Promoter methylation as biomarkers for diagnosis of melanoma: A systematic review and meta‐analysis

Guo, Yu; Long, Junling; Lei, Shaorong

doi:10.1002/jcp.27495

Cited by 23 publications

(19 citation statements)

References 54 publications

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“…Hypermethylation has been associated to the silencing of genes and to decreased gene expression of tumour suppressors, whilst hypomethylation can potentially result in genomic instability and reactivation of oncogenes (Litovkin et al 2014(Litovkin et al , 2015Paska and Hudler 2015;Weisenberger 2014). Based on genome-wide studies, abnormal methylation patterns have been detected in melanoma patients, highlighting potential markers for disease progression and also providing an important strategy for tumour diagnosis and treatment (Fu et al 2017;Guo et al 2018;Koga et al 2009). Nevertheless, as the proteome represents a link between DNA and phenotype, proteins likely provide a more accurate depiction of the cell state.…”

Section: Linking Genes To Protein Expression and Functionmentioning

confidence: 99%

Clinical protein science in translational medicine targeting malignant melanoma

et al. 2019

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Melanoma of the skin is the sixth most common type of cancer in Europe and accounts for 3.4% of all diagnosed cancers. More alarming is the degree of recurrence that occurs with approximately 20% of patients lethally relapsing following treatment. Malignant melanoma is a highly aggressive skin cancer and metastases rapidly extend to the regional lymph nodes (stage 3) and to distal organs (stage 4). Targeted oncotherapy is one of the standard treatment for progressive stage 4 melanoma, and BRAF inhibitors (e.g. vemurafenib, dabrafenib) combined with MEK inhibitor (e.g. trametinib) can effectively counter BRAFV600E-mutated melanomas. Compared to conventional chemotherapy, targeted BRAFV600E inhibition achieves a significantly higher response rate. After a period of cancer control, however, most responsive patients develop resistance to the therapy and lethal progression. The many underlying factors potentially causing resistance to BRAF inhibitors have been extensively studied. Nevertheless, the remaining unsolved clinical questions necessitate alternative research approaches to address the molecular mechanisms underlying metastatic and treatment-resistant melanoma. In broader terms, proteomics can address clinical questions far beyond the reach of genomics, by measuring, i.e. the relative abundance of protein products, post-translational modifications (PTMs), protein localisation, turnover, protein interactions and protein function. More specifically, proteomic analysis of body fluids and tissues in a given medical and clinical setting can aid in the identification of cancer biomarkers and novel therapeutic targets. Achieving this goal requires the development of a robust and reproducible clinical proteomic platform that encompasses automated biobanking of patient samples, tissue sectioning and histological examination, efficient protein extraction, enzymatic digestion, mass spectrometry-based quantitative protein analysis by label-free or labelling technologies and/or enrichment of peptides with specific PTMs. By combining data from, e.g. phosphoproteomics and acetylomics, the protein expression profiles of different melanoma stages can provide a solid framework for understanding the biology and progression of the disease. When complemented by proteogenomics, customised protein sequence databases generated from patient-specific genomic and transcriptomic data aid in interpreting clinical proteomic biomarker data to provide a deeper and more comprehensive molecular characterisation of cellular

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Section: Linking Genes To Protein Expression and Functionmentioning

confidence: 99%

Clinical protein science in translational medicine targeting malignant melanoma

et al. 2019

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“…Due to the lack of direct genetic components in transcriptional reprogramming, studying the epigenetic factors that may promote cellular plasticity leading to increased invasion and metastasis is reasonable . Based on the Cancer Genome Atlas Network (TCGA), the well‐established mutational classifications of melanomas are not in agreement with gene expression patterns, which could explain not only the low response rate of therapies targeting the aforementioned mutations but also the concerns raised against the durability of such interventions .…”

