Mechanisms of peripheral neuropathy associated with bortezomib and vincristine in patients with newly diagnosed multiple myeloma: a prospective analysis of data from the HOVON-65/GMMG-HD4 trial

Broyl, Annemiek; Corthals, Sophie L.; Jongen, Joost L.M.; Holt, Bronno van der; Kuiper, Rowan; Knegt, Yvonne de; Duin, Mark van; Jarari, Laila el; Bertsch, Uta; Lokhorst, Henk M.; Durie, Brian G.M.; Goldschmidt, Hartmut; Sonneveld, Pieter

doi:10.1016/s1470-2045(10)70206-0

Cited by 206 publications

(157 citation statements)

References 27 publications

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“…The selected SNPs of FOS gene were also studied in Chinese patients with high myopia, and the obtained data indicated that they are scarcely to be important in predisposing humans to high myopia [51]. In case of JUN rs11688 SNP, Broyl et al presented its association with bortezomib-induced and vincristine-induced peripheral neuropathy [52]. At present no study reported association of IER5 polymorphisms and diseases.…”

Section: Citationmentioning

confidence: 99%

Variations in Immediate-early Genes Encoding c-Fos, c-Jun and IER5 Transcription Factors are Associated with Ischemic Stroke

G¹

2015

Adv Genet Eng

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Transcription factors make a great contribution in the regulation of mechanisms, which are involved in the preand post-stroke events. The main goal of the current study was to evaluate the potential association of single nucleotide polymorphisms FOS (rs7101, rs1063169), JUN (rs11688) and IER5 (rs6425663) with ischemic stroke in Armenian population. A total 161 patients with ischemic stroke and 165 controls were involved in this study. Transcription factors were genotyped using polymerase chain reaction with sequence-specific primers (PCR-SSP). Association of genotype, allelic and carriage frequencies with ischemic stroke was assessed using Pearson's Chisquare test. Multiple test corrected p values less than 0.05 were considered significant. The data obtained demonstrated a significant negative association between the FOS rs1063169*T, JUN rs11688*A and IER5 rs6425663*T minor alleles with ischemic stroke. On the other hand, the frequency distribution of rs7101*T minor allele of FOS gene and its carriage rate in the group of patients were significantly higher than in controls. Our results indicate that the minor alleles of FOS rs1063169, JUN rs11688 and IER5 rs6425663 SNPs can be considered as protective against ischemic stroke, whereas the minor allele of FOS rs7101 SNP represents a risk factor for this disease.

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Section: Citationmentioning

confidence: 99%

Variations in Immediate-early Genes Encoding c-Fos, c-Jun and IER5 Transcription Factors are Associated with Ischemic Stroke

G¹

2015

Adv Genet Eng

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“…20,21 Most recently, very promising data on bortezomib as consolidation and maintenance therapy are emerging both in patients not receiving transplantation 22,23 and in transplantation patients. 24,25 Its ability to maintain efficacy but markedly reduce attendant neuropathy when used weekly 26 or subcutaneously 27 has also been shown. Gene profiling can define signatures predictive of response 12 and for the development of neuropathy 25 to bortezomib.…”

Section: Development Of Next-generation Agents Targeting the Tumor Cementioning

confidence: 99%

“…24,25 Its ability to maintain efficacy but markedly reduce attendant neuropathy when used weekly 26 or subcutaneously 27 has also been shown. Gene profiling can define signatures predictive of response 12 and for the development of neuropathy 25 to bortezomib. In addition, functional assays can be used to show that MM cells with high proteasome load and low proteasome capacity have high proteasome stress and are therefore susceptible to proteasome inhibition.…”

Section: Development Of Next-generation Agents Targeting the Tumor Cementioning

confidence: 99%

New Insights into Therapeutic Targets in Myeloma

Anderson

2011

Hematology

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Patient outcome in multiple myeloma (MM) has been remarkably improved due to the use of combination therapies including proteasome inhibitors and immunomodulatory drugs, which target the tumor in its BM microenvironment. Ongoing efforts to improve the treatment paradigm even further include using oncogenomics to better characterize molecular pathogenesis and to develop refined patient stratification and personalized medicine in MM; using models of MM in its BM milieu to identify novel targets and to validate next-generation therapeutics directed at these targets; developing immune-based therapies including mAbs, immunotoxins targeting MM cells and cytokines, and novel vaccine strategies; and using functional oncogenomics to inform the design of novel combination therapies. With continued rapid evolution of progress in these areas, MM will be a chronic illness with sustained complete response in a significant number of patients.

