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

Autor: Grafiati
Publicado: 14 de marzo de 2023

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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 <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 > 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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11

Faruq, Faruq, Davidson Zhao, Jian Wu, Jonahunnatha Nesson George William, Min Zhang, and Hong Chang. "Downregulation of MDM2 Leads to Anti-Proliferative Effects through Activation of p53-Associated Pathway Mediated By Both Dual Inhibitor MX69 and Mir-548c-3p in Multiple Myeloma." Blood 134, Supplement_1 (2019): 4419. http://dx.doi.org/10.1182/blood-2019-129430.

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Multiple myeloma (MM) is a plasma cell malignancy characterized by abnormal proliferation of clonal plasma cells in the bone marrow. MM remains an incurable disease with a high rate of relapse and development of drug resistance. Mouse double minute 2 homolog (MDM2) has been characterized as an oncogene that is associated with cancer development and radio/chemotherapy resistance in cancer. However, the mechanism(s) underlying MDM2 overexpression and its association with drug resistance in MM have not been fully explored. In addition, the effect of the newly discovered dual inhibitor MX69, which
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12

Saha, Manujendra N., Hua Jiang, Yijun Yang, Donna Reece, and Hong Chang. "PRIMA-1Met/APR-246 Displays High Antitumor Activity in Multiple Myeloma By Induction of p73 and Noxa." Molecular Cancer Therapeutics 12, no. 11 (2013): 2331–41. http://dx.doi.org/10.1158/1535-7163.mct-12-1166.

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13

Abdi, Jahangir, Manujendra N. Saha, Mona Sobhani, Qian Shi, and Hong Chang. "Bone Marrow Stromal Cells Induce Bortezomib Resistance Partly through a Transcriptome Modulation in Multiple Myeloma Cells." Blood 124, no. 21 (2014): 3392. http://dx.doi.org/10.1182/blood.v124.21.3392.3392.

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Abstract INTRODUCTION It has been suggested that environment-mediated drug resistance (EMDR) might account for the intrinsic (de novo) resistance to therapy in some myeloma patients developing in early stages of the disease and contribute to acquired drug resistance in the course of treatment. Understanding the mechanisms exploited by bone marroe stromal cells (BMSCs) to generate such resistance has long been sought. Furthermore, knowledge of the role that changes in expression of various genes could play is scanty. In this study we explored how BMSCs could induce resistance to bortezomib and
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14

Nagoshi, Hisao, Tomohiko Taki, Kazuhiro Nishida, et al. "Identification of the Novel Chimeric Gene, PVT1-WWOX, in Multiple Myeloma with 8q24 Abnormality." Blood 120, no. 21 (2012): 1823. http://dx.doi.org/10.1182/blood.v120.21.1823.1823.

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Abstract Abstract 1823 Genetic abnormalities play a crucial role in the pathogenesis of various malignancies, including multiple myeloma (MM). Secondary cytogenetic abnormalities implicated in MM progression include 8q24 rearrangements, gain of the long arm of chromosome 1 (1q+), and loss of the short arm of chromosome 17 (17p-). The 8q24 rearrangements, including MYC and PVT1, have been identified by conventional cytogenetic analysis in 3.5–5.0% of MM patients and by fluorescence in situ hybridization (FISH) and spectral karyotyping (SKY) in 9.5–20%. 8q24 rearrangements are frequently associa
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15

Doudican, Nicole A., Shireen Vali, Shweta Kapoor, et al. "Predictive Simulation Based Design and Validation Of Repurposed Novel Therapeutics With Multi-Target Mechanisms For Multiple Myeloma." Blood 122, no. 21 (2013): 3859. http://dx.doi.org/10.1182/blood.v122.21.3859.3859.

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Abstract Introduction Development of resistance to single agent therapy is a significant clinical obstacle in the treatment of multiple myeloma (MM). Genetic mutations and the bone marrow micro-environment are major determinants of MM resistance mechanisms. Given the complexity of MM, the need for combinatorial therapeutic regimens targeting multiple biological mechanisms of action is pressing. Repurposing has the advantage of using drugs with known clinical history. Methodology We used a predictive simulation-based approach that models MM disease physiology in plasma cells by integrating and
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16

Teoh, Phaik Ju, Chonglei Bi, Chirackal Sintosebastian, Liang Seah Tay, Rafael Fonseca, and Wee Joo Chng. "PRIMA-1 targets the vulnerability of multiple myeloma of deregulated protein homeostasis through the perturbation of ER stress via p73 demethylation." Oncotarget 7, no. 38 (2016): 61806–19. http://dx.doi.org/10.18632/oncotarget.11241.

