Advanced Research in Melanoma Metastasis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (30 June 2026) | Viewed by 584

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Guest Editor
HUN-REN-DE Public Health Research Group, Department of Public Health and Epidemiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary
Interests: melanoma; metastasis; cell invasion

Special Issue Information

Dear Colleagues,

Metastatic disease remains the leading cause of mortality in melanoma patients. The mechanisms of melanoma progression, invasion, and metastasis formation have been the focus of extensive studies for decades, as melanoma has been observed as having one of the highest metastatic potentials among human cancers. The metastasis formation of primary tumors is a balance of cellular interactions between the host (‘soil’) and the tumor (‘seed’), characterized by altered crosstalk between cells, a mechanism determined by both the intrinsic properties of the tumor cells and the host response. According to the ‘seed and soil’ hypothesis, the primary tumor contributes to the preparation of secondary sites for tumor cell invasion and development, known as the pre-metastatic niche (PMN). The distribution of the targeted organ is especially variable depending on the type of cancer; however, melanoma has the unique property of having a fully comprehensive metastatic potential; hence, any organ or tissue can host melanoma metastasis. The site of distant metastasis is an important and independent predictor of the survival of melanoma patients with metastatic disease.

This Special Issue focuses on experimental insights into melanoma progression, invasion, and metastasis formation, with particular attention to tumor–host interactions, the pre-metastatic niche, and organ-specific metastatic patterns. We welcome laboratory medicine and experimental studies that advance the mechanistic understanding of melanoma dissemination and may reveal new therapeutic targets. Purely clinical studies will not be considered.

Dr. Viktória Koroknai
Guest Editor

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Keywords

  • melanoma
  • metastasis
  • tumor–host interactions
  • pre-metastatic niche
  • tumor microenvironment
  • organ-specific metastasis
  • molecular mechanisms
  • therapeutic targets

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Published Papers (1 paper)

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21 pages, 2785 KB  
Article
Role of Organ-Specific Endothelial Cells in Melanoma Adhesion Patterns
by Marwa Hamdan, István Szász, Tünde Várvölgyi, Margit Balázs and Viktória Koroknai
Biomedicines 2026, 14(7), 1409; https://doi.org/10.3390/biomedicines14071409 - 23 Jun 2026
Viewed by 310
Abstract
Background: The metastatic dissemination of melanoma involves adhesion of circulating tumor cells within organ-specific vascular beds; however, the relative contribution of the endothelial environment versus that of the melanoma-intrinsic molecular state remains unclear. Materials and Methods: We quantified the in vitro [...] Read more.
Background: The metastatic dissemination of melanoma involves adhesion of circulating tumor cells within organ-specific vascular beds; however, the relative contribution of the endothelial environment versus that of the melanoma-intrinsic molecular state remains unclear. Materials and Methods: We quantified the in vitro adhesion of primary (n = 5) and metastatic (n = 3) melanoma cell lines to human hepatic, brain, and pulmonary endothelial cells under co-culture conditions, and we profiled the expression of 86 adhesion- and extracellular-matrix-related genes in melanoma and endothelial cells. Results: Adhesion was highest for the hepatic endothelium, intermediate for the pulmonary endothelium, and lowest for the brain endothelium. This endothelial preference was conserved in both primary and metastatic melanoma cells, though metastatic cells exhibited higher absolute adhesion. The linear mixed-effect models revealed that the effects of adhesion state on melanoma gene expression were modest and varied by endothelial type, whereas melanoma origin had more widespread and larger effects (mean absolute standardized coefficients of 0.32–0.47 versus 0.60–0.87, respectively). The expression of three genes (SPP1, ITGA11, and MMP2) was associated with melanoma origin in all endothelial types. Spearman’s co-expression analysis revealed endothelial-type-specific gene networks, and within-sample permutation confirmed the non-random coordination in all three endothelial types. Conclusions: Our findings support a model in which endothelial organ specificity contributes to melanoma cell adhesion behavior and associated transcriptional patterns, highlighting the importance of the vascular interface as a biologically active mediator of early metastatic cell–endothelium interactions. Full article
(This article belongs to the Special Issue Advanced Research in Melanoma Metastasis)
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