Melanoma brain metastasis mimicking cortical laminar necrosis
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Background: Metastatic lesions to the brain are common in patients with melanoma. Imaging characteristics can support the diagnosis of metastatic melanoma, but alternative diagnoses should be considered. Case Description: Here, we present a case of a 57-year-old man in whom a metastatic melanoma initially mimicked the imaging characteristics of cortical laminar necrosis. Conclusion: This comprises the first report of melanoma brain metastasis presenting with these imaging characteristics and emphasizes the importance of maintaining a high index of suspicion for metastatic lesions in patients with known cancer.Background: Metastatic lesions to the brain are common in patients with melanoma. Imaging characteristics can support the diagnosis of metastatic melanoma, but alternative diagnoses should be considered. Case Description: Here, we present a case of a 57-year-old man in whom a metastatic melanoma initially mimicked the imaging characteristics of cortical laminar necrosis. Conclusion: This comprises the first report of melanoma brain metastasis presenting with these imaging characteristics and emphasizes the importance of maintaining a high index of suspicion for metastatic lesions in patients with known cancer.
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The inhibitory effect of tumor necrosis serum (TNS) on the artificial metastasis of B-16 melanoma cells and the spontaneous metastasis of Lewis lung carcinoma cells was investigated. The results obtained were as follows: 1) When tumor necrosis serum (TNS) was administered either 20 min or 2 days after injection of B-16 melanoma cells, a very strong inhibitory effect (99%) relative to the control was noted. 2) TNS showed a 60% inhibitory effect on spontaneous metastasis, and the weight of the original tumor regressed by 60%. 3) No histological changes in normal tissues were observed microscopically following TNS injection. The above results confirm that TNS is extremely effective in preventing metastasis.
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Abstract Brain metastasis occurs in a large proportion of metastatic melanoma patients and is associated with a dismal prognosis. However, the molecular mechanisms that govern melanoma tropism to the brain remain poorly understood. MicroRNAs (miRNAs) play essential roles in many physiological and pathological processes, and have been recently shown to exert key roles during cancer metastasis. In this study we find that specific miRNAs may be important mediators of melanoma dissemination to the brain. First, we conducted a miRNA microarray analysis of metastatic melanoma tissues that revealed a subset of miRNAs differentially expressed in brain metastases (n=11) relative to other sites (n=48). A brain-specific signature comprised of seven miRNAs was further validated in an independent cohort of metastatic melanoma samples (n=36; 9 brain metastatic specimens). Then, we analyzed the trend of expression of those miRNAs during tumor progression by comparing their levels in primary tumors and their paired metastasis from patients with or without recurrence in the brain (n=18). Differential expression of some miRNAs was already evident at diagnosis in primary tumors that recurred in the brain, while for others it was acquired in the transition from primary to metastasis, suggesting that it may be a later event in tumor progression. Furthermore, in vitro modulation of specific signature miRNAs significantly altered the ability of melanoma cells to execute processes such as adhesion and transmigration through human brain endothelial cells and proliferation in human astrocytes conditioned media. Additionally, using an in vivo model of melanoma brain metastasis, we confirmed the capacity of specific miRNA alterations to promote melanoma cells’ competence to reach the brain. Finally, the analysis of potential downstream mediators of select miRNAs revealed the involvement of immuno-suppressive molecules, as well as inflammatory and chemotactic mediators in this process. Collectively, our results expand our understanding of the mechanisms that control melanoma brain metastasis, potentially revealing novel therapeutic avenues for patients for whom no viable approaches are currently available. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1946.
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Primary tumor
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Abstract. The process of cancer metastasis is sequential and selective and contains stochastic elements. The growth of melanoma metastases represents the endpoint of many lethal events that few tumor cells can survive. Primary tumors consist of multiple subpopulations of cells with heterogeneous metastatic properties, and the outcome of metastasis depends on the interplay of metastatic tumor cells with various host factors. This viewpoint is more optimistic than that of metastasis as a random process. A selective biological process is regulated by the interaction of tumor cells with their host, and these complex interactions can now be studied and manipulated.
