Project description:There are two datasets:
1. scRNA-seq of human cutaneous immune cells from psoriasis patients. These include pre- and post-Tildrakizumab treated patients and come in a BAM file format.
19006FL-25-01
19006FL-38-01
19006FL-32-01-03
19006FL-33-01
19006FL-28-01-05
19006FL-35-01-01
2. RNA-seq of ZFP36L2 CRISPIR deleted Human T cells are FASTQ files.
19006XR-30-05
19006XR-30-04
19006XR-30-02
19006XR-30-01
19006XR-26-05
19006XR-26-04
19006XR-26-02
19006XR-26-01
19006R-22-04
19006R-22-08
19006R-22-05
19006R-22-01
Project description:MLS000408882-01 and MLS000573813-01 were identified through a cell based screen that measures the reactivation of an epigenetically silenced transgene. MLS000408882-01 and MLS000573813-01 shows selectivity for cancer vs. normal cells affecting both transcriptional patterns and cell viability in a cancer specific manner.
Project description:Abstract Background: YSCH-01, a recombinant L-IFN adenovirus injection, is an oncolytic virus- based anticancer drug with dual anti-tumor effects. In previous studies, we have confirmed the potential of YSCH-01 in the treatment of malignant gliomas. Additionally, YSCH-01 has emerged as a promising candidate for osteosarcoma treatment, exhibiting significant antitumor properties. However, its specific role in osteosarcoma and the underlying mechanisms remain poorly understood. Methods: We evaluated the infectivity and efficacy of YSCH-01 in osteosarcoma cells by collecting clinical samples of osteosarcoma and conducting experiments using osteosarcoma cell lines both in vitro and in vivo. Additionally, we studies the impact of YSCH-01 on interferon overexpression at the RNA and protein levels to highlight its potential antitumor properties. Furthermore, RNA-seq analysis of tumor samples treated with YSCH-01 provided valuable insights into the altered gene expression profiles and signaling pathways, helping to elucidate the molecular basis of its antitumor effects. Results: Our findings demonstrated the dose-dependent infectivity of YSCH-01 in osteosarcoma cells, with varying effects observed across different cell lines. Both in vitro and in vivo studies showed that YSCH-01 effectively inhibited osteosarcoma cell proliferation. In CDX and PDX animal models, YSCH-01 exhibited potent therapeutic effects, particularly in terms of its distant effects. Additionally, IFN-αsignaling pathway was activated in the tumor tissues with YSCH-01 treatment. Conclusions: The initial findings of this study revealed the complex molecular pathways through which YSCH-01 exerts its antitumor effects in osteosarcoma. By elucidating the correlation between key molecular markers in osteosarcoma and patient outcomes, we have identified potential therapeutic targets, presenting a promising avenue for osteosarcoma treatment. Keywords: Osteosarcoma; Oncolytic Virus; YSCH-01; L-IFN.