Papel de las quimiocinas en la progresión del melanoma

Monteagudo, Carlos; Pellín-Carcelén, Ana; Martín, J.M.; Ramos, David

doi:10.1016/j.ad.2011.03.004

Cited by 11 publications

(8 citation statements)

References 58 publications

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“…This observation corroborates what other studies have shown—that disseminated melanoma cells can be directed to and/or selectively retained within the brain by external cues originating in the parenchymal milieu, such as chemokines or brain-derived ligands. Chemokine stimulation of their respective receptors is known to induce cellular responses of altered adhesion, migration, proliferation, and apoptosis [ 15 ]. Brain-derived signals promote melanoma cell adhesion to the intracranial vasculature and concomitantly foster melanoma metastases formation, which is the “seed and soil” hypothesis of cancer cell metastasis originally proposed by Paget in 1889 [ 16 ].…”

Section: Mechanisms Of Melanoma Brain Metastasismentioning

confidence: 99%

Melanoma Brain Metastasis: Mechanisms, Models, and Medicine

Kircher

Silvis

Cho

et al. 2016

IJMS

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The development of brain metastases in patients with advanced stage melanoma is common, but the molecular mechanisms responsible for their development are poorly understood. Melanoma brain metastases cause significant morbidity and mortality and confer a poor prognosis; traditional therapies including whole brain radiation, stereotactic radiotherapy, or chemotherapy yield only modest increases in overall survival (OS) for these patients. While recently approved therapies have significantly improved OS in melanoma patients, only a small number of studies have investigated their efficacy in patients with brain metastases. Preliminary data suggest that some responses have been observed in intracranial lesions, which has sparked new clinical trials designed to evaluate the efficacy in melanoma patients with brain metastases. Simultaneously, recent advances in our understanding of the mechanisms of melanoma cell dissemination to the brain have revealed novel and potentially therapeutic targets. In this review, we provide an overview of newly discovered mechanisms of melanoma spread to the brain, discuss preclinical models that are being used to further our understanding of this deadly disease and provide an update of the current clinical trials for melanoma patients with brain metastases.

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Section: Mechanisms Of Melanoma Brain Metastasismentioning

confidence: 99%

Melanoma Brain Metastasis: Mechanisms, Models, and Medicine

Kircher

Silvis

Cho

et al. 2016

IJMS

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“…Genes with the most markedly increased expression included CXCL2, CXCL3, and IL-8. All of these genes, as well as the more moderately increased CXCL1, have been shown to be important both in neutrophil chemotaxis and in melanoma growth [15, 16]. Increased expression of PTGS2 (cyclo-oxygenase-2 (COX-2)) is reminiscent of the situation in nonmelanoma skin cancer.…”

Section: Resultsmentioning

confidence: 99%

“…This makes these molecules potentially valuable therapeutic targets in prevention and treatment of melanoma [8, 15, 16, 21]. For example, COX-2 inhibitors have been shown to be cytotoxic and cytostatic for human melanoma cells in vitro and to have potentially beneficial effects in melanoma therapy [44, 45].…”

Section: Discussionmentioning

confidence: 99%

Ultraviolet Radiation and the Slug Transcription Factor Induce Proinflammatory and Immunomodulatory Mediator Expression in Melanocytes

Shirley

Grimm²,

Kusewitt

2012

Journal of Skin Cancer

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Despite extensive investigation, the precise contribution of the ultraviolet radiation (UVR) component of sunlight to melanoma etiology remains unclear. UVR induces keratinocytes to secrete proinflammatory and immunomodulatory mediators that promote inflammation and skin tumor development; expression of the slug transcription factor in keratinocytes is required for maximal production of these mediators. In the present studies we examined the possibility that UVR-exposed melanocytes also produce proinflammatory mediators and that Slug is important in this process. Microarray studies revealed that both UVR exposure and Slug overexpression altered transcription of a variety of proinflammatory mediators by normal human melanocytes; some of these mediators are also known to stimulate melanocyte growth and migration. There was little overlap in the spectra of cytokines produced by the two stimuli. However IL-20 was similarly induced by both stimuli and the NFκB pathway appeared to be important in both circumstances. Further exploration of UVR-induced and Slug-dependent pathways of cytokine induction in melanocytes may reveal novel targets for melanoma therapy.

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“…Understanding the different molecular mechanisms which may conceivably enable melanoma tumour progression is an essential step that could allow us improve prediction and help develop effective therapies for this disease 22. Cancer cells are ‘rogue’ cells that do not respond to a normal homeostatic regulation.…”

Section: Discussionmentioning

confidence: 99%