1,721,101 research outputs found
Guidelines for Molecular Analysis in Archive Tissues capitolo 15 MicroRNA extraction from formalin-fixed paraffin-embedded tissues
No full textLung cancer and molecular testing in small biopsies versus cytology: The Logics of Worlds
No full textThe 8th Annual National Molecular Cytopathology Meeting, held in Naples, Italy, on December 2 to 3, 2019, addressed updates in diagnostic cytopathology and molecular classifications and specifically focused on lung cancer biomarker testing in cytology samples. Lung cancer continues to be the most commonly diagnosed noncutaneous malignancy in the world. In the majority of patients, lung cancers are frequently identified when they cannot be surgically accessed, and this leads to the use of cytology for a diagnosis and theragnostic testing. The meeting was an international forum for discussing new roles and updates for cytopathology in molecular testing as the basis for provoking new trends and novel approaches. The relevant literature is referenced. The significance of these updates for the practice of pathology in general is discussed
Apoptomirs: Small molecules have gained the license to kill
No full textApoptosis is a tightly regulated form of cell death and represents an important process during normal development. In the past years, the scientific community has produced remarkable advances in our understanding of cancer biology, realizing that apoptosis and the genes that control it have a profound effect on the malignant phenotype. Recently, a new class of non-coding RNA genes, known as microRNA (miRNA or miR), have been demonstrated to play important roles in diverse biological processes, including development, cell differentiation, proliferation, and apoptosis. This suggests that other oncogenic mechanisms are needed to produce selective pressure to override apoptosis during multistage carcinogenesis. Intriguingly, since most cytotoxic anticancer agents induce apoptosis, it is possible that defects in apoptotic programs may contribute to treatment failure. Several studies strongly suggest a role for microRNAs in modulating sensitive/resistant phenotypes to cytotoxic therapy, calling for further investigation and validation of microRNA functions and targets in order to improve sensitivity to cancer treatments, thus ultimately improving prognosis and survival. Here, we review the current findings about microRNAs focusing on their involvement in the apoptotic process. © 2010 Society for Endocrinology Printed in Great Britain
LESIONI ULCERATIVE DELLA VULVA, DELLA VAGINA E DEL CAVO ORALE IN PAZIENTE IMMUNOCOMPETENTE: CASE REPORT
No full textEmerging role of miR-106b-25/miR-17-92 clusters in the control of transforming growth factor beta signaling
No full textc-Met and miRs in cancer
Full text linkc-Met, a member of the receptor tyrosine kinase family, is involved in a wide range of cellular processes, including tumor survival, cell growth, angiogenesis and metastasis, and resulting in overexpression in many human cancers, leading to a constitutive activation of the downstream pathways. Recently identified MicroRNAs are a family of small noncoding RNA molecules, extensively studied in cancer, that exert their action by inhibiting gene expression at the posttranscriptional level in several biological processes. Aberrant regulation of microRNAs expression has been implicated in the pathogenesis of different human neoplasia. Several publications point out the connections between c-Met and its ligand hepatocyte growth factor (HGF) and microRNAs. This review summarizes the current knowledge about the interplay between c-Met/HGF and microRNAs and provides evidence that microRNAs are a novel and additional system to regulate c-Met expression in tumors. In the future, microRNAs connected to c-Met may provide an additional option to inhibiting this oncogene from orchestrating an invasive growth program
<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
Take your "M" time
No full textBoth entry and exit from mitosis are driven through the fine modulation of Cdk1 activity by several proteins or protein complexes. It is well established that to enter into the M-phase a cell requires Cdk1 to be fully activated in the nucleus by the Cdc25A, B and C phosphatases. Then, at the onset of anaphase Cdk1 activity suddenly drops mainly due to Cyclin B1 degradation, thus allowing exit from M-phase. Recent data demonstrate that high Cdk1 activity is necessary also for proper chromosome segregation, since its premature drop determines acceleration of the progression from prophase to metaphase eventually with incorrect division of the DNA content. A primary role in maintaining high Cdk1 activity during prophase and metaphase is played by Cdc25C phosphatase. During the M-phase, the activity of Cdc25C is regulated by the FEZ1/LZTS1 (LZTS1) tumor suppressor gene, which is able to prevent Cdc25C degradation in mitotic cells. As a consequence, Lzts1 absence in mice results in accelerated mitotic progression, improper chromosome segregation and, eventually, in increased incidence of both spontaneous and carcinogen-induced cancer formation. © 2007 Landes Bioscience
Immunohistochemical expression of polypeptide specific (TPS) antigen in normal and neoplastic tissue.
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