Section: Introductionmentioning

confidence: 99%

DNA hypermethylation is associated with invasive phenotype of malignant melanoma

Koroknai

Szász

Hernández-Vargas

et al. 2019

Experimental Dermatology

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Tumor cell invasion is one of the key processes during cancer progression, leading to life-threatening metastatic lesions in melanoma. As methylation of cancer-related genes plays a fundamental role during tumorigenesis and may lead to cellular plasticity which promotes invasion, our aim was to identify novel epigenetic markers on selected invasive melanoma cells. Using Illumina BeadChip assays and Affymetrix Human Gene 1.0 microarrays, we explored the DNA methylation landscape of selected invasive melanoma cells and examined the impact of DNA methylation on gene expression patterns. Our data revealed predominantly hypermethylated genes in the invasive cells affecting the neural crest differentiation pathway and regulation of the actin cytoskeleton. Integrative analysis of the methylation and gene expression profiles resulted in a cohort of hypermethylated genes (IL12RB2, LYPD6B, CHL1, SLC9A3, BAALC, FAM213A, SORCS1, GPR158, FBN1 and ADORA2B) with decreased expression. On the other hand, hypermethylation in the gene body of the EGFR and RBP4 genes was positively correlated with overexpression of the genes. We identified several methylation changes that can have role during melanoma progression, including hypermethylation of the promoter regions of the ARHGAP22 and NAV2 genes that are commonly altered in locally invasive primary melanomas as well as during metastasis. Interestingly, the down-regulation of the methylcytosine dioxygenase TET2 gene, which regulates DNA methylation, was associated with hypermethylated promoter region of the gene. This can probably lead to the observed global hypermethylation pattern of invasive cells and might be one of the key changes during the development of malignant melanoma cells. K E Y W O R D S cell invasion, DNA methylation, gene body, malignant melanoma, TET2

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“…A systematic review and meta-analysis by Guo et al found up to 50 genes, associated with risk of melanoma, in the context of promoter methylation. 6 Moreover, hypomethylation-mediated inactivation of CLDN11 is reported in melanoma. Hypermethylation of tumor-related genes such as RASSF1A, 47 APC, 48 DAPK 49 HOXB13, 50 MGMT, 18 WIF1, 51 RARB, 19 INK4A, 52 SYK, 53 TFPI2 41 and SOCS1 54 are found to be associated with advanced melanoma and poor prognosis.…”

Section: Dna Methylation In Melanomamentioning

confidence: 99%

“…3 Skin cancers are one of the most prevalent groups of cancersthe two broad groups being melanoma and non-melanoma cancers. [4][5][6] Melanoma is the 19 th most commonly occurring cancer in men and women, with about 300,000 new cases reported in 2018. 7 Although melanoma accounts for a smaller percentage of all skin cancers when compared to nonmelanoma cancers, it is the cause for most skin cancer-related deaths.…”

Section: Introductionmentioning

confidence: 99%

Malignant melanoma: Underlying epigenetic mechanisms

Sabit¹,

Kaliyadan²,

Menezes³

2020

Indian J Dermatol Venereol Leprol

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Although malignant melanoma is not the most common type of skin cancer, it is the most aggressive and fatal type as it can spread out and metastasize progressively. Early diagnosis and interventions lead to improved patient survival. The incidence rate of melanoma is dramatically increasing, with a few newer therapeutic options available. Therefore, establishing a reliable genetic or epigenetic-based diagnostic and prognostic tool is really important. In this review, we highlight the underlying epigenetic mechanisms involved in melanoma. Furthermore, the epigenetic-based therapeutic options will be also discussed. One of the key areas of discussion will be microRNA which is a small, single-stranded RNA molecule that serves as a regulatory element and found to regulate nearly a third of human genes. MicroRNAs play a role in a wide range of diseases including cancer. In malignant cells, it regulates cell proliferation, invasion, and metastasis.

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Promoter methylation as biomarkers for diagnosis of melanoma: A systematic review and meta‐analysis

Cited by 23 publications

References 54 publications

Clinical protein science in translational medicine targeting malignant melanoma

Clinical protein science in translational medicine targeting malignant melanoma

DNA hypermethylation is associated with invasive phenotype of malignant melanoma

Malignant melanoma: Underlying epigenetic mechanisms

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