Deciphering mechanisms of brain metastasis in melanoma - the gist of the matter
Open accessAbstract
Metastasis to distant organs and particularly the brain still represents the most serious obstacle in melanoma therapies. Melanoma cells acquire a phenotype to metastasize to the brain and successfully grow there through complex mechanisms determined by microenvironmental than rather genetic cues. There do appear to be some prerequisites, including the presence of oncogenic BRAF or NRAS mutations and a loss of PTEN. Further mediators of the brain metastatic phenotype appear to be the high activation of the PI3K/AKT or STAT3 pathway or high levels of PLEKHA5 and MMP2 in metastatic cells. A yet undefined subset of brain metastases exhibit a high level of expression of CD271 that is associated with stemness, migration and survival. Hence, CD271 expression may determine specific properties of brain metastatic melanoma cells. Environmental cues - in particular those provided by brain parenchymal cells such as astrocytes - seem to help specifically guide melanoma cells that express CCR4 or CD271, potential "homing receptors". Upon entering the brain, these cells interact with brain parenchyma cells and are thereby reprogrammed to adopt a neurological phenotype. Several lines of evidence suggest that current therapies may have a negative effect by activating a program that drives tumor cells toward stemness and metastasis. Yet significant improvements have expanded the therapeutic options for treating brain metastases from melanoma, by combining potent BRAF inhibitors such as dabrafenib with checkpoint inhibitors or stereotactic surgery. Further progress toward developing new therapeutic strategies will require a more profound understanding of the mechanisms that underlie brain metastasis in melanoma.
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Cancer cells may enter the meninges via the choroid plexus, the brain, by crossing pial blood vessels or by vascular channels that connect the bone marrow and meninges.
“Cancer cells may enter the meninges via the choroid plexus, the brain, by crossing pial blood vessels or by vascular channels that connect the bone marrow and meninges”
From Living on the Edge of the CNS: Meninges Cell Diversity in Health and Disease (2021) · cites this paper as Redmer, 2018
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- Authors
- Redmer, T.
- Affiliations
- University of Veterinary Medicine Vienna (AT)
- Corresponding author
- Redmer, Torben
- ORCID
- Redmer, Torben
- Venue
- Molecular Cancer
- Published
- 2018-07-27
- Volume
- 17
- Issue
- 1
- Pages
- 106-106
- ISSN
- 1476-4598 (ISSN-L)
- PMC
- PMC6064184
- OpenAlex
- W2884489621
- Cited by
- 67
- References
- 170
- Citations by year
- 2026: 4 · 2025: 11 · 2024: 3 · 2023: 15 · 2022: 9 · 2021: 8 · 2020: 9 · 2019: 8
- FWCI
- 1.11
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Molecular Cancer (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft (RE 4210/1-1)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Brain Metastases and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- melanoma brain metastases, BRAF mutation, NRAS mutation, PTEN loss, PI3K/Akt signaling, STAT3 pathway, MMP-2, p75 neurotrophin receptor, CCR4, homing receptors, tumor microenvironment, astrocytes, cancer stemness, dabrafenib, immune checkpoint inhibitors, stereotactic surgery
- MeSH terms
- Antineoplastic Agents, Brain Neoplasms, Humans, Melanoma, Neoplastic Stem Cells, Gene Expression Regulation, Neoplastic, Cell Line, Tumor, Gene Regulatory Networks
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