Background: Skin cutaneous melanoma (SKCM) is one of the most malignant and aggressive cancers, causing about 72% of deaths in skin carcinoma. Although extensive study has explored the mechanism of recurrence and metastasis, the tumorigenesis of cutaneous melanoma remains unclear. Exploring the tumorigenesis mechanism may help identify prognostic biomarkers that could serve to guide cancer therapy. Method: Integrative bioinformatics analyses, including GEO database, TCGA database, DAVID, STRING, Metascape, GEPIA, cBioPortal, TRRUST, TIMER, TISIDB and DGIdb, were performed to unveil the hub genes participating in tumor progression and cancer-associated immunology of SKCM. Furthermore, immunohistochemistry (IHC) staining was performed to validate differential expression levels of hub genes between SKCM tissue and normal tissues from the First Affiliated Hospital of Soochow University cohort. Results: A total of 308 differentially expressed genes (DEGs) and 12 hub genes were found significantly differentially expressed between SKCM and normal skin tissues. Functional annotation indicated that inflammatory response, immune response was closely associated with SKCM tumorigenesis. KEGG pathways in hub genes include IL-10 signaling and chemokine receptors bind chemokine signaling. Five chemokines members (CXCL9, CXCL10, CXCL13, CCL4, CCL5) were associated with better overall survival and pathological stages. IHC results suggested that significantly elevated CXCL9, CXCL10, CXCL13, CCL4 and CCL5 proteins expressed in the SKCM than in the normal tissues. Moreover, our findings suggested that IRF7, RELA, NFKB1, IRF3 and IRF1 are key transcription factors for CCL4, CCL5, CXCL10. In addition, the expressions of CXCL9, CXCL10, CXCL13, CCL4 and CCL5 were positively correlated with infiltration of six immune cells (B cell, CD8 + T cells, CD4 + T cells, macrophages, neutrophils, dendritic cells) and 28 types of TILs. Among them, high levels of B cells, CD8 + T cells, neutrophils and dendritic cells were significantly related to longer SKCM survival time. Conclusion: In summary, this study mainly identified five chemokine members (CXCL9, CXCL10, CXCL13, CCL4, CCL5) associated with SKCM tumorigenesis, progression, prognosis and immune infiltrations, which might help us evaluate several immune-related targets for cutaneous melanoma therapy.

BackgroundPsoriasis is a chronic, prolonged, and recurrent skin inflammatory disease. However, the pathogenesis of psoriasis is not completely clear, thus we aimed to explore potential molecular basis of it.MethodsTwo datasets were downloaded from the Gene Expression Omnibus database. After identifying the differentially expressed genes of psoriasis skin lesion samples and healthy controls, three kinds of analyses, namely functional annotation, protein-protein interaction (PPI) network, and immune infiltration analyses, were performed.ResultsA total of 152 up-regulated genes and 38 down-regulated genes were selected for subsequent analyses. Evaluation of the PPI network identified the most important module containing 13 hub genes. Gene ontology analysis showed that the hub genes have a significant enrichment effect on positive regulation of cell migration, defense response to the other organism and epithelial cell differentiation. KEGG signaling pathway analysis showed that the hub genes were significantly enriched in chemokine signaling, Toll-like receptor signaling pathway, and IL-17 signaling pathway. Compared with the normal control sample, naive B cells, CD8+ T cells, activated memory CD4+ T cells, follicular helper T cells, gamma delta T cells, resting NK cells, monocytes, M0 macrophages, M1 macrophages, activated dendritic cells and neutrophils infiltrated more, while memory B cells, naive CD4+ T cells, regulatory T cells (Tregs), activated NK cells, resting mast cells, and eosinophils infiltrated less.ConclusionTo conclude, the hub genes and pathways identified from psoriasis lesions and normal controls along with the immune infiltration profile may provide new insights into the study of psoriasis.

