In situ targeted gene expression analysis of Marjolin ulcers
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1055953 | ENA |
REPOSITORIES: ENA
Similar Datasets
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.
2024-07-21 | GSE251937 | GEO
Project description:Single-cell and In Situ Spatial Transcriptomics of Marjolin ulcers
| PRJNA1055946 | ENA
Project description:Circular RNA (circRNA) microarray analysis was performed to examine the expression profiles of circRNAs in diabetic foot ulcers (DFU) and in human excisional skin wounds 7 days after injury.
2019-10-01 | GSE114248 | GEO
Project description:We performed RNAseq on ulcers and distant normal tissue from biopsy-wounded wild-type and Bmp4-overexpressing (Vil1-Cre;Rosa26-Bmp4) mice to investigate differences in gene expression between tissue states and genotypes. Biopsy wounding was performed by taking three biopsies from well-separated areas in the colon wall using forceps. Small tissue pieces were excised from the ulcers and distant normal colon tissue and collected for RNA sequencing.
2021-05-09 | E-MTAB-10238 | biostudies-arrayexpress
Project description:In situ targeted gene expression analysis of healing skin on SD0 post-wounding in Wildtype and Rnasel knock out wounds
| PRJNA1167251 | ENA
Project description:Long-lasting Analgesia via Targeted in situ Repression of NaV1.7
| PRJNA670519 | ENA
Project description:Profiling RNA at chromatin targets in situ by antibody-targeted tagmentation.
| PRJNA801630 | ENA
Project description:Diabetic foot ulcers (DFUs) are a devastating complication of diabetes. In order to identify systemic and local factors associated with DFU healing, we examined the cellular landscape of DFUs by single-cell RNA-seq analysis of foot and forearm skin specimens, as well as PBMC samples, from 10 non-diabetic subjects, and 17 diabetic patients, 11 with, and 6 without DFU. Our analysis shows enrichment of a unique inflammatory fibroblast population in DFU patients with healing wounds. The patients with healing DFUs also depicted enrichment of macrophages with M1 polarization, as opposed to more M2 macrophages in non-healing wounds. These findings were verified using Immunohistochemistry and Spatial Transcriptomics.
2021-11-01 | GSE165816 | GEO
Project description:Single-cell transcriptomics of Marjolin ulcers
| PRJNA983741 | ENA
Project description:Chronic non-healing venous leg ulcers (VLUs) are a widespread debilitating disease with high morbidity and associated costs, as approximately $15 billion annually are spent on the care of VLUs. Despite their socioeconomic burden, there is a paucity of novel treatments targeted towards healing VLUs, which can be attributed to both lack of pathophysiologic insight into VLU development as well as lack of knowledge regarding biologic actions of VLU-targeted therapies. Currently, the bioengineered bilayered living cellular construct (BLCC) skin substitute is the only FDA-approved biologic treatment for healing VLUs. To elucidate the mechanisms through which the BLCC promotes healing of chronic VLUs, we conducted a clinical trial (NCT01327937) in which patients with non-healing VLUs were treated with either standard care (compression therapy) or with BLCC together with standard care. Tissue was collected from the VLU edge before and 1 week after treatment, and samples underwent comprehensive microarray, mRNA and protein analyses. Ulcers treated with BLCC skin substitute displayed three distinct patterns suggesting the mechanisms by which BLCC shifted a non-healing into a healing tissue response: it modulated inflammatory and growth factor signaling; it activated keratinocytes; and it attenuated Wnt/β-catenin signaling. In these ways, BLCC application orchestrated a shift of the chronic non-healing ulcer microenvironment into a distinctive healing milieu resembling that of an acute, healing wound. Our findings also provide first patient-derived in vivo evidence of specific biologic processes that can be targeted in the design of therapies to promote healing of chronic VLUs.
2016-09-01 | GSE84571 | GEO