Publications by authors named "T Yugawa"

Article Synopsis
  • * Ectopic expression of oncogenes MYC and PIK3CAE545K enhances growth in these cells but enables tumor initiation only after several cell passages, despite lower expression levels of HPV E6 and E7 in late-passaged cells.
  • * To achieve tumorigenicity, additional activation of the RAS-MEK pathway is necessary, indicating that while HPV16 and certain oncogenes play a role, multiple genetic events are needed for cervical neoplasia progression.
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Article Synopsis
  • - Infection by high-risk HPV types, particularly HPV16, significantly increases the risk of developing oral squamous cell carcinomas (OSCCs), but the exact process by which this occurs is not fully understood.
  • - The study found that the E6 protein from HPV16 suppresses key transporters (TAP1 and TAP2) responsible for moving viral peptides into immune cells, which contributes to immune evasion.
  • - Analysis of cancer data revealed that in HPV-positive OSCC samples, the expression of TAP genes was lower while certain signaling pathways (LTαβ and LTβR) were elevated, indicating a complex relationship between HPV expression and tumor immune response.
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The success rate of establishing human cancer cell lines is not satisfactory and the established cell lines often do not preserve the molecular and histological features of the original tissues. In this study, we developed a novel culture method which can support proliferation of almost all primary epithelial ovarian cancer cells, as well as primary normal human oviductal epithelial cells. Cancer cells from fresh or frozen specimens were enriched by the anti-EpCAM antibody-conjugated magnetic beads, plated on Matrigel-coated plate and cultivated under the optimized culture conditions.

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Oncogenic mutations of RAS genes, found in about 30% of human cancers, are considered to play important roles in cancer development. However, oncogenic RAS can also induce senescence in mouse and human normal fibroblasts. In some cell lines, oncogenic RAS has been reported to induce non-apoptotic programed cell death (PCD).

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The high-risk human papillomavirus E6 proteins have been shown to interact with and lead to degradation of PDZ-domain-containing proteins through its carboxy-terminal motif. This PDZ-binding motif plays important roles in transformation of cultured cells and carcinogenesis of E6-transgenic mice. However, its biological effects on the natural host cells have not been elucidated.

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