Skin cutaneous melanoma (SKCM) is the deadliest cancer among commonly encountered skin malignant tumours due to its extreme aggressiveness and dissemination. 1 At present, SKCM is usually diagnosed in the late grades of metastatic tumours, which could drive patients to a poor response to the therapeutic strategies. 2 Therefore, we need to explore the potential biomarkers and therapeutic targets to improve the diagnosis and therapy of invasive melanoma. The malignant transformation of melanocytes is a multistep process. Melanocytes change their characteristics throughout the process, which enables them to proliferate and migrate. 2 Numerous methods such as assessing excised tumours, utilization of biomarkers and imaging techniques had been applied to detect and monitor

Background Melanoma has the highest mortality rate of all skin tumors, and metastases are the major cause of death from it. The molecular mechanism leading to melanoma metastasis is currently unclear. Methods With the goal of revealing the underlying mechanism, three data sets with accession numbers GSE8401, GSE46517 and GSE7956 were downloaded from the Gene Expression Omnibus (GEO) database. After identifying the differentially expressed gene (DEG) of primary melanoma and metastatic melanoma, three kinds of analyses were performed, namely functional annotation, protein-protein interaction (PPI) network and module construction, and co-expression and drug-gene interaction prediction analysis. Results A total of 41 up-regulated genes and 79 down-regulated genes was selected for subsequent analyses. Results of pathway enrichment analysis showed that extracellular matrix organization and proteoglycans in cancer are closely related to melanoma metastasis. In addition, seven pivotal genes were identified from PPI network, including CXCL8, THBS1, COL3A1, TIMP3, KIT, DCN, and IGFBP5, which have all been verified in the TCGA database and clinical specimens, but only CXCL8, THBS1 and KIT had significant differences in expression. Conclusions To conclude, CXCL8, THBS1 and KIT may be the hub genes in the metastasis of melanoma and thus may be regarded as therapeutic targets in the future.

Background：Skin cutaneous melanoma (SKCM) is one of the most malignant and aggressive cancers, causing about 72% of deaths in skin carcinoma. Although extensive study has explored the mechanism of recurrence and metastasis, the tumorigenesis of cutaneous melanoma remains unclear. Exploring the tumorigenesis mechanism may help identify prognostic biomarkers that could serve to guide cancer therapy. Methods：Integrative bioinformatics analyses, including GEO database, TCGA database, DAVID, STRING, Metascape, GEPIA, cBioPortal, TRRUST, TIMER, TISIDB and DGIdb, were performed to unveil the hub genes participating in tumor progression and cancer-associated immunology of SKCM. Furthermore, immunohistochemistry (IHC) staining was performed to validate differential expression levels of hub genes between SKCM tissue and normal tissues from the First Affiliated Hospital of Soochow University cohort. Results: A total of 308 differentially expressed genes (DEGs) and 12 hub genes were found significantly differentially expressed between SKCM and normal skin tissues. Functional annotation indicated that inflammatory response, immune response was closely associated with SKCM tumorigenesis. KEGG pathways in hub genes include IL-10 signaling and chemokine receptors bind chemokine signaling. Five chemokines members (CXCL9, CXCL10, CXCL13, CCL4, CCL5) were associated with better overall survival and pathological stages. IHC results suggested that significantly elevated CXCL9, CXCL10, CXCL13, CCL4 and CCL5 proteins expressed in the SKCM than in the normal tissues. Moreover, our findings suggested that IRF7, RELA, NFKB1, IRF3 and IRF1 are key transcription factors for CCL4, CCL5, CXCL10. In addition, the expressions of CXCL9, CXCL10, CXCL13, CCL4 and CCL5 were positively correlated with infiltration of six immune cells (B-cell, CD8+T cells, CD4+T cells, macrophages, neutrophils, dendritic cells) and 28 types of TILs. Among them, high levels of B cells, CD8+T cells, neutrophils and dendritic cells were significantly related to longer SKCM survival time. Conclusion: In summary, this study mainly identified five chemokine members (CXCL9, CXCL10, CXCL13, CCL4, CCL5) associated with SKCM tumorigenesis, progression, prognosis and immune infiltrations, which might help us evaluate several immune-related targets for cutaneous melanoma therapy.

