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Artículos de revistas

Literatura académica sobre el tema "P73, multiple myeloma"

Autor: Grafiati

Publicado: 14 de marzo de 2023

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Artículos de revistas sobre el tema "P73, multiple myeloma"

1

Hao, Mu, Yu Qin, Meirong Zang, et al. "Hypermethylation of TAp73 Suppresses ABL1-Involved DNA Damage Response in Multiple Myeloma." Blood 124, no. 21 (2014): 3374. http://dx.doi.org/10.1182/blood.v124.21.3374.3374.

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Abstract Background: More recently, multiple myeloma (MM) cells evade apoptosis despite pervasive DNA damage was demonstrated. However, the relevance of ongoing DNA damage and the mechanisms by which apoptosis is suppressed remain to be fully elucidated. p53 deletion and mutations do not appear to be a pivotal event in the evolution from pre-malignancy toward malignancy in MM. The protooncogene ABL1 was an alternative pathway to p53 down stream of ATM/ATR, which is commonly translocated in Chronic Myelogenous Leukemia (CML). ABL1 forms a complex with the tumor suppressor gene TP73, which belon

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2

Schultheis, B., A. Krämer, A. Willer, U. Hegenbart, H. Goldschmidt, and R. Hehlmann. "Analysis of p73 and p53 gene deletions in multiple myeloma." Leukemia 13, no. 12 (1999): 2099–103. http://dx.doi.org/10.1038/sj.leu.2401609.

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3

Lunghi, Paolo, Nicola Giuliani, Laura Mazzera, et al. "Targeting MEK/MAPK Signal Transduction Module Potentiates Arsenic Trioxide (ATO)-Induced Apoptosis in Multiple Myeloma Cells through Multiple Signaling Pathways." Blood 110, no. 11 (2007): 1517. http://dx.doi.org/10.1182/blood.v110.11.1517.1517.

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Abstract Multiple Myeloma (MM) cells are extremely resistant to apoptosis and currently new potential drug combinations are under investigation. We have shown that the combined treatment with the MEK1/2 inhibitor PD184352 (PD) and Arsenic Trioxide (ATO) resulted in the synergistic (Combination Index &lt;1.0) induction of apoptosis in 7 human myeloma cell lines (HMCLs: XG1, XG6, OPM2, JJN3, RPMI, H929, Sultan) analyzed, irrespective of their p53 status. The combined treatment was also a highly potent inducer of apoptosis and mitochondrial damage in the majority of the primary multiple myelo

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4

Raab, Marc S., Klaus Podar, Jing Zhang, et al. "Targeting Proteinkinase C Alters ER-Stress and b-Catenin Signaling in Multiple Myeloma: Therapeutic Implications." Blood 110, no. 11 (2007): 258. http://dx.doi.org/10.1182/blood.v110.11.258.258.

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Abstract We have previously shown that the novel orally available small molecule inhibitor of PKC enzastaurin (Eli Lilly and Company) inhibits MM cell growth, survival and angiogenesis both in vitro and in vivo. To date, however, the downstream effects contributing to growth inhibition and cell death remain to be determined. Here, we performed global gene expression profiling on enzastaurin treated MM cells and identified 200 Genes to be differentially regulated with a &gt; 2-fold cut off. Strikingly, two major groups of up-regulated probe sets were associated with either of two pathways -

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5

Lunghi, Paolo, Nicola Giuliani, Laura Mazzera, et al. "Targeting MEK/MAPK signal transduction module potentiates ATO-induced apoptosis in multiple myeloma cells through multiple signaling pathways." Blood 112, no. 6 (2008): 2450–62. http://dx.doi.org/10.1182/blood-2007-10-114348.

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Abstract We demonstrate that blockade of the MEK/ERK signaling module, using the small-molecule inhibitors PD184352 or PD325901 (PD), strikingly enhances arsenic trioxide (ATO)–induced cytotoxicity in human myeloma cell lines (HMCLs) and in tumor cells from patients with multiple myeloma (MM) through a caspase-dependent mechanism. In HMCLs retaining a functional p53, PD treatment greatly enhances the ATO-induced p53 accumulation and p73, a p53 paralog, cooperates with p53 in caspase activation and apoptosis induction. In HMCLs carrying a nonfunctional p53, cotreatment with PD strikingly elevat

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6

Shammas, Masood A., Paola Neri, Hemanta Koley, et al. "Specific killing of multiple myeloma cells by (-)-epigallocatechin-3-gallate extracted from green tea: biologic activity and therapeutic implications." Blood 108, no. 8 (2006): 2804–10. http://dx.doi.org/10.1182/blood-2006-05-022814.