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17

Robak, Pawel, Anna Linke, Barbara Cebula, Lorenzo M. Leoni, Tadeusz Robak, and Piotr Smolewski. "Cytotoxic Effect of R-Etodolac (SDX-101) in Combination with Purine Analogues or Monoclonal Antibodies on Ex-Vivo B-Cell Chronic Lymphocytic Leukemia Cells." Blood 106, no. 11 (2005): 2122. http://dx.doi.org/10.1182/blood.v106.11.2122.2122.

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Abstract Background: SDX-101 (R-etodolac) is the R isomer of the non-steroidal anti-inflammatory drug Etodolac. SDX-101 decreased the in vitro survival of B-cell chronic lymphocytic leukemia (B-CLL) cells and showed synergistic activity with chlorambucil. In multiple myeloma cells, SDX-101 showed cytotoxic activity and displayed a synergistic cytotoxic effect with dexamethasone. Currently, SDX-101 is being tested in phase II clinical trial for treatment of refractory B-CLL in combination with chlorambucil. Aims: To evaluate the ex-vivo cytotoxic effect of SDX-101 in combination with agents pro
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18

Liao, Chengcheng, Srikanth Talluri, Subodh Kumar, et al. "Base Excision Repair and Homologous Recombination Pathway Intermediates Drive Genomic Instability and Evolution in Myeloma." Blood 136, Supplement 1 (2020): 27–28. http://dx.doi.org/10.1182/blood-2020-141042.

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Multiple myeloma (MM) cells demonstrate significant genomic instability with acquisition of new genomic events over time. In an effort to decipher the pathways utilized by MM cells to genomically evolve and to acquire proliferative advantage as well as develop drug resistance, we have investigated role of various pathway intermediates. Based on our prior results showing elevated homologous recombination (HR) contributing to genomic instability and development of drug resistance, we have further studied RAD51, the key HR gene. Also based on the dysfunctional base excision repair (BER) that can
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19

Lunghi, Paolo, Laura Mazzera, Attilio Corradi, et al. "Arsenic Trioxide (ATO) Interacts Synergistically with MEK Inhibitors to Induce Apoptosis in STI571-Resistant Bcr-Abl Mutants." Blood 114, no. 22 (2009): 2177. http://dx.doi.org/10.1182/blood.v114.22.2177.2177.

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Abstract Abstract 2177 Poster Board II-154 Resistance toward Imatinib and other Bcr-Abl tyrosine kinase inhibitors remains an increasing clinical problem in the treatment of advanced stages of chronic myeloid leukemia. Thus novel therapeutic strategies are needed to address the emerging problem of Imatinib resistance. Previous preclinical studies reported that the MEK inhibitors PD184352 or PD0325901 (Pfizer), strikingly enhances ATO-mediated apoptosis in Acute Myelogenous Leukemia and in Multiple myeloma. The aim of this study was to investigate whether the combined treatment with PD184352 (P
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20

Terragna, Carolina, Marina Martello, Sandra Durante, et al. "High Number of Copy Number Alterations and Over-Expression of Genes Involved in the Response Mechanisms to Genotoxic Stress Both Characterize Newly Diagnosed Multiple Myeloma (MM) Patients Carrying Amplified MDM4 and/or Deleted p53,." Blood 118, no. 21 (2011): 3935. http://dx.doi.org/10.1182/blood.v118.21.3935.3935.

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Abstract Abstract 3935 Background The p53 tumor suppressor pathway is tightly kept in check, or completely silenced in cancer cells. A potent inhibitor of p53 is represented by MDM4, which is critical for the control of p53 activity during the response to stress and is often amplified in several types of cancer. TP53 mutations are rare in newly diagnosed MM, while occur more frequently as late event in the course of the disease and are related to survival. Recently, the adverse prognostic impact of chr. 1q amplification, described in almost 40% of newly diagnosed MM pts, has been reported. The
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21

Gaken, Joop, Louisa Pericleous, Farzin Farzaneh, Ghulam J. Mufti, and Mahvash Tavassoli. "TAT-Apoptin Mediated Induction of Apoptosis in Leukaemic Cells." Blood 108, no. 11 (2006): 1900. http://dx.doi.org/10.1182/blood.v108.11.1900.1900.

