Navegando por Palavras-chave "tumorigenesis"

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    Cancer stem cell genomics: the quest for early markers of malignant progression
    (Expert Reviews, 2009-09-01) Okamoto, Oswaldo Keith [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Biologically distinct populations of neoplastic stem cells have been identified in a variety of human cancers, in which they are associated with the initial steps of tumorigenesis. the intrinsic properties of self-renewal, clonogenicity and multipotency, along with a longer half-life within the body, may render normal adult stem cells more prone to accumulate genetic mutations leading to neoplastic transformation, as predicted by the cancer stem cell hypothesis. Tumor formation is also associated with the pluripotency of embryonic stem cells and may be induced as a consequence of complete dedifferentiation of mature cells, as recently reported for induced pluripotent stem cells. the tumor-initiating cell phenotype may result from genetic alterations affecting the expression of critical genes regulating typical stem cell processes such as self-renewal and pluripotency, in addition to genes determining stem cell senescence or longevity. Detailed genome-wide analysis of cancer stem cells and respective normal counterparts will help elucidate the cellular and molecular nature of tumors, providing fundamental information about the initial steps toward malignant transformation. Devising ways of detecting such genetic and epigenetic alterations and cell populations displaying them would allow medical interventions at the early phases of cancer development, thereby improving the chances of favorable clinical outcomes.
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    RNAi-mediated knockdown of E2F2 inhibits tumorigenicity of human glioblastoma cells
    (Spandidos Publ Ltd, 2014-10-01) Nakahata, Adriana Miti [UNIFESP]; Suzuki, Daniela Emi [UNIFESP]; Rodini, Carolina de Oliveira [UNIFESP]; Fiuza, Mayara L.; Okamoto, Oswaldo K.; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)
    In a previous genome-wide expression profiling study, we identified E2F2 as a hyperexpressed gene in stem-like cells of distinct glioblastoma multiforme (GBM) specimens. Since the encoded E2F2 transcription factor has been implicated in both tumor suppression and tumor development, we conducted a functional study to investigate the pertinence of E2F2 to human gliomagenesis. E2F2 expression was knocked down by transfecting U87MG cells with plasmids carrying a specific silencing shRNA. Upon E2F2 silencing, in vitro cell proliferation was significantly reduced, as indicated by a time-course analysis of viable tumor cells. Anchorage-independent cell growth was also significantly inhibited after E2F2 silencing, based on cell colony formation in soft agar. Subcutaneous and orthotopic xenograft models of GBM in nude mice also indicated inhibition of tumor development in vivo, following E2F2 silencing. As expression of the E2F2 gene is associated with glioblastoma stem cells and is involved in the transformation of human astrocytes, the present findings suggest that E2F2 is involved in gliomagenesis and could be explored as a potential therapeutic target in malignant gliomas.