Relevant bibliographies by topics / Peripheral neuropathy, murine models, bortezomib, multiple myeloma

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Peripheral neuropathy, murine models, bortezomib, multiple myeloma'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "Peripheral neuropathy, murine models, bortezomib, multiple myeloma"

1

Berenson, James R., Ori Yellin, Ravi Patel, et al. "A Phase II Study of Pegylated Liposomal Doxorubicin, Bortezomib and Dexamethasone (DVD) for Patients with Previously Untreated Multiple Myeloma (MM)." Blood 114, no. 22 (2009): 4936. http://dx.doi.org/10.1182/blood.v114.22.4936.4936.

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Abstract Abstract 4936 Despite recent advances in the treatment of MM, the disease remains incurable and many of the most effective, newer combination therapies are accompanied by significant side effects that have a major negative impact on the patient's quality of life. Pegylated liposomal doxorubicin (PLD) and bortezomib have shown anti-MM efficacy in the laboratory and for the treatment of previously treated MM patients, leading to FDA approval for patients who have failed one prior therapy. Using our severe combined immunodeficiency-hu murine models of human MM, we have previously demonst
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Dave, Ami Atulkumar, Jaime K. Lewis, and Agne Paner. "Retrospective review of chronic pain causes and management in multiple myeloma patients." Journal of Clinical Oncology 38, no. 15_suppl (2020): e20552-e20552. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e20552.

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e20552 Background: The survival of patients with multiple myeloma has improved dramatically since the introduction of proteasome inhibitors such as bortezomib, which can have the adverse effect of peripheral neuropathy. This study retrospectively examines causes of chronic pain in myeloma patients and the modalities and duration of treatments used for pain control. Methods: Rush University Medical Center multiple myeloma patients who were diagnosed and treated between 2000-2019 were included. Outcome measures were abstracted from the medical record and included: classes of pain medication used
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Mavis, Cory, Juan Gu, Joseph Skitzki, Francisco Hernandez, and Myron S. Czuczman. "Ixazomib, An Investigational Orally Bioavailable Proteasome Inhibitor, Increases p21 Expression Inducing Caspase-Dependent Cell Death, Cell-Cycle Arrest, and In B-Cell Lymphoma Pre-Clinical Models." Blood 122, no. 21 (2013): 1828. http://dx.doi.org/10.1182/blood.v122.21.1828.1828.

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Abstract Pharmacological inhibition of the proteasome with bortezomib (BTZ) has translated into an improved clinical outcome in patients with multiple myeloma and mantle cell lymphoma. Despite the observed clinical activity, BTZ anti-tumor activity in B-cell lymphoma has been partially hindered by treatment-related toxicities (peripheral neuropathy) preventing further dose escalation and emergence of acquired resistance. To further develop therapeutic strategies targeting the proteasome system, we studied the anti-tumor activity and mechanisms-of-action of ixazomib (MLN2238), a reversible prot
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Uy, Geoffrey L., Matthew S. Holt, Nicholas M. Fisher, et al. "Bortezomib Alters Peripheral Blood Lymphocyte Subsets in Patients with Multiple Myeloma." Blood 106, no. 11 (2005): 2387. http://dx.doi.org/10.1182/blood.v106.11.2387.2387.

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Abstract Bortezomib (VELCADE®) is a potent inhibitor of the proteasome which exerts its antimyeloma effect in part by blocking the activation of NF-κB. As NF-κB is critical for lymphocyte development and survival, there is great interest in harnessing the potential immunomodulatory effects of bortezomib. In murine hematopoietic transplantation models, bortezomib inhibits in vitro mixed lymphocyte responses and promotes the apoptosis of alloreactive T cells protecting against acute graft-versus-host disease. However, no data exists on the in vivo effects of bortezomib on human T cells. To chara
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5

Zhou, Jialin, Hanheng Mai, Yunqing Liu, et al. "Genetic Insusceptibility Mediated Inflammation Contributes to Bortezomib-Induced Peripheral Neuropathy." Blood 144, Supplement 1 (2024): 1961. https://doi.org/10.1182/blood-2024-201966.

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Introduction: Chemotherapy-induced peripheral neuropathy (CIPN) is a disabling pain condition resulting from chemotherapy for cancer. CIPN-inducing drug bortezomib is widely used in multiple myeloma (MM) treatment. The pathogenesis of bortezomib-induced peripheral neuropathy (BIPN) is poorly understood. Our study reported here elucidates the murine transcriptomic modifications in oxaliplatin- and cisplatin-induced CIPN and whole exome sequencing (WES) features in MM patients with BIPN. Methods: RNA sequencing (RNA-seq) data of murine spinal cords were retrieved under the GEO accession numbers
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Anchoori, Ravi K., Vidyasagar Anchoori, Brandon Lam, et al. "Development and anticancer properties of Up284, a spirocyclic candidate ADRM1/RPN13 inhibitor." PLOS ONE 18, no. 6 (2023): e0285221. http://dx.doi.org/10.1371/journal.pone.0285221.

