Project description:Marjolin's ulcer is a a rare and aggressive cutaneous malignancy that can arise on previously injured skin, established scars, and chronic non-healing wounds. It is most often found in burn scars, but it can also occur in other types of wounds, including venous stasis ulcers, pressure sores, and vaccination sites. The most common histological type of Marjolin’s ulcers is squamous cell carcinoma, however basal cell carcinomas, malignant melanomas, and sarcomas have also been reported. All parts of the body could potentially be affected yet the lower extremities are the anatomic sites most commonly involved. While SCCs commonly have a metastasis rate of 0.5 to 3.0 percent, those arising from burn scars metastasize at a rate in excess of 30 percent. The 5-year survival after a diagnosis of Marjolin’s ulcer was found to be 50 percent. The transformation to a malignancy can occur either chronically, over a period of more than 35 years, or occasionally within a year of the original injury. The exact mechanism of this transformation is not fully understood, but it is thought to be related to chronic keratinocyte dysfunction during the healing process of severe burn wounds. Surgical excision is the main treatment for Marjolin's ulcer and provides the best chance of survival. In a previous study, we investigated the bulk transcriptional changes that lead to Marjolin's ulcer by comparing global gene expression changes between squamous cells present in a squamous cell carcinoma versus those present within Marjolin's ulcer (MU) (Sinha et. al. JBCR 2017). This imparted novel insights into mechanisms underlying divergent clinical features of these cutaneous cancers. The goal of our current study is to characterize a new case of Marjolin's ulcer in a patient under our care by analyzing the cell types, their frequencies, and their individual transcriptional responses within a burn scar versus within Marjolin's ulcer. To achieve this, we conducted single-cell RNA sequencing on two excised tissues: 1. a sample from the center of the tumor (tumor core), and 2. another sample from the margin of tumor-free scar tissue.

Project description:To analyze the gene expression of human gastric epithelial cells (GES-1) regulated by paeonifl or in based on transcript tome sequencing; to identify and analyze key genes; to study the mechanism of paeoniflorin on Leuk-1cells; and to explore its medicinal value. Method: Different doses of Ulcer-healing Decoction were used to treat GES-1, and its activity was assessed by MTT assay. Transcriptome sequencing analysis was then performed to identify differentially expressed genes (DEGs). The function and pathways of the DEGs were annotated using GO and KEGG enrichment analysis. Result: The survival rate of GES-1 cells was significantly increased under different concentrations of ulcer-healing decoction intervention (P < 0.05 or P < 0.01). After 24 hours of treatment with 80 µ g/mL ulcer-healing decoction, a total of 312 crucial DEGs were observed in GES-1 cells, of which 233 DEGs were upregulated and 79 DEGs were downregulated. The top five differentially expressed genes include CYP1A1, IL24, IKBKGP1, GDF15, SCUBE1 and OASL, ADAMTS5, SULF1, ID2, and DDX60. The functions of these genes are mainly related to promoting wound,cell proliferation and migration,immunity and inflammation.GO enrichment analysis showed that the DEGs were significantly enriched in the extracellular region and involved in biological processes such as cytokine production and response, stimulus response, and exerting molecular functions such as proliferation factor receptor activity. KEGG pathway enrichment showed that the DEGs were significantly enriched in various signaling pathways. Immunohistochemistry and other methods were used to detect differentially expressed proteins in GES-1 cells induced by ulcer-healing decoction, and the results were consistent with those from RNA-seq, thereby validating the accuracy of sequencing technologies. Conclusion: The role of ulcer-healing decoction in GES-1 is primarily reflected in regulating inflammatory factors and growth factors, promoting cell proliferation, and supporting the regeneration and repair of gastric mucosal epithelial cells.

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RNA-seq strategy to study Mycobacterium ulcerans adaptation within our original mouse model of spontaneous healing.

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