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Abstract We have studied the specific targeting of leukaemic cells using the Chicken Anaemia Virus (CAV)-derived protein VP3 (Apoptin) linked to the protein transduction domain (PTD) from HIV TAT with the aim of using this strategy for in vitro purging. Apoptin is a 13.6 kDa protein which induces apoptosis specifically in cancer cells whilst leaving normal cells unaffected. Expression of Apoptin in normal cells results in its cytoplasmic localisation. In tumour cells Apoptin resides initially in the cytoplasm and subsequently translocates to the nucleus and induces apoptosis. Apoptin is phosph
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Laane, Edward, Purushothama Nanjappa, Subodh Kumar, et al. "XRCC5 Plays an Important Role in Homologous Recombination, Genome Stability and Survival of Myeloma Cells." Blood 126, no. 23 (2015): 1218. http://dx.doi.org/10.1182/blood.v126.23.1218.1218.

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Abstract Understanding mechanisms underlying genomic instability is critical in delineating pathogenesis and development of new treatments for prevention and treatment of cancer. We have previously shown that dysregulated homologous recombination (HR) significantly contributes to genomic instability and progression in multiple myeloma (MM). To identify the regulators of HR and genome stability in MM, we conducted a functional shRNA screen and identified XRCC5 (Ku80) as a novel regulator of HR in MM cells. XRCC5 has been known to work as part of DNA ligase IV-XRCC4 complex in the repair of DNA
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23

Mello, Mariana Rezende Bandeira, Dulcinéia Martins Albuquerque, Krizzia Borges Albanez, et al. "Chromatin Texture and Molecular Features Are Independent Prognostic Factors In AML." Blood 116, no. 21 (2010): 4850. http://dx.doi.org/10.1182/blood.v116.21.4850.4850.

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Abstract Abstract 4850 Introduction: The WHO 2008 classification of acute myeloid leukemia (AML) is based on morphology, cytogenetics and molecular features. Among them, mutations and internal tandem duplications of FLT3 in AML with a normal karyotype have been associated to a poor prognosis. Mutated NPM1 in the absence of FLT3-ITD is associated to a favorable. On the other hand, variables of nuclear chromatin texture have been described as independent risk factors in several malignancies (ALL, melanoma and multiple myeloma). Aim: To compare the influence on overall survival of the chromatin f
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24

Martínez-Baños, Déborah, Beatríz Sánchez-Hernández, Guadalupe Jiménez, Georgina Barrera-Lumbreras, and Olga Barrales-Benítez. "Global methylation and promoter-specific methylation of the P16, SOCS-1, E-cadherin, P73 and SHP-1 genes and their expression in patients with multiple myeloma during active disease and remission." Experimental and Therapeutic Medicine 13, no. 5 (2017): 2442–50. http://dx.doi.org/10.3892/etm.2017.4274.

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Levy, Daphna, Amos M. Cohen, and Jeremy Don. "Dual Role of Pim-2 Depends on the Associated Proteome." Blood 108, no. 11 (2006): 4334. http://dx.doi.org/10.1182/blood.v108.11.4334.4334.

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Abstract Pim-2, a Ser/Thr kinase, is a proto-oncogene originally identified as common proviral insertion sites in T and B cell lymphomas in mice. Deregulation of Pim-2 expression has been documented in several human malignancies, including leukemia, lymphoma, multiple myeloma and prostate cancer. In human non-Hodgkin’s lymphomas and in chronic lymphocytic leukemia Pim-2 is up-regulated and its expression correlates with disease activity. Pim-2 promotes cell survival in response to a wide variety of proliferative signals. Pim-2 promotes cell survival by phosphorylation of Bad and Cot. The goal
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26

Paydas, S., B. Sahin, E. Seyrek, and S. Zorludemir. "p53 mutations in multiple myeloma." Molecular Pathology 50, no. 6 (1997): 329. http://dx.doi.org/10.1136/mp.50.6.329-a.

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27

Teoh, P. J., and W. J. Chng. "p53 Abnormalities and Potential Therapeutic Targeting in Multiple Myeloma." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/717919.