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AbstractEpigallocatechin-3-gallate (EGCG), a polyphenol extracted from green tea, is an antioxidant with chemopreventive and chemotherapeutic actions. Based on its ability to modulate growth factor-mediated cell proliferation, we evaluated its efficacy in multiple myeloma (MM). EGCG induced both dose- and time-dependent growth arrest and subsequent apoptotic cell death in MM cell lines including IL-6-dependent cells and primary patient cells, without significant effect on the growth of peripheral blood mononuclear cells (PBMCs) and normal fibroblasts. Treatment with EGCG also led to significan

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7

Shammas, Masood A., Ramesh B. Batchu, Hemanta Koley, et al. "A Green Tea Polyphenol, Epigallocatechin-3-Gallate, Induces Selective Apoptosis in Multiple Myeloma Cells: Mechanism of Action and Therapeutic Potential." Blood 106, no. 11 (2005): 1590. http://dx.doi.org/10.1182/blood.v106.11.1590.1590.

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Abstract Epigallocatechin-3-gallate (EGCG), a polyphenol extracted from green tea, induces dose and time dependent cell death in both IL-6-dependent and independent multiple myeloma cell lines and primary patient cells, with minimal or no effect on the growth of normal cells. The cell death is apoptotic as determined by annexin V staining and is not inhibited by IL-6. Evaluation of molecular mechanism of action by gene expression profiling indicated that EGCG had a profound effect on transcription of major regulatory genes involved in distinct pathways controlling cell growth arrest and apopto

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8

Cottini, Francesca, Teru Hideshima, Martin Sattler, Federico Caligaris-Cappio, Kenneth C. Anderson, and Giovanni Tonon. "The Role of the ABL1/YAP1/P73 Axis in Prevention of DNA Damage-Mediated Apoptosis in Multiple Myeloma." Blood 120, no. 21 (2012): 725. http://dx.doi.org/10.1182/blood.v120.21.725.725.

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Abstract Abstract 725 Background: Genome integrity plays a crucial role in the development of normal plasma cells to eliminate aberrant ones. Multiple myeloma (MM) is a plasma cell malignancy characterized by complex heterogeneous cytogenetic abnormalities. MM cells show constitutive DNA Damage Response (DDR) and activate compensatory mechanisms to prevent DNA-damage mediated apoptosis. Here we define the molecular mechanisms of these protective effects. Methods: A panel of 15 MM cell lines was used. Blood and BM samples from healthy volunteers and MM patients were obtained after informed cons

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9

Raab, Marc S., Iris Breitkreutz, Giovanni Tonon, et al. "Targeting PKC: A Novel Role for Beta-catenin in ER Stress and Apoptotic Signaling." Blood 112, no. 11 (2008): 2763. http://dx.doi.org/10.1182/blood.v112.11.2763.2763.

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Abstract Targeting protein kinase C (PKC) isoforms by the small molecule inhibitor enzastaurin has shown promising pre-clinical activity in a wide range of tumor cells. In this study, we further delineated its mechanism of action in multiple myeloma (MM) cells and found a novel role of b-catenin in regulating growth and survival of tumor cells. Inhibition of PKC leads to rapid accumulation of b-catenin by preventing the phosphorylation required for its proteasomal degradation. Specifically, b-catenin was dephosphorylated at Ser33,37,41 and accumulated in a dose- and time-dependent manner in al

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10

Raab, Marc S., Iris Breitkreutz, Giovanni Tonon, et al. "Targeting PKC: a novel role for beta-catenin in ER stress and apoptotic signaling." Blood 113, no. 7 (2009): 1513–21. http://dx.doi.org/10.1182/blood-2008-05-157040.

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Abstract Targeting protein kinase C (PKC) isoforms by the small molecule inhibitor enzastaurin has shown promising preclinical activity in a wide range of tumor cells. We further delineated its mechanism of action in multiple myeloma (MM) cells and found a novel role of β-catenin in regulating growth and survival of tumor cells. Specifically, inhibition of PKC leads to rapid accumulation of β-catenin by preventing the phosphorylation required for its proteasomal degradation. Microarray analysis and small-interfering RNA (siRNA)–mediated gene silencing in MM cells revealed that accumulated β-ca

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