1,721,107 research outputs found
Ultrastructural and biological observations on neoplastic growth control obtained by contact inhibition
No full textultrastructural and biological observations on neoplastic growth control obtained by contact inhibition
No full textA role for endogenous reverse transcriptase in tumorigenesis and as a target in differentiating cancer therapy
No full textAn unexpected result emerging from completion of the genome sequencing project is that a large portion of mammalian genomes is constituted by retrotransposons. A large body of published data supports the conclusion that retrotransposons are biologically active elements and indicates that retrotransposition is an ongoing process in mammalian genomes. Retroelements can act as insertional mutagens altering the coding integrity of genes and, recently, have been found to also affect the expression of cellular genes at the epigenetic level: in this light, they are a potential threat in that these events can trigger the onset of several pathologies including cancer. Retroelement genes, and particularly the gene coding for reverse transcriptase (RT), are typically expressed at high levels in transformed cells and tumors. In recent work, we have found that drug-mediated inhibition of the endogenous RT activity, or silencing of expression of active retrotransposons of the LINE-1 family by RNA interference, down-regulate cell growth and induce the activation of differentiating functions in several cancer cell lines. Moreover, the inhibition of endogenous RT activity in vivo antagonizes the growth of human tumors in animal models. In this review, we discuss newly emerging concepts on the role of retrotransposons and suggest that an abnormally high level of the RT activity that they encode may contribute to the loss of control in the proliferation and differentiation programs typical of transformed cells. In this light, RT-coding elements may be regarded as promising targets in the development of novel, differentiation-inducing approaches to cancer therapy. © 2005 Wiley-Liss, Inc
Human endogenous retroviruses role in cancer cell stemness
No full textCancer incidence and mortality, metastasis, drug resistance and recurrence are still the critical issues of oncological diseases. In this scenario, increasing scientific evidences demonstrate that the activation of human endogenous retroviruses (HERVs) is involved in the aggressiveness of tumors such as melanoma, breast, germ cell, renal, ovarian, liver and haematological cancers. In their dynamic regulation, HERVs have also proved to be important determinants of pluripotency in human embryonic stem cells (ESC) and of the reprogramming process of induced pluripotent stem cells (iPSCs). In many types of tumors, essential characteristics of aggressiveness have been associated with the achievement of sternness features, often accompanied with the identification of defined subpopulations, termed cancer stern cells (CSCs), which possess stem cell-like properties and sustain tumorigenesis. Indeed, CSCs show high self -renewal capacity with a peculiar potential in tumor initiation, progression, metastasis, heterogeneity, recurrence, radiotherapy and drug resistance. However, HERVs role in CSCs biology is still not fully elucidated. In this regard, CD133 is a widely recognized marker of CSCs, and our group demonstrated, for the first time, the requirement of HERV-K activation to expand and maintain a CD133+ melanoma cell subpopulation with sternness features in response to microenvironmental modifications. The review will discuss HERVs expression as cancer hallmark, with particular focus on their role in the regulation of cancer sternness features and the potential involvement as targets for therapy
influence of genetic and physiological properties of the host cell on the cytopathic expression of herpes simplex virus.
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Glicoproteine virus-indotte in presenza di un bis-guanilidrazone che modifica la citopatologia del virus dell’herpes simplex
No full textAntiviral activity of guanylhydrazones. effect of a bis-derivative on herpes simplex virus infection in vitro.
No full textModifications of mitochondria in human tumor cells during anthracycline-induced apoptosis.
No full textPublisher:
Athens, Greece : s.n., 1981- (Athens, Greece : Potamitis Press
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