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p53 abnormalities are regarded as an independent prognostic marker in multiple myeloma. Patients harbouring this genetic anomaly are commonly resistant to standard therapy. Thus, various p53 reactivating agents have been developed in order to restore its tumour suppressive abilities. Small molecular compounds, especially, have gained popularity in its efficacy against myeloma cells. For instance, promising preclinical results have steered both nutlin-3 and PRIMA-1 into phase I/II clinical trials. This review summarizes different modes of p53 inactivation in myeloma and highlights the current p
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28

Sundan, Anders, Torstein B. Ro, Janne Bonhorst, Anders Waage, and Magne Borset. "Bmps(Bone Morphogenetic Proteins) Inhibit Growth in Multiple Myeloma Cells by p53 Activation." Blood 104, no. 11 (2004): 3354. http://dx.doi.org/10.1182/blood.v104.11.3354.3354.

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Abstract Only a few naturally occurring cytokines are able to inhibit myeloma cell growth, and among them BMP-4 is a potent inhibitor of growth as well as an inductor of apoptosis in myeloma cells. To study the mechanism behind BMP-4-induced growth inhibition, we performed gene expression profiling by microarrays in two human myeloma cell lines after BMP-4 stimulation for 4 hours. We found that BMP-4 upregulated several known p53 target genes like p21/Cip1, Bax, cyclin G, Gadd45 and dual specificity phosphatases, suggesting a role for p53 in BMP-mediated growth inhibition of myeloma cells. p53
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29

Yang, Yonghui, Joseph Gera, and Alan Lichtenstein. "Targeting Deptor in Multiple Myeloma." Blood 120, no. 21 (2012): 575. http://dx.doi.org/10.1182/blood.v120.21.575.575.

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Abstract Abstract 575 DEPTOR is an mTOR binding protein specifically over-expressed in some genetic subtypes of multiple myeloma (MM). DEPTOR binds mTOR in TORC1 and TORC2 complexes and inhibits their kinase activity. As a result, p70 and 4E-BP1 phosphorylation, substrates of TORC1, are decreased. However, TORC1/p70 down-regulation results in marked feedback activation of the PI3K/AKT pathway and AKT becomes activated even though DEPTOR restrains TORC2. Most importantly, DEPTOR knockdown is deleterious to over-expressing MM cell lines, resulting in apoptosis. We hypothesized that compounds pre
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30

Owen, R. G., S. A. Davis, J. Randerson, et al. "p53 gene mutations in multiple myeloma." Molecular Pathology 50, no. 1 (1997): 18–20. http://dx.doi.org/10.1136/mp.50.1.18.

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31

Markovic, Olivera, Dragomir Marisavljevic, Vesna Cemerikic, Maja Perunicic, and Milica Colovic. "The expression of p53 protein in patients with multiple myeloma." Srpski arhiv za celokupno lekarstvo 135, no. 1-2 (2007): 43–47. http://dx.doi.org/10.2298/sarh0702043m.

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Introduction: Although mutations of p53 are one of the most often acquired genetic changes in malignant tumors, these mutations are rare events in patients with newly diagnosed multiple myeloma (MM). Moreover, there are a few literature data about clinical significance of p53 overexpression in multiple myeloma. Objective The aim of our study was to evaluate the clinical significance of p53 immunoexpression in multiple myeloma. Method A total of 58 patients with newly diagnosed MM (26 females and 32 males, mean age 62 years) were enrolled in the study. The diagnosis of MM was made according to
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32

Stühmer, Thorsten, Manik Chatterjee, Martin Hildebrandt, et al. "Nongenotoxic activation of the p53 pathway as a therapeutic strategy for multiple myeloma." Blood 106, no. 10 (2005): 3609–17. http://dx.doi.org/10.1182/blood-2005-04-1489.

