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Miriam Galvonas Jasiulionis

Researcher at Federal University of São Paulo

Publications -  68
Citations -  1664

Miriam Galvonas Jasiulionis is an academic researcher from Federal University of São Paulo. The author has contributed to research in topics: Melanoma & Epigenetics. The author has an hindex of 22, co-authored 60 publications receiving 1329 citations. Previous affiliations of Miriam Galvonas Jasiulionis include Ludwig Institute for Cancer Research.

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The Role of SIRT1 on DNA Damage Response and Epigenetic Alterations in Cancer

TL;DR: The recent findings on the interplay among SIRT1, oxidative stress, and DNA repair machinery and its impact on normal and cancer cells are discussed.
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Oxidative Stress Modulates DNA Methylation during Melanocyte Anchorage Blockade Associated with Malignant Transformation

TL;DR: In this article, increased intracellular oxidative species and nitric oxide levels, as well as alterations in the DNA methylation, were observed after melan-a detachment, which were also associated with a decrease in the Hcy element in the methionine (universal methyl donor) cycle.
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Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation.

TL;DR: The results show that Timp1 is assembled in a supramolecular complex containing CD63 and β1-integrins along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway, independently of Akt phosphorylation.
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Enhanced OXPHOS, glutaminolysis and β-oxidation constitute the metastatic phenotype of melanoma cells.

TL;DR: The results indicate that progression to metastasis requires mitochondrial function, and 4C11+ cells could be grouped as a subpopulation with a profile that was quite distinct from the other cells investigated in the present study.
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Melanocyte transformation associated with substrate adhesion impediment.

TL;DR: This model corroborates the role of adhesion state as a promoting agent in transformation process and demonstrates that cell adhesion disturbances may act as carcinogenic stimuli, at least for a nontumorigenic immortalized melanocyte lineage.