BackgroundDecubitus ulcers are common skin injuries in plastic and burn surgery departments, usually occur in patients with a long disease course and poor underlying health. Designing a reconstruction procedure with safety blood supply to a large volume soft tissue and resulting in minimal trauma is a priority for surgeons.MethodsThe free-style perforators on the potential donor sites surrounding the ulcers were detected by Doppler, and the area of the ulcer was divided into several sections based on the location of pre-design perforator flaps. According to the insertion point of the perforators, small V-Y advancement flaps, propeller flaps and rotation flaps pedicled with freestyle perforators were formed and moderately modified during surgery. All of the small flaps were transplanted from donor sites to the defect and reassembled into a new composite flap to repair the ulcer. The donor sites were directly closed. The area of the flaps ranged from 7.0 × 10.5 cm to 8.0 × 22.0 cm and the diameter of the pedicle perforators ranged from 0.5 to 4.0 mm.ResultsIn 30 patients, 65 flaps were constructed, and all of the flaps survived with direct closure of all donor sites. One case with effusion healed 1 month postoperatively through draining and application of a mild pressure dressing. After a 3–24 months follow-up period, all of the patients were satisfied with post-operative function and appearance, and only one case had a local recurrence 6 months postoperatively.ConclusionThe jigsaw puzzle flap based on freestyle perforators can repair the large skin and soft tissue defects caused by decubitus ulcers on the buttocks, with direct donor flap area closure. This method is easy to perform with a safe blood supply and minimal trauma resulting from the avoidance of microvascular anastomosis and the conventional myocutaneous flap.

Background: Melanoma has the highest mortality rate of all skin tumors, and metastases are the major cause of death from it. The molecular mechanism leading to melanoma metastasis is currently unclear. Methods: With the goal of revealing the underlying mechanism, three data sets with accession numbers GSE8401, GSE46517 and GSE7956 were downloaded from the Gene Expression Omnibus (GEO) database. After identifying the differentially expressed gene (DEG) of primary melanoma and metastatic melanoma, three kinds of analyses were performed, namely functional annotation, protein‐protein interaction (PPI) network and module construction, and co-expression and drug-gene interaction prediction analysis. Results: A total of 41 up-regulated genes and 79 down-regulated genes was selected for subsequent analyses. Results of pathway enrichment analysis showed that extracellular matrix organization and proteoglycans in cancer are closely related to melanoma metastasis. In addition, seven pivotal genes were identified from PPI network, including CXCL8, THBS1, COL3A1, TIMP3, KIT, DCN, and IGFBP5, which have all been verified in the TCGA database and clinical specimens, but only CXCL8, THBS1 and KIT had significant differences in expression. Conclusions: To conclude, CXCL8, THBS1 and KIT may be the hub genes in the metastasis of melanoma and thus may be regarded as therapeutic targets in the future.

Background: Infantile hemangiomas (IH) and venous malformations (VM) are the most common types of vascular abnormalities that seriously affect the health of children. Although there is evidence that these two diseases share some common genetic changes, the underlying mechanisms need to be further studied.Methods: The microarray datasets of IH (GSE127487) and VM (GSE7190) were downloaded from GEO database. Extensive bioinformatics methods were used to investigate the common differentially expressed genes (DEGs) of IH and VM, and to estimate their Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Trough the constructing of protein-protein interaction (PPI) network, gene models and hub genes were obtained by using Cytoscape and STRING. Finally, we analyzed the co-expression and the TF-mRNA-microRNA regulatory network of hub genes.Results: A total of 144 common DEGs were identified between IH and VM. Functional analysis indicated their important role in cell growth, regulation of vasculature development and regulation of angiogenesis. Five hub genes (CTNNB1, IL6, CD34, IGF2, MAPK11) and two microRNA (has-miR-141-3p, has-miR-150-5p) were significantly differentially expressed between IH and normal control (p < 0.05).Conclusion: In conclusion, our study investigated the common DEGs and molecular mechanism in IH and VM. Identified hub genes and signaling pathways can regulate both diseases simultaneously. This study provides insight into the crosstalk of IH and VM and obtains several biomarkers relevant to the diagnosis and pathophysiology of vascular abnormalities.