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AbstractMutation of p53 is a rare event in multiple myeloma, but it is unknown if p53 signaling is functional in myeloma cells, and if targeted nongenotoxic activation of the p53 pathway is sufficient to kill tumor cells. Here, we demonstrate that treatment of primary tumor samples with a small-molecule inhibitor of the p53–murine double minute 2 (MDM2) interaction increases the level of p53 and induces p53 targets and apoptotic cell death. Significantly, given the importance of the bone marrow microenvironment for the support and drug resistance of myeloma cells, tumor cells undergo effective
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33

Stühmer, Thorsten, Angela Zöllinger, Manik Chatterjee, Kurt Bommert, and Ralf C. Bargou. "Selective Induction of the p53-Pathway as Treatment for Multiple Myeloma." Blood 106, no. 11 (2005): 3382. http://dx.doi.org/10.1182/blood.v106.11.3382.3382.

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Abstract The p53 pathway is central to cellular defences against neoplastic transformation, and mutations that impair p53 function are prominent oncogenic events. However, certain malignancies, such as multiple myeloma (MM), rarely present with p53 defects except in late stages. MM might therefore be vulnerable to p53 induction therapy, but it is unknown if the p53 pathway remains actually functional in this disease, and if it can be sufficiently well triggered to induce tumor cell death. We have used nutlin-3, a newly developed small-molecule antagonist against the p53 suppressor murine doubl
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34

Turner, Joel G., Jana L. Dawson, Steven Grant, et al. "Melphalan and XPO1 Inhibitor Combination Therapy for the Treatment of Multiple Myeloma." Blood 124, no. 21 (2014): 2084. http://dx.doi.org/10.1182/blood.v124.21.2084.2084.

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Abstract Introduction High-dose melphalan chemotherapy with autologous stem cell transplant remains the standard of care for the treatment of multiple myeloma. However, patients eventually develop drug resistance and die from progressive disease despite the introduction of therapies using proteosome inhibitors (PIs) and immunomodulatory drugs (IMIDs). The incurable nature of multiple myeloma clearly demonstrates the need for novel agents and treatments. Here, our aim was to investigate whether the use of XPO1 (exportin 1, CRM1) inhibitors (XPO1i) could sensitize de novo and acquired drug-resis
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35

Ikeda, H., T. Hideshima, G. Perrone, et al. "Effect of the specific P53 stabilizer CBS9106 on multiple myeloma (MM)." Journal of Clinical Oncology 27, no. 15_suppl (2009): 8601. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.8601.

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8601 Background: The mutations of P53 tumor suppressor protein are associated with progressive in Multiple Myeloma (MM), conversely, stabilization of P53 leads to cell cycle arrest and apoptosis. In this study, we examined p53 protein expression and demonstrated the effect of P53 stabilization using a novel specific P53 stabilizer CBS9106 in MM. Method: We examined P53 protein expression using Immunoblot analysis, as well as the growth inhibitory effect of CBS9106 in MM cell lines and primary tumor cells from MM patients. We also defined whether CBS9106 can overcome the growth promoting effect
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36

Kumar, Shaji, Michael Timm, Michael P. Kline, et al. "Mi-63, a Small Molecule Inhibitor of MDM2-p53 Interaction, Has Significant In Vitro Activity in Multiple Myeloma." Blood 108, no. 11 (2006): 3464. http://dx.doi.org/10.1182/blood.v108.11.3464.3464.

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Abstract Background: Multiple myeloma (MM) is a plasma cell proliferative disorder that results in considerable morbidity and mortality. As it is incurable with the current therapeutic approaches, more effective therapies based on better understanding of the pathobiology of the disease are needed. In MM, malignant plasma cells are characterized by low proliferative and apoptotic rates compared to other malignancies. The tumor suppressor gene p53, responsible for induction of cellular apoptosis in response to genotoxic stimuli, is relatively intact in most cases of myeloma. However, p53 mutatio
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37

Sagawa, Morihiko, Hiroto Ohguchi, Takeshi Harada, et al. "Targeting Ribonucleotide Reductase M1 and M2 in Multiple Myeloma." Blood 128, no. 22 (2016): 360. http://dx.doi.org/10.1182/blood.v128.22.360.360.

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Abstract Ribonucleotide reductase (RR) is an enzyme that catalyzes the conversion of ribonucleotide diphosphate to deoxyribonucleotide diphosphate and is essential for de novo DNA synthesis, DNA repair, and cell growth. RR primarily exists as a heterodimer tetramer composed of regulatory subunit RRM1, and catalytic subunit RRM2. Overexpression or polymorphisms of RR are described non-small cell lung, pancreas, breast, and ovarian cancers. Moreover, RRM1 and RRM2 expression is highly correlated with patient survival in non-small cell lung and pancreas cancers. To date, the biologic significance
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38

Drach, Johannes, Jutta Ackerman, Hannes Kaufmann, Robert Königsberg, and Heinz Huber. "Deletions Of The p53 Gene In Multiple Myeloma." British Journal of Haematology 108, no. 4 (2000): 886. http://dx.doi.org/10.1046/j.1365-2141.2000.01908.x.

