Histology and histopathology Vol.22, nº 8 (2007)

Ir a Estadísticas

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    Mammalian target of rapamycin: Master regulator of cell growth in the nervous system
    (Murcia : F. Hernández, 2007) Sandsmark, D.K.; Pelletier, C.; Weber, J.D.; Gutmann, D.H.
    The mammalian target of rapamycin (mTOR) is a highly conserved serine/threonine protein kinase that regulates a number of diverse biologic processes important for cell growth and proliferation, including ribosomal biogenesis and protein translation. In this regard, hyperactivation of the mTOR signaling pathway has been demonstrated in numerous human cancers, including a number of inherited cancer syndromes in which individuals have an increased risk of developing benign and malignant tumors. Three of these inherited cancer syndromes (Lhermitte-Duclos disease, neurofibromatosis type 1, and tuberous sclerosis complex) are characterized by significant central nervous system dysfunction and brain tumor formation. Each of these disorders is caused by a genetic mutation that disrupts the expression of proteins which negatively regulate mTOR signaling, indicating that the mTOR signaling pathway is critical for appropriate brain development and function. In this review, we discuss our current understanding of the mTOR signaling pathway and its role in promoting ribosome biogenesis and cell growth. We suggest that studies of this pathway may prove useful in identifying molecular targets for biologically-based therapies of brain tumors associated with these inherited cancer syndromes as well as sporadic central nervous system tumors.
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    Advances of MUC1 as a target for breast cancer immunotherapy
    (Murcia : F. Hernández, 2007) Yang, E.; Hu, X.F.; Xing, P.X.
    MUC1 is a potential target in breast cancer immunotherapy as MUC1 is overexpressed in breast cancer, and is absent or expressed in low level in normal mammary gland. In addition, MUC1 is mostly aberrantly underglycosylated in cancer and the antigens on the cancer surface are different from normal cell. Therefore targeting MUC1 for cancer immunotherapy can exploit the difference between cancer and normal cells, and eliminating the cancerous cells while leaving the normal mammary cells unharmed. This review will focus on the recent advance of MUC1 breast cancer immunotherapy currently being investigated.
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    Cell proliferation and apoptosis in stromal corneal dystrophies
    (Murcia : F. Hernández, 2007) Szentmáry, N.; Takács, L.; Berta, Andras; Szende, B.; Süveges, I.; Módis, L.
    The aim of our study was to evaluate corneal cell proliferation and apoptosis in cases of granular, macular and lattice dystrophy, and to provide evidence which may help to clarify whether apoptosis is a pathogenic factor in any of these dystrophies. The study group comprised 39 eyes (from 33 patients) which had undergone penetrating keratoplasty (PK) for stromal dystrophies: these comprised 12 eyes (from 9 patients, 55.5% males) with granular dystrophy, 13 eyes (12 patients, 33.3% males) with macular dystrophy, and 14 eyes (13 patients, 61.5% males) with lattice type I dystrophy. A further 4 corneal buttons from enucleated eyes of 4 patients with choroideal melanoma served as controls. Immunocytochemical analysis of Ki67 (DNAcon Kit, DakoCytomation A/S, Glostrup, Denmark) was used for evaluation of cell proliferation. Apoptosis was detected by use of the TUNEL (terminal deoxyribonucleotidyl transferase-mediated dUTPdigoxigenin nick-end labelling) assay method (Apoptag reagent, Q-Biogene, Strasbourg, France). Statistical comparisons were made using the Mann-Whitney test. No Ki67-positive cells were detected in the studygroup or control corneas. In control corneas no apoptotic activity was found. In the study group the mean (normalised) apoptotic keratocyte number was 1.1±1.7 in granular dystrophy and 0.5±1.1 in lattice type I The aim of our study was to evaluate corneal cell proliferation and apoptosis in cases of granular, macular and lattice dystrophy, and to provide evidence which may help to clarify whether apoptosis is a pathogenic factor in any of these dystrophies. The study group comprised 39 eyes (from 33 patients) which had undergone penetrating keratoplasty (PK) for stromal dystrophies: these comprised 12 eyes (from 9 patients, 55.5% males) with granular dystrophy, 13 eyes (12 patients, 33.3% males) with macular dystrophy, and 14 eyes (13 patients, 61.5% males) with lattice type I dystrophy. A further 4 corneal buttons from enucleated eyes of 4 patients with choroideal melanoma served as controls. Immunocytochemical analysis of Ki67 (DNAcon Kit, DakoCytomation A/S, Glostrup, Denmark) was used for evaluation of cell proliferation. Apoptosis was detected by use of the TUNEL (terminal deoxyribonucleotidyl transferase-mediated dUTPdigoxigenin nick-end labelling) assay method (Apoptag reagent, Q-Biogene, Strasbourg, France). Statistical comparisons were made using the Mann-Whitney test. No Ki67-positive cells were detected in the studygroup or control corneas. In control corneas no apoptotic activity was found. In the study group the mean (normalised) apoptotic keratocyte number was 1.1±1.7 in granular dystrophy and 0.5±1.1 in lattice type I controls, the difference was statistically significant only for macular dystrophy (1.6±1.2; p = 0.01). Keratocyte apoptosis seems to be a concomitant or pathogenic factor in macular dystrophy. However, the pathways that are triggered to result in increased apoptotic cell death remain to be clarified.
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    New insights into the cytoplasmic function of PML
    (Murcia : F. Hernández, 2007) Salomoni, P.; Bellodi, C.
    PML is a tumour suppressor inactivated in Acute Promyelocytic Leukaemia (APL). PML is the essential component of a subnuclear structure called the PML nuclear body (PML-NB), which is disrupted in APL. By targeting different cellular proteins to this structure, PML can either hamper or potentiate their functions. The PML transcript undergoes alternative splicing to generate both nuclear and cytoplasmic isoforms. Most of the research in this field has focused its attention on studying nuclear PML. Nevertheless, new exciting studies show that cytoplasmic PML may control essential cellular functions, thus opening new avenues for investigation.
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    Diagnosis of Hodgkin`s disease: an update on histopathological and immunophenotypical features
    (Murcia : F. Hernández, 2007) Fraga, M.; Forteza, J.
    The Hodgkin lymphoma (HL) is a B-cell lymphoma, as was proved by molecular studies with single-cell PCR. Histologically, it is characterized by a minority of neoplastic cells, Reed-Sternberg cells and its variants, related to a variable non-neoplastic inflammatory background. Nowadays, (WHO classification) the following types of HL are recognized: Nodular Paragranuloma and the Classical Hodgkin Lymphoma, the latter including Nodular Sclerosis, Mixed Cellularity, Lymphocyte-rich Classical Hodgkin Lymphoma and Lymphocyte Depletion. Morphology together with immunohistochemical studies allows to classify the different forms of Hodgkin lymphoma and to make a differential diagnosis with non-Hodgkin lymphomas. All classical Hodgkin lymphomas are treated similarly, and chances for remission and survival are currently good. Molecular parameters should be added to the current classification and patients could benefit from new therapeutic targets.