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LONG-TERM EVALUATION OF THE SAFETY AND EFFECTIVENESS OF NEURAL STEM CELL TRANSPLANTATION FOR CHRONIC THORACIC SPINAL CORD INJURY Harmin; Maharani, Hanisa Aulia
Journal of Stem Cell Research and Tissue Engineering Vol. 9 No. 1 (2025): JOURNAL OF STEM CELL RESEARCH AND TISSUE ENGINEERING
Publisher : Stem Cell Research and Development Center, Universitas Airlangga

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20473/jscrte.v9i1.73556

Abstract

Spinal cord injury (SCI) is a debilitating neurological condition that leads to partial or complete loss of motor and sensory function, depending on the injury’s severity and location. Conventional therapies focus on surgical stabilization, prevention of secondary damage, and rehabilitation. However, these approaches often fall short in restoring long-term functionality. In recent years, cell-based therapies have emerged as promising alternatives, particularly those involving neural stem cells (NSCs). This literature review explores the long-term safety and effectiveness of NSC transplantation for chronic thoracic SCI, based on studies published between 2010 and 2025. Research shows that fetal-derived NSCs, such as HuCNS-SC, demonstrate a high safety profile and low risk of tumor formation due to their committed neural lineage. Clinical trials report early signs of motor improvement and reduced spasticity in chronic SCI patients following transplantation. Additionally, mesenchymal stem cells (MSCs) have shown the ability to migrate to injury sites and exert therapeutic effects, though these benefits tend to be short-lived. The post-injury inflammatory microenvironment poses a significant barrier to the success of NSC therapies by impairing stem cell differentiation and survival. Therefore, immunosuppressive regimens are often employed to enhance NSC efficacy by creating a more supportive environment. Overall, while both NSCs and MSCs offer promising avenues for SCI treatment, long-term recovery likely requires multimodal approaches that address both neural regeneration and immune modulation. Continued research is essential to optimize these therapies and translate them into effective clinical treatments for patients with chronic SCI.
DECODING YAP-DRIVEN MALIGNANT REPROGRAMMING IN ORAL EPITHELIAL STEM CELLS THROUGH SINGLE-CELL ANALYSIS Putri, Indah Salsabila Febriana; Harmin; Maharani, Hanisa Aulia
Journal of Stem Cell Research and Tissue Engineering Vol. 9 No. 1 (2025): JOURNAL OF STEM CELL RESEARCH AND TISSUE ENGINEERING
Publisher : Stem Cell Research and Development Center, Universitas Airlangga

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20473/jscrte.v9i1.73558

Abstract

Oral squamous cell carcinoma (OSCC), a major subtype of head and neck squamous cell carcinoma (HNSC), is characterized by high mortality rates and cellular heterogeneity that complicates early detection and treatment. Recent advances in cancer biology suggest that tumorigenesis involves reprogramming of epithelial progenitor cells into cancer stem-like cells (CSCs), driven by oncogenic signaling such as Yes-associated protein (YAP) activation. YAP, a key effector of the Hippo pathway, regulates transcriptional programs involved in cell proliferation, dedifferentiation, and inhibition of differentiation. However, the specific mechanisms by which YAP reprograms oral epithelial stem cells remain incompletely understood. This literature review systematically explores findings from studies published between 2020 and 2025 that investigate the role of YAP in malignant reprogramming, particularly through single-cell analysis approaches. Articles were sourced from PubMed and Google Scholar using defined inclusion criteria, focusing on original studies involving in vitro, in vivo, or bioinformatic models. The review highlights that YAP activation in oral epithelial cells induces stemness-associated genes (e.g., SOX2, NANOG, OCT4), represses differentiation pathways (Notch, p63), and promotes epithelial-mesenchymal transition (EMT) markers (ZEB1, SNAI2, VIM). Single-cell RNA sequencing (scRNA-seq) has revealed dynamic and hybrid cell states, supporting the view that YAP-driven transformation is gradual and reversible. YAP also shapes the tumor microenvironment by inducing cytokines that recruit tumor-supportive immune and stromal cells. Key YAP-regulated targets such as CTGF, AXL, and ITGA6 emerge as potential therapeutic entry points, as their inhibition reduces proliferation and stemness. These findings underscore YAP’s central role in oral carcinogenesis and its promise as a molecular target for early intervention and therapy.