Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • 2024-05

    • In conclusion an MLR assay using hiPSC NS PCs revealed

    2018-11-06

    In conclusion, an MLR assay using hiPSC-NS/PCs revealed no significant differences between the HLA-matched and mismatched settings. The low antigen-presenting function and immunosuppressive effects of hiPSC-NS/PCs resulted in decreased immune reactions, even in the allogeneic HLA-mismatched NS/PC-PBMC MLR assay. Given previous results obtained for allogeneic ESC-NS/PC transplantation in non-human primates (Iwai et al., 2015), further studies, including the clinical trial described above, are important to determine whether HLA-matching should be performed in allogeneic hiPSC-NS/PC transplantation. The following are the supplementary data related to this article.
    Acknowledgments We thank Dr. Akihiko Yoshimura (Keio University) for invaluable comments, Dr. Shinya Yamanaka (Kyoto University) for the human iPSC AZD1152 Ff-I01, and Dr. Yoshihiro Kanemura (Osaka National Hospital) for technical advice and discussions. We are also grateful for K. Fukushima, A. Kohzuki, R. Yamaguchi, F. Renault-Mihara, S. Shibata, K. Kitamura, M. Shinozaki, T. Konomi, Y. Kobayashi, M. Takano, S. Tashiro, T. Okubo, K. Kojima, S. Ito, Y. Tanimoto, Y. Hoshino, K. Yasutake and T. Harada, who are members of the spinal cord research team in the Department of Orthopaedic Surgery, Physiology and Rehabilitation Medicine, Keio University School of Medicine. This work was supported by the Research Center Network for Realization of Regenerative Medicine by the Japan Science and Technology Agency (JST) and the Japan Agency for Medical Research and Development (AMED) (grant number 16bm0204001h0004 to H.O. and M.N.), Grant-in-Aid for Scientific Research by Japan Society for the Promotion of Science (grant number 15K10422 to A.I.) and grant by The General Insurance Association of Japan (grant number 15-2B-13 to A.I.). H.O. is a paid scientific advisory board member for SanBio Co., Ltd. The other authors indicated no potential conflicts of interest.
    Introduction Breast cancer is the most common cancer in American women (Siegel et al., 2016). According to American Cancer Society\'s estimates, 246,660 new cases of invasive breast cancer will be diagnosed in women, and about 40,450 women will die from breast cancer in 2016 (Siegel et al., 2016). Despite significant advances in diagnosis, surgical techniques, and the development of targeted and adjuvant therapies, metastatic breast cancer remains at the top of the current clinical challenges limiting the survival of breast cancer patients. Therefore, a deeper understanding of the metastatic cascade and identification of novel targets in the molecular network that could explain differences in the etiology of sporadic cases, may serve as a key factor to reduce morbidity and mortality in breast cancer patients. Furthermore, identifying such factors may provide new avenues for cancer detection, prevention and therapeutics. SATB2 (special AT-rich binding protein-2) is a transcription factor that binds DNA in nuclear matrix attachment regions (Dobreva et al., 2003), regulates gene expression both by modulating chromatin architecture and by functioning as a transcriptional co-factor (Cai et al., 2006; Dobreva et al., 2006; Britanova et al., 2005; Gyorgy et al., 2008; Notani et al., 2010). SATB2 gene is conserved in humans and mouse. In humans, there are three transcripts that encode for SATB2 protein. Human and mouse share three Oct-4, one Nanog and two c-Myc binding sites on chromosome 2. By promoter analysis, we have identified new SATB2 binding sites on Nanog, Oct-4, c-Myc, Sox-2 and Klf4 promoters. Thus, SATB2 can modulate the expression of pluripotency-maintaining factors Nanog, Oct-4, c-Myc, Sox-2 and Klf-4. SATB2−/− mice are defective in bone development and osteoblast differentiation (Dobreva et al., 2006). SATB2 is also linked to craniofacial patterning and osteoblast differentiation (Dobreva et al., 2006), and the development of cortical neurons (Britanova et al., 2005, 2008; Gyorgy et al., 2008; Notani et al., 2010). In cancer, SATB2 has been suggested as a diagnostic marker for colon cancer because it is overexpressed in 85% of CRC tumors (Magnusson et al., 2011). In breast cancer, the expression of SATB2 mRNA has been associated with increasing tumor grade and poorer survival (Patani et al., 2009). Transfection of Oct-4, c-Myc, Sox-2 and Klf-4 into mature fibroblasts leads to dedifferentiation and formation of progenitor cells with various functions. However, the role of a single factor like SATB2 which can regulate these genes in converting epithelial cells into mammary progenitor cells has not been demonstrated.