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39

Vadikoliou, C., C. Lalayianni, A. Papalexadri, et al. "P073 Treatment-related AML/MDS in multiple myeloma." Leukemia Research 33 (May 2009): S101. http://dx.doi.org/10.1016/s0145-2126(09)70153-5.

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40

Teoh, P. J., T. H. Chung, S. Sebastian, et al. "p53 haploinsufficiency and functional abnormalities in multiple myeloma." Leukemia 28, no. 10 (2014): 2066–74. http://dx.doi.org/10.1038/leu.2014.102.

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41

Nardiello, Tricia, Achim A. Jungbluth, Anna Mei, et al. "MAGE-A Inhibits Apoptosis In Proliferating Multiple Myeloma Cells." Blood 116, no. 21 (2010): 785. http://dx.doi.org/10.1182/blood.v116.21.785.785.

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Abstract Abstract 785 The type I Melanoma Antigen GEne (MAGE) MAGE-A3 is commonly present in primary multiple myeloma cells and its expression is correlated with advanced disease and proliferation. MAGE-A3 belongs to the Cancer-Testis antigen (CTAg) family of tumor-associated proteins, which are present in many cancers, but their normal expression is limited to developing germ cells and placental trophoblast. This unique expression pattern fuels speculation on a role for CTAg in oncogenesis; however, very little is known about their function. In gene expression analyses of primary myeloma cell
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42

Chng, W. J., T. Price-Troska, S. Van Wier, et al. "Clinical and biological implication of defective p53 pathway in multiple myeloma (MM)." Journal of Clinical Oncology 24, no. 18_suppl (2006): 17516. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.17516.

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17516 Background: The p53 tumor suppressor is commonly inactivated by mutations. Even in tumors without mutations, there are defects in the response to p53 activation. In MM, the prognostic significance of p53 mutation is unknown, while there has been no systematic study of p53 function. We seek to address these issues in this study. Methods: p53 mutation was studied by conformation sensitive gel electrophoresis with primers encompassing exons 1 to 10 followed by sequencing of DNA fragments with altered electrophoretic pattern in newly diagnosed MM patients entered into ECOG E9486 trial where
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43

Coyne, Mark R. E., Seán Naughton, Patrick J. Hayden, Alessia Montagnoli, Michael E. O'Dwyer, and Corrado Santocanale. "Targeting Cdc7 Kinase in Multiple Myeloma." Blood 114, no. 22 (2009): 3847. http://dx.doi.org/10.1182/blood.v114.22.3847.3847.

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Abstract Abstract 3847 Poster Board III-783 Introduction Myeloma remains an incurable cancer and the development of new therapeutic approaches is of fundamental importance. A key feature of progressive myeloma is deregulation of the mechanisms that control progression through the cell cycle, in particular, the increase in the activity of S-phase promoting factors and the loss of cell cycle brakes such as the tumour suppressor protein p53. Moreover, high expression of Mcl-1, a potent anti-apoptotic Bcl2 family member, and defects in the p53 pathway are now known to be instrumental in inhibiting
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44

Zhuang, Junling, Fazal Shirazi, Ram Kumar Singh, et al. "Ubiquitin-activating enzyme inhibition induces an unfolded protein response and overcomes drug resistance in myeloma." Blood 133, no. 14 (2019): 1572–84. http://dx.doi.org/10.1182/blood-2018-06-859686.

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Abstract Three proteasome inhibitors have garnered regulatory approvals in various multiple myeloma settings; but drug resistance is an emerging challenge, prompting interest in blocking upstream components of the ubiquitin-proteasome pathway. One such attractive target is the E1 ubiquitin-activating enzyme (UAE); we therefore evaluated the activity of TAK-243, a novel and specific UAE inhibitor. TAK-243 potently suppressed myeloma cell line growth, induced apoptosis, and activated caspases while decreasing the abundance of ubiquitin-protein conjugates. This was accompanied by stabilization of
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45

John, Lukas, Maria Theresa Krauth, Klaus Podar, and Marc-Steffen Raab. "Pathway-Directed Therapy in Multiple Myeloma." Cancers 13, no. 7 (2021): 1668. http://dx.doi.org/10.3390/cancers13071668.

