Melanoma Microbiome
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR658019.fastq.gz | Fastqsanger.gz | |||
| ERR658020.fastq.gz | Fastqsanger.gz | |||
| ERR658021.fastq.gz | Fastqsanger.gz | |||
| ERR658022.fastq.gz | Fastqsanger.gz | |||
| ERR658023.fastq.gz | Fastqsanger.gz |
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Project description:Despite malignant cutaneous melanoma is relatively rare compared to other skin cancers, it is still responsible for 80% of all skin cancer-related deaths. To identify molecular signatures of melanoma progression, excisional biopsies from 18 common melanocytic nevi (CMN), 8 primary radial growth phase melanomas (RGPM), 15 primary vertical growth phase melanomas (VGPM) and 5 melanoma metastases (MTS) were profiled using whole genome oligo-microarrays. Differentially expressed genes for each progression step were identified, and validation of selected transcripts by qRT-PCR was performed on an independent cohort of fixed samples. The comparison between CMN and RGPM showed an enrichment of Gene Ontology (GO) terms related to inter and intra-cellular junctions, whereas the transition from RGPM to VGPM was characterized by the deregulation of WNT3, MAPK and AKT pathways. In this step, enrichment analysis underlined the alteration of biological processes linked to apoptosis. Upregulation of genes involved into DNA double-strand breaks repair and downregulation of cellular adhesion genes were observed in MTS respect to VGPM. Futhermore, the gene expression profiles of 11 dysplastic nevi (DN) were compared to all the others. Some genes controlling proliferation were found more expressed than in CMN. Overall, DN displayed an heterogeneous behaviour, with relevant oncogenes, such as MYC and BCL6, less expressed than in RGPM, and a modulation pattern similar to VGPM for a subset of gene families, such as mismatch repair. This suggests that DN is not an intermediate step within melanoma progression, but a separate entity with an independent risk of progression to melanoma Keywords: Melanoma progression, gene expression profiling, qPCR
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Project description:Recent studies revealed trajectories of mutational events in early melanomagenesis, but the accompanying changes in gene expression are far less understood. Therefore, we performed a comprehensive RNA-Seq analysis of laser-microdissected melanocytic nevi (n=23) and primary melanoma samples (n=57) and characterized the molecular mechanisms of early melanoma development. Using self-organizing maps, unsupervised clustering and analysis of pseudotime (PT) dynamics to identify evolutionary trajectories, we describe here two transcriptomic types of melanocytic nevi (N1 and N2) and primary melanomas (M1 and M2). N1/M1 lesions are characterized by pigmentation-type and MITF gene signatures, and a high prevalence of NRAS mutations in M1 melanomas. N2/M2 lesions are characterized by inflammatory-type and AXL gene signatures with an equal distribution of wild type and mutated BRAF and low prevalence of NRAS mutations in M2 melanomas. Interestingly, N1 nevi and M1 melanomas and N2 nevi and M2 melanomas, respectively, cluster together, but there is no clustering in a stage-dependent manner. Transcriptional signatures of M1 melanomas harbour signatures of BRAF/MEK inhibitor resistance and M2 melanomas harbour signatures of anti-PD-1 antibody treatment resistance. Transcriptomic signatures suggest that the epigenetic regulators SMARCA2 and SMARCA4 are differentially involved in the epigenetic programming of the two melanoma types. Pseudotime dynamics of nevus and melanoma samples reflect a switch-like immune-escape mechanism in melanoma development with downregulation of immune genes paralleled by an increasing expression of a cell cycle signature in late-stage melanomas. Taken together, the transcriptome analysis identifies gene signatures and mechanisms underlying development of melanoma in early and late stages with relevance for diagnostics and therapy.
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