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Bortezomib has been successful for treatment of multiple myeloma, but not against solid tumors, and toxicities of neuropathy, thrombocytopenia and the emergence of resistance have triggered efforts to find alternative proteasome inhibitors. Bis-benzylidine piperidones such as RA190 covalently bind ADRM1/RPN13, a ubiquitin receptor that supports recognition of polyubiquitinated substrates of the proteasome and their subsequent deububiqutination and degradation. While these candidate RPN13 inhibitors (iRPN13) show promising anticancer activity in mouse models of cancer, they have suboptimal drug
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7

Kuhn, Deborah J., Sally A. Hunsucker, Qing Chen, Peter M. Voorhees, Marian Orlowski, and Robert Z. Orlowski. "Targeted inhibition of the immunoproteasome is a potent strategy against models of multiple myeloma that overcomes resistance to conventional drugs and nonspecific proteasome inhibitors." Blood 113, no. 19 (2009): 4667–76. http://dx.doi.org/10.1182/blood-2008-07-171637.

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Abstract Proteasome inhibition is a validated strategy for therapy of multiple myeloma, but this disease remains challenging as relapses are common, and often associated with increasing chemoresistance. Moreover, nonspecific proteasome inhibitors such as bortezomib can induce peripheral neuropathy and other toxicities that may compromise the ability to deliver therapy at full doses, thereby decreasing efficacy. One novel approach may be to target the immunoproteasome, a proteasomal variant found predominantly in cells of hematopoietic origin that differs from the constitutive proteasome found
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8

Ikeda, Hiroshi, Teru Hideshima, Mariateresa Fulciniti та ін. "PI3K/p110δ is a novel therapeutic target in multiple myeloma". Blood 116, № 9 (2010): 1460–68. http://dx.doi.org/10.1182/blood-2009-06-222943.

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In this study, we demonstrate expression and examined the biologic sequelae of PI3K/p110δ signaling in multiple myeloma (MM). Knockdown of p110δ by small interfering RNA caused significant inhibition of MM cell growth. Similarly, p110δ specific small molecule inhibitor CAL-101 triggered cytotoxicity against LB and INA-6 MM cell lines and patient MM cells, associated with inhibition of Akt phosphorylation. In contrast, CAL-101 did not inhibit survival of normal peripheral blood mononuclear cells. CAL-101 overcame MM cell growth conferred by interleukin-6, insulin-like growth factor-1, and bone
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Steinberg, Jeffrey A., Jing Shen, Eric Sanchez, et al. "Alpha Lipoic Acid (ALA) Inhibits the Anti-Myeloma Effects of Bortezomib." Blood 114, no. 22 (2009): 3832. http://dx.doi.org/10.1182/blood.v114.22.3832.3832.

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Abstract Abstract 3832 Poster Board III-768 Introduction ALA is an antioxidant often used in the management of peripheral neuropathy (PN) for patients with multiple myeloma (MM). A clinical trial evaluating ALA in diabetic neuropathy showed this drug to be effective for patients with both somatic and autonomic neuropathies. It also normalized the endoneural blood flow, reduced oxidative stress and improved vascular dysfunction. Bortezomib (Velcade®), the first-in-class proteasome inhibitor (PI), which is approved for the treatment of patients with MM, may cause PN. As a result, patients are of
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10

Moreau, Philippe, Asher A. Chanan-Khan, Andrew W. Roberts, et al. "Venetoclax Combined with Bortezomib and Dexamethasone for Patients with Relapsed/Refractory Multiple Myeloma." Blood 128, no. 22 (2016): 975. http://dx.doi.org/10.1182/blood.v128.22.975.975.

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Abstract Background: BCL-2 and MCL-1 promote multiple myeloma (MM) cell survival. Venetoclax (VEN) is a potent, selective, orally bioavailable small-molecular inhibitor of BCL-2. When combined with bortezomib, which can inhibit MCL-1, VEN can enhance the activity of bortezomib in MM cell lines and xenograft models. Methods: In this Phase 1b, open label, dose escalation study, patients with relapsed/refractory (R/R) MM received daily VEN (50 - 1200 mg per designated dose cohort) with bortezomib and dexamethasone. The objectives of the study were to assess the safety, pharmacokinetics, maximum t
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Dissertations / Theses on the topic "Peripheral neuropathy, murine models, bortezomib, multiple myeloma"

1

SALA, BARBARA. "Caratterizzazione neurofisiologica, neuropatologica e comportamentale della neuropatia periferica da Bortezomib in moldelli murini." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/49728.

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In the last 20 years several in vivo rat models of peripheral neuropathy induced by antineoplastic drugs clarified the phatophysiological mechanisms involved in peripheral neurotoxicity. Moreover these models allowed to identify neuroprotection strategies for preventing sensory nerve and dorsal root ganglia (DRG) neurons damages. Only a few cancer cell lines is able to induce the development of cancer in immunocompetent rats, therefore these models do not represent the best way to investigate, at the same time, the antineoplastic activity and the neurotoxic effects of these drugs; by contr
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