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Multiple Myeloma (MM) is a malignant plasma cell disorder with an unmet medical need, in particular for relapsed and refractory patients. Molecules within deregulated signaling pathways, including the RAS/RAF/MEK/ERK, but also the PI3K/AKT-pathway belong to the most promising evolving therapeutic targets. Rationally derived compounds hold great therapeutic promise to target tumor-specific abnormalities rather than general MM-associated vulnerabilities. This paradigm is probably best depicted by targeting mutated BRAF: while well-tolerated, remarkable responses have been achieved in selected pa
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46

Stanganelli, Carmen, Jorge Arbelbide, Juliana Zimerman, Dorotea Beatriz Fantl, Claudia Corrado, and Irma Slavutsky. "Aberrant Gene Promoter Methylation of Tumor Suppressor Genes in Plasma Cell Disorders." Blood 110, no. 11 (2007): 2487. http://dx.doi.org/10.1182/blood.v110.11.2487.2487.

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Abstract There is increasing evidence that, in addition to genetic aberrations, epigenetic processes play a major role in carcinogenesis. Particularly, hypermethylation of CpG islands of the promoter regions of tumor suppressor genes (TSG) is now considered as an important epigenetic mechanism for gene inactivation. Multiple myeloma (MM) is characterized by neoplastic proliferation of monoclonal plasma cells. The natural course of disease may progress through monoclonal gammopathy of undetermined significance (MGUS) to MM. During this process, multiple genetic alterations are sequentially acqu
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47

Munawar, Umair, Santiago Barrio, Markus Roth, et al. "Implications of TP53 alterations for Therapy Response in Multiple Myeloma." Blood 132, Supplement 1 (2018): 3189. http://dx.doi.org/10.1182/blood-2018-99-118658.

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Abstract Deletion of the tumor suppressor gene TP53is significantly associated with an unfavorable clinical course of Multiple Myeloma (MM). In addition, point mutations that abrogate p53 function similarly shorten survival. Most recently 'double hit', bi-allelic TP53inactivated MM was identified as an ultimate high risk feature of MM, affecting 3.7% of newly diagnosed MM patients (NDMM, Walker et al., Leukemia 2018). For TP53genetic analysis we combined data from two targeted sequencing M3P cohorts with targeted sequencing and FISH data, one of NDMM (n=142, Kortüm et al. Blood Cancer J. 2016)
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48

Liu, Qun, and Yair Gazitt. "Potentiation of dexamethasone-, paclitaxel-, and Ad-p53–induced apoptosis by Bcl-2 antisense oligodeoxynucleotides in drug-resistant multiple myeloma cells." Blood 101, no. 10 (2003): 4105–14. http://dx.doi.org/10.1182/blood-2002-10-3067.

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Abstract Overexpression of Bcl-2 in myeloma cells results in resistance to drugs such as dexamethasone (DEX), adenovirus-mediated delivery of p53 (Ad-p53), and paclitaxel (TAX), which work through the intrinsic apoptotic pathway. Bcl-2 antisense oligodeoxynucleotides (Bcl-2-ASO) have been shown to induce apoptosis in cancer cells, as a single agent or, better, in combination with chemotherapy. We hypothesized that down-regulation of Bcl-2 by Bcl-2-ASO will sensitize drug-resistant myeloma cells to undergo apoptosis. In this paper we report a detailed time/dose study of the effect of Bcl-2-ASO
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49

Preudhomme, Claude, Thierry Facon, Marc Zandecki, et al. "Rare occurrence of P53 gene mutations in multiple myeloma." British Journal of Haematology 81, no. 3 (1992): 440–43. http://dx.doi.org/10.1111/j.1365-2141.1992.tb08253.x.

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50

Ortega, Manoela M., Helen N. Honma, Lair Zambon, et al. "GSTM1 and codon 72 P53 polymorphism in multiple myeloma." Annals of Hematology 86, no. 11 (2007): 815–19. http://dx.doi.org/10.1007/s00277-007-0347-x.

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