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Four of five patients with brain metastases from melanoma had increased lofetamine I 123 uptake in the region of the tumor deposits. A comparison group of five patients with melanoma with no clinical or radiologic evidence of brain involvement and 46 of 47 patients without malignant melanoma but with known brain tumors of other histologic types had normal or decreased iofetamine I 123 brain uptake in the region of the tumor. An exception was one patient whose metastatic small cell lung cancer to the brain showed focally increased uptake. These findings suggest that certain brain tumors such as melanoma are capable of selectively binding iofetamine I 123 because of specific chemical properties of the radiopharmaceutical. Increased uptake of iofetamine I 123 in brain lesions in a patient at risk for metastatic melanoma may be a useful aid to differential diagnosis.
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Malignant melanoma as a cause of inflammatory metastasis to the skin is a rare phenomenon referred to as in-transit metastasis (ITM). We report an unusual case of a patient who developed left leg lesions resembling lymphangiectasis. Punch biopsy results revealed atypical cells consistent with melanoma. The patient had a history of high-risk melanoma involving the left side of the lower extremity. This case highlights the need for a high index of suspicion for ITM in patients with a history of melanoma. Therapeutic options are discussed.
Melanoma diagnosis
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Malignant melanoma has a high incidence. Malignant melanoma metastasis can develop in all viscera, including brain. They are encephalophiles. Rarely, the primary tumor remains unknown. Treatment of this metastasis is complex.A 50-year-old man in an excellent clinical condition was diagnosed with multiple metastasis. Lesions were diagnosed using modem imaging methods: MRI, PET-scan. They were treated by chemotherapy, radiotherapy and immunotherapy. In the evolution of the disease, appeared brain metastases.The chemotherapy, radiotherapy and immunotherapy have not stopped the evolution of visceral lesions which increased in number and size. They had not toxic effects. The general condition of the patient was very good, with KPS=100. The brain metastases had no response to RCS. His surgical excision improved the neurological condition but, thereafter, general condition get worse and the patient died 3 months after surgical intervention. Biopsies from subcutaneous nodes and brain lesion sustained the malignant melanoma diagnosis.In rare instances there are malignant melanoma metastases without a primary tumor. The patient was in a very good condition, although the treatment methods have not produced a regression of stabilization of the disease. The results of melanoma metastasis treatment are not satisfactory.
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Abstract Brain metastasis is a significant cause of morbidity and mortality in multiple cancer types and represents an unmet clinical need. The mechanisms that mediate metastatic cancer growth in the brain parenchyma are largely unknown. Melanoma, which has the highest rate of brain metastasis among common cancer types, is an ideal model to study how cancer cells adapt to the brain parenchyma. Our unbiased proteomics analysis of melanoma short-term cultures revealed that proteins implicated in neurodegenerative pathologies are differentially expressed in melanoma cells explanted from brain metastases compared with those derived from extracranial metastases. We showed that melanoma cells require amyloid beta (Aβ) for growth and survival in the brain parenchyma. Melanoma-secreted Aβ activates surrounding astrocytes to a prometastatic, anti-inflammatory phenotype and prevents phagocytosis of melanoma by microglia. Finally, we demonstrate that pharmacologic inhibition of Aβ decreases brain metastatic burden. Significance: Our results reveal a novel mechanistic connection between brain metastasis and Alzheimer's disease, two previously unrelated pathologies; establish Aβ as a promising therapeutic target for brain metastasis; and demonstrate suppression of neuroinflammation as a critical feature of metastatic adaptation to the brain parenchyma. This article is highlighted in the In This Issue feature, p. 1171
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Choroidal melanoma primarily metastasizes to the liver. Isolated extrahepatic metastases have rarely been reported and they generally resulted in death within 6 months. We describe a patient who developed an isolated brain metastasis 27 years after his left eye was enucleated for choroidal melanoma. The metastasis was successfully treated with surgery and radiotherapy. The patient is alive and disease free 3 years after treatment of the metastasis. Posterior location and other clinical and morphologic characteristics of primary choroidal melanoma could explain the unusually long latency of this solitary extrahepatic metastatic disease. Lifelong surveillance to detect early signs of metastasis is mandatory for any patient treated for choroidal melanoma.
Choroidal Melanoma
Choroid
Ocular Melanoma
Eye Enucleation
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