1,721,209 research outputs found
Emerging role of miR-106b-25/miR-17-92 clusters in the control of transforming growth factor beta signaling
No full textmiRNAs in precancerous lesions of the gastrointestinal tract.
Full text linkIn spite of the well-established understanding of the phenotypic lesions occurring in the shift from native epithelia to invasive (adeno) carcinoma, the molecular typing of the precancerous changes in the gastrointestinal tract remains unreliable. In recent years, no biomarkers have aroused as much interest as the miRNAs, a class of non-coding RNA molecules that function as endogenous silencers of numerous target genes. Aberrant miRNA expression is a hallmark of human disease, including cancer. Unlike most mRNAs, miRNAs are both long-living in vivo and very stable in vitro. Such characteristics allow their testing in paraffin-embedded tissue samples, which is essential in the biological profiling of small (phenotypically characterized) preneoplastic lesions of the gastrointestinal tract (as well as in other fields of human pathology). The upcoming challenge lies in the reliable identification of disease-specific targets of dysregulated miRNAs, to enable miRNA testing in the clinical management of the secondary prevention of gastrointestinal cancer
Tp44 molecules involved in antigen-independent T cell activation are expressed on human plasma cells.
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Leucemia mieloide cronica: terapia molecolare
No full textLa Leucemia Mieloide Cronica (LMC) è una patologia della cellila staminale emopoietica caratterizzata dalla presenza del gene di fusione BCR-ABL, che codifica per una proteina con attività tirosin-kinasica responsabile del fenotipo neoplastico. La terapia della LMC è stata rivoluzionata dall'avvento dei farmaci inibitori delle tirosin-kinasi, il cui capostipite è l'imatinib mesilato. Nel capitolo viene discussa in dettaglio la terapia di prima linea e la terapia di salvataggio dei pazienti affetti da LMC, ed il monitoraggio della risposta
<it>Fez1/Lzts1 </it>a new mitotic regulator implicated in cancer development
No full textAbstract Considerable evidence has accumulated suggesting that cancer has genetic origin, based on the development of genomic alterations, such as deletions, mutations, and/or methylations in critical genes for homeostasis of cellular functions, including cell survival, DNA replication and cell cycle control. Mechanism controlling the precise timing and sequence of cell cycle events as well as checkpoints insuring fidelity of those events are key targets that when disrupted could result in tumorigenesis. Mitosis is the process by which a cell duplicates its genetic information (DNA), in order to generate two, identical, daughter cells. In addition each daughter cell must receive one centrosome and the appropriate complements of cytoplasm and organelles. This process is conventionally divided in to five distinct stages: prophase, prometaphase, metaphase, anaphase and telophase that correspond to a different morphology of the cell. The entry into mitosis (M) is under the control of the cyclin dependent kinase Cdk1. During G2, the kinases Wee1 and Myt1 phosphorylate Cdk1 at T14/Y15 residues, rendering it inactive. The transition from G2 to M is promoted by the activation of Cdk1 via dephosphorylation by the Cdk1 phosphatase Cdc25C. Activated Cdk1 complexes translocate into the nucleus during prophase where phosphorylate numerous substrates in order to enhance their activation as the cells progresses trough prophase, prometaphase, and metaphase. Recently we identified a new player: FEZ1/LZTS1 that contributes to the fine-tuning of the molecular events that determine progression through mitosis, and here will review its role in cancer development and in M phase regulation.</p
A human REV7 homolog that interacts with the polymerase zeta catalytic subunit hREV3 and the spindle assembly checkpoint protein hMAD2.
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