1,721,080 research outputs found
ISOLATION OF SLOW CYCLING STEM-LIKE MELANOMA SPHERES FROM mGluR1 POSITIVE MELANOMA CELL LINE
No full textHuman malignant melanoma is a highly aggressive and drug-resistant tumour of neuro-ectodermal origin. Tumor heterogeneity, undifferentiated molecular signatures, and increased tumorigenicity of melanoma subsets with embryonic-like differentiation plasticity, strongly suggests the presence and involvement of cancer a stem cells in the initiation and propagation of melanoma. Parallel to the role that normal stem cells play in organogenesis, cancer stem cells are thought to be crucial for tumorigenesis. Many investigators, indeed, propose that melanoma stem cells (MSCs) may be responsible for tumour chemoresistance, invasiveness, and neoplastic progression and that targeted abrogation of a MSCs population could therefore ultimately lead to stable remissions and perhaps cure of metastatic melanoma. However, the high percentage of cells expressing different markers of undifferentiated and partially differentiated stages that form the bulk of the melanoma tumour has made the isolation of melanoma stem cells a challenging goal. In fact, no peculiar marker of stemness has been identified so far that may consistently flag up a stem cell population different from the highly heterogenic melanoma cell population.
Glutamate has been proposed to play an important role in the in biology of stem/progenitor cells (Melchiorri et al, 2007) and cancer-initiating stem cells (Nicoletti et al., 2007, Ciceroni et al, 2008). Results from previous studies suggest that the ectopic expression of the type 1 metabotropic glutamate receptor gene (GRM1) is sufficient to transform melanocytes in vitro and cause malignant melanoma in vivo (Pollock et al. 2003). In addition, it has been documented that the GRM1 gene is aberrantly expressed in about 60% of human melanomas cell lines and biopsies (Pollock et al. 2003, Ortiz P. 2007).
By culturing the type 1 metabotropic glutamate receptor-positive metastatic melanoma cell line, C8161, under conditions that are known to allow the isolation of neural stem cells, we were able to isolate a highly tumorigenic, drug resistant, slow-cycling cell population that could represent a good cell model to study Melanoma resistance and recurrence both in vitro and in vivo
ISOLATION OF SLOW CYCLING STEM-LIKE MELANOMA SPHERES FROM mGluR1 POSITIVE MELANOMA CELL LINE
No full textHuman malignant melanoma is a highly aggressive and drug-resistant tumour of neuro-ectodermal origin. Tumor heterogeneity, undifferentiated molecular signatures, and increased tumorigenicity of melanoma subsets with embryonic-like differentiation plasticity, strongly suggests the presence and involvement of cancer a stem cells in the initiation and propagation of melanoma. Parallel to the role that normal stem cells play in organogenesis, cancer stem cells are thought to be crucial for tumorigenesis. Many investigators, indeed, propose that melanoma stem cells (MSCs) may be responsible for tumour chemoresistance, invasiveness, and neoplastic progression and that targeted abrogation of a MSCs population could therefore ultimately lead to stable remissions and perhaps cure of metastatic melanoma. However, the high percentage of cells expressing different markers of undifferentiated and partially differentiated stages that form the bulk of the melanoma tumour has made the isolation of melanoma stem cells a challenging goal. In fact, no peculiar marker of stemness has been identified so far that may consistently flag up a stem cell population different from the highly heterogenic melanoma cell population.
Glutamate has been proposed to play an important role in the in biology of stem/progenitor cells (Melchiorri et al, 2007) and cancer-initiating stem cells (Nicoletti et al., 2007, Ciceroni et al, 2008). Results from previous studies suggest that the ectopic expression of the type 1 metabotropic glutamate receptor gene (GRM1) is sufficient to transform melanocytes in vitro and cause malignant melanoma in vivo (Pollock et al. 2003). In addition, it has been documented that the GRM1 gene is aberrantly expressed in about 60% of human melanomas cell lines and biopsies (Pollock et al. 2003, Ortiz P. 2007).
By culturing the type 1 metabotropic glutamate receptor-positive metastatic melanoma cell line, C8161, under conditions that are known to allow the isolation of neural stem cells, we were able to isolate a highly tumorigenic, drug resistant, slow-cycling cell population that could represent a good cell model to study Melanoma resistance and recurrence both in vitro and in vivo
MELATONIN REDUCES BOTH BASAL AND BACTERIAL LIPOPOLYSACCHARIDE-INDUCED LIPID PEROXIDATION IN VITRO
No full textI.P. 2001: 5.0
H2O2-induced lipid peroxidation in rat brain homogenates is greatly reduced by melatonin.
No full textMelatonin reduces H2O2-induced lipid peroxidation in homogenates of different rat brain regions.
No full textMelatonin reduces kainate-induced lipid peroxidation in homogenates of different brain regions.
No full text
A reappraisal of the role of the various opioid receptor subtypes in cell-mediated immunity.
No full textOpioid peptides have been shown by several studies to modulate various parameters of the immune response, but scant experimental findings exist on the role played by specific opioid receptor subtypes in the control of immune mechanisms. This study focuses on the in vitro influences of [Trp4,Asn7]dermorphin, a mu-selective agonist, [D-Ala2]deltorphin I, a delta-selective agonist and U50,488, a kappa-selective agonist, on the proliferative response of splenocytes to concanavalin A (Con A). [Trp4,Asn7]dermorphin at low concentrations (10(-11P) and 10(-12) M) enhanced the proliferative response to Con A, whereas higher concentrations (10(-6) to 10(-7) M) inhibited it. Both effects were antagonized by naloxone. [D-Ala2]deltorphin I at very low concentrations (10(-12) to 10(-13) M) also produced a significant increase in the proliferative response of splenocytes to Con A. This effect was significantly antagonized by natrindole, a specific delta-receptor antagonist. Finally U50,488 at concentrations ranging from 10(-8) to 10(-9) M inhibited the proliferative response to Con A. The effects of U50,488 were mediated by the stimulation of the kappa-opioid receptors, since a preincubation of splenocytes with the selective antagonist norbinaltorphimine significantly reduced or abolished the U50,488-induced suppression of the mitotic response. In conclusion, our results clearly indicate that the different opioid receptor subtypes play a different role in the control of immune mechanisms and suggest that immunoenhancing effects of opioid peptides are very likely due to the stimulation of mu- and delta-receptors, whereas the immunosuppressive effects are mediated through the stimulation of kappa-opioid receptors
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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