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  1. Article ; Online: The Role of Glycosylation in Melanoma Progression.

    De Vellis, Chiara / Pietrobono, Silvia / Stecca, Barbara

    Cells

    2021  Volume 10, Issue 8

    Abstract: Malignant melanoma is the most aggressive form of skin cancer, which originates from the malignant transformation of melanocytes, the melanin-producing cells of the skin. Melanoma progression is typically described as a stepwise process in which ... ...

    Abstract Malignant melanoma is the most aggressive form of skin cancer, which originates from the malignant transformation of melanocytes, the melanin-producing cells of the skin. Melanoma progression is typically described as a stepwise process in which metastasis formation ensues late during disease. A large body of evidence has shown that the accumulation of genetic and epigenetic alterations drives melanoma progression through the different steps. Mortality in melanoma is associated with metastatic disease. Accordingly, early-stage melanoma can be cured in the majority of cases by surgical excision, while late-stage melanoma is a highly lethal disease. Glycosylation is a post-translational modification that involves the transfer of glycosyl moieties to specific amino acid residues of proteins to form glycosidic bonds through the activity of glycosyltransferases. Aberrant glycosylation is considered a hallmark of cancer as it occurs in the majority of tumor types, including melanoma. The most widely occurring glycosylation changes in melanoma are represented by sialylation, fucosylation, and N- and I-glycan branching. In this review, we discuss the role of glycosylation in melanoma and provide insights on the mechanisms by which aberrant glycosylation promotes melanoma progression through activation of invasion and metastasis, immune evasion and cell proliferation.
    MeSH term(s) Animals ; Cell Transformation, Neoplastic/metabolism ; Glycosylation ; Humans ; Melanoma/metabolism ; Polysaccharides/metabolism
    Chemical Substances Polysaccharides
    Language English
    Publishing date 2021-08-19
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10082136
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Radiosensitisation of Hepatocellular Carcinoma Cells by Vandetanib.

    Znati, Sami / Carter, Rebecca / Vasquez, Marcos / Westhorpe, Adam / Shahbakhti, Hassan / Prince, Jessica / Vlckova, Petra / De Vellis, Chiara / Bascal, Zainab / Loizidou, Marilena / Sharma, Ricky A

    Cancers

    2020  Volume 12, Issue 7

    Abstract: Hepatocellular Carcinoma (HCC) is increasing in incidence worldwide and requires new approaches to therapy. The combination of anti-angiogenic drug therapy and radiotherapy is one promising new approach. The anti-angiogenic drug vandetanib is a tyrosine ... ...

    Abstract Hepatocellular Carcinoma (HCC) is increasing in incidence worldwide and requires new approaches to therapy. The combination of anti-angiogenic drug therapy and radiotherapy is one promising new approach. The anti-angiogenic drug vandetanib is a tyrosine kinase inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2) and RET proto-oncogene with radio-enhancement potential. To explore the benefit of combined vandetanib and radiotherapy treatment for HCC, we studied outcomes following combined treatment in pre-clinical models.
    Methods: Vandetanib and radiation treatment were combined in HCC cell lines grown
    Results: Vandetanib IC 50 s were measured in 20 cell lines and the drug was found to significantly enhance radiation cell kill and to inhibit both cell migration and invasion
    Conclusion: In 2D and 3D studies
    Language English
    Publishing date 2020-07-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers12071878
    Database MEDical Literature Analysis and Retrieval System OnLINE

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