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“…Administration of bortezomib leads to intracytoplasmatic vacuolization in dorsal root ganglia (DRG) satellite cells, probably due to mitochondrial and endoplasmic reticulum enlargement [24]. All these intracellular modifications are probably related to the ability of bortezomib to activate mitochondrial-based apoptotic pathways, including activation of caspases [25] and dysregulation of calcium homeostasis [26]. Inhibitors of the mitochondrial electron transport chain (mETC) attenuate mechanical hyperalgesia in both CIPN models and after tumor necrosis factor-(TNF-) treatment [17].…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, it has been demonstrated that the antioxidant agent -lipoic acid, by regulating essential mitochondrial proteins with antioxidant and chaperone properties, exerts neuroprotective effects against chemotherapy-induced neurotoxicity in sensory neurons [27]. Finally, significant changes in the expression of various genes, including those controlling mitochondrial dysfunction associated with vincristine-and bortezomib-evoked peripheral neuropathy, have been demonstrated in humans [25].…”

Section: Introductionmentioning

confidence: 99%

Transient Receptor Potential Channels in Chemotherapy-Induced Neuropathy

Nassini¹,

Benemei²,

Fusi³

et al. 2013

TOPAINJ

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Chemotherapy-Induced Peripheral Neuropathy (CIPN) is a common dose-limiting side effect of many chemotherapeutic drugs, including platinum-based compounds (e.g., cisplatin and oxaliplatin), taxanes (e.g., paclitaxel), vinca alkaloids (e.g., vincristine), and the first-in-class proteasome inhibitor, bortezomib. Among the various sensory symptoms of CIPN, paresthesia, dysesthesia, spontaneous pain, and mechanical and thermal hypersensitivity are prominent. Inflammation, oxidative stress, loss of intraepidermal nerve fibers, modifications of mitochondria, and various ion channels alterations are part of the several mechanisms contributing to CIPN. Because attempts to mitigate chemotherapeutic-induced acute neuronal hyperexcitability and the subsequent peripheral neuropathy have yielded unsatisfactory results, a more in-depth understanding of the mechanism(s) responsible for the neurotoxic action of anticancer drugs is required.Some members of the transient receptor potential (TRP) family of channels, as the TRPV1 and TRPV4 (vanilloid), TRPA1 (ankyrin) and TRPM8 (melastatin) are expressed on the plasma membrane of primary sensory neurons (nociceptors), where they are activated by an unprecedented series of physical and chemical stimuli. There is evidence that TRPV1, TRPV4, TRPA1 and TRPM8 are prominent contributors of mechanical and thermal hypersensitivity in models of CIPN. In particular, in vitro and in vivo studies have pointed out the unique role of TRPA1 and oxidative stress in the mechanism responsible for cold and mechanical hyperalgesia in rodent models of CIPN.

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Mechanisms of peripheral neuropathy associated with bortezomib and vincristine in patients with newly diagnosed multiple myeloma: a prospective analysis of data from the HOVON-65/GMMG-HD4 trial

Cited by 206 publications

References 27 publications

Variations in Immediate-early Genes Encoding c-Fos, c-Jun and IER5 Transcription Factors are Associated with Ischemic Stroke

Variations in Immediate-early Genes Encoding c-Fos, c-Jun and IER5 Transcription Factors are Associated with Ischemic Stroke

New Insights into Therapeutic Targets in Myeloma

Transient Receptor Potential Channels in Chemotherapy-Induced Neuropathy

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