentially phosphorylated serine 445 (S445) of MYPT1. An MYPT1 mutant
Meta-analysis of RCTs and observational studies suggest that lymphadenectomy was associated with improved OS in advanced- and early-stage EOC. However, results from RCTs demonstrate that lymphadenectomy was not associated with improved OS in advanced- and early-stage EOC.
Precision medicine based on cancer genomics is being applied in clinical practice. However, patients do not always derive benefits from genomic testing. Here, we performed targeted amplicon exome sequencing-based panel tests, including 160 cancer-related genes (PleSSision-160), on 88 malignant ovarian tumors (high-grade serous carcinoma, 27; endometrioid carcinoma, 15; clear cell carcinoma, 30; mucinous carcinoma, 6; undifferentiated carcinoma, 4; and others, 6 (immature teratoma, 1; carcinosarc
Mutations in the breast cancer susceptibility gene 1 (<i>BRCA1</i>) are associated with an increased risk of developing epithelial ovarian cancer. However, beyond the role of BRCA1 in DNA repair, little is known about other mechanisms by which BRCA1 impairment promotes carcinogenesis. Given that altered metabolism is now recognized as important in the initiation and progression of cancer, we asked whether the loss of BRCA1 changes metabolism in the cells of origin of ovarian cancer. The findings
Epithelioid sarcoma of the vulva is an extremely rare and aggressive tumor. This tumor most commonly occurs on the labia majora in women of reproductive age. The molecular pathogenesis remains largely unknown. Only 20 cases of vulvar epithelioid sarcoma have been reported to date and more than half have had poor outcomes. We report a successfully treated case of vulvar epithelioid sarcoma in a 33-year-old woman. We performed a radical vulvectomy with flap reconstruction. Three years after surger
TFI from second-line chemotherapy may predict a survival benefit of third-line chemotherapy.
•Cervical cancer occurring in patients with OHVIRA syndrome is very rare.•This case reports on HPV-negative adenocarcinoma located in the nonvisible cervix.•Colposcopy and imaging are essential for cervical cancer with uterine malformation.•In OHVIRA syndrome, cervical malignancies may be overlooked.
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