Meta-analysis of clinical trials comparing the efficacy and safety of liposomal cisplatin versus conventional nonliposomal cisplatin in nonsmall cell lung cancer (NSCLC) and squamous cell carcinoma of the head and neck (SCCHN)

Xu, Bei; Zeng, Min; Zeng, Jiawei; Feng, Jiafu; Yu, Lin

doi:10.1097/md.0000000000013169

Cited by 28 publications

(16 citation statements)

References 21 publications

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“…First, platinum‐compounds are being formed with novel attached side groups (eg, phenanthriplatin), which cause diverse DNA adducts less susceptible to known mechanisms of drug resistance. Second, new platinum formulations have been developed that alter drug pharmacokinetics, such as liposomal cisplatin, which has been purported to be less neurotoxic . Finally, platinum drugs are being conjugated with bioactive compounds in order to increase efficacy and better target cancer.…”

Section: Discussionmentioning

confidence: 99%

Platinum‐induced peripheral neurotoxicity: From pathogenesis to treatment

Staff

Cavaletti

Islam

et al. 2019

J Peripheral Nervous Sys

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Platinum-induced peripheral neurotoxicity (PIPN) is a common side effect of platinum-based chemotherapy that may cause dose reduction and discontinuation, with oxaliplatin being more neurotoxic. PIPN includes acute neurotoxicity restricted to oxaliplatin, and chronic non-length-dependent sensory neuronopathy with positive and negative sensory symptoms and neuropathic pain in both upper and lower limbs.Chronic sensory axonal neuropathy manifesting as stocking-and-glove distribution is also frequent. Worsening of neuropathic symptoms after completing the last chemotherapy course may occur. Motor and autonomic involvement is uncommon. Ototoxicity is frequent in children and more commonly to cisplatin. Platinum-based compounds result in more prolonged neuropathic symptoms in comparison to other chemotherapy agents. Patient reported outcomes questionnaires, clinical evaluation and instrumental tools offer complementary information in PIPN. Electrodiagnostic features include diffusely reduced/abolished sensory action potentials, in keeping with a sensory neuronopathy. PIPN is dependent on cumulative dose but there is a large variability in its occurrence. The search for additional risk factors for PIPN has thus far yielded no consistent findings. There are currently no neuroprotective strategies to reduce the risk of PIPN, and symptomatic treatment is limited to duloxetine that was found effective in a single phase III intervention study. This review critically examines the pathogenesis, incidence, risk factors (both clinical and pharmacogenetic), clinical phenotype and management of PIPN.

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Section: Discussionmentioning

confidence: 99%

Platinum‐induced peripheral neurotoxicity: From pathogenesis to treatment

Staff

Cavaletti

Islam

et al. 2019

J Peripheral Nervous Sys

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“…Cisplatin (CP) is a chemotherapeutic drug that has been used clinically for decades in patients with malignant tumors; however, nephrotoxicity, which is the major side effect of CP treatment, has greatly limited its application as a treatment ( 1 , 2 ). Thus, there is an urgent requirement to develop a novel therapeutic agent that protects against CP-induced renal injury and obtain novel insights into the treatment of patients with cancer undergoing CP-based chemotherapy regimens ( 3 , 4 ).…”

Section: Introductionmentioning

confidence: 99%

Treatment with catalpol protects against cisplatin‑induced renal injury through Nrf2 and NF‑κB signaling pathways

Zhang

Liu

et al. 2020

Exp Ther Med

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Cisplatin (CP) is one of the most widely used chemotherapy drugs for cancer treatment, but it often leads to nephrotoxicity. It is well known that catalpol exhibits antioxidant and anti-inflammatory functions, thus the present study aimed to investigate the potential protective effects of catalpol on CP-induced kidney injury in rats, in addition to determining the underlying mechanisms. Sprague-Dawley rats were treated with 25, 50 or 100 mg/kg catalpol for two days, injected with 20 mg/kg cisplatin and catalpol on day 3 and sacrificed on day 4. The histological analysis of isolated kidney tissues was performed using hematoxylin and eosin staining, cleaved caspase-3 expression levels were analyzed using western blotting and the expression levels of inflammatory cytokines in the tissues, including tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-6, IL-8, IL-10 and inducible nitric oxide synthase (iNOS) were evaluated using ELISAs. Furthermore, the mRNA and protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1), kelch-like ECH-associated protein 1 (Keap1), NF-κB and inhibitory κB (IκB) were determined using reverse transcription-quantitative PCR and western blotting, respectively. The results revealed that the treatment with catalpol prevented the histopathological injury and renal dysfunction caused by CP. In addition, catalpol significantly suppressed the CP-induced apoptosis of tubular cells, inhibited the CP-induced upregulation of TNF-α, IL-1β, IL-6, IL-8 and iNOS and promoted the production of the anti-inflammatory cytokine IL-10. Additionally, the mRNA and protein expression levels of Nrf2, HO-1 and IκB in the kidney tissues were increased, whereas the expression levels of Keap1 and NF-κB were significantly decreased following the treatment with catalpol. In conclusion, these results suggested that catalpol may inhibit CP-induced renal injury and suppress the associated inflammatory response through activating the Nrf2 and inhibiting the NF-κB signaling pathways, respectively.

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“…Canta et al, 2011, showed that lipoplatin, a liposomal formulation of cisplatin, reduced the systemic toxicity of cisplatin; and this formulation was markedly less nephrotoxic and induced less neurotoxicity than conventional cisplatin [ 30 ]. There are data that show that lipoplatin does not cause damage to the proximal kidney tubules as does cisplatin for several reasons: cisplatin remains protected by the lipid capsule, and the entrance of lipoplatin particles into the kidney tubule cells is limited; additionally, lipoplatin is released through the kidney with a half-life of 60–117 h compared to 6.5 h for conventional cisplatin, these pharmacokinetic differences could also explain the low renal toxicity [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Liposomes Co-Encapsulating Cisplatin/Mifepristone Improve the Effect on Cervical Cancer: In Vitro and In Vivo Assessment

et al. 2020

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Cervical cancer is usually diagnosed in the later stages despite many campaigns for early detection and continues to be a major public health problem. The standard treatment is cisplatin-based chemotherapy plus radiotherapy, but patient response is far from ideal. In the research for new drugs that enhance the activity of cisplatin, different therapeutic agents have been tested, among them the antiprogestin mifepristone. Nevertheless, the efficacy of cisplatin is limited by its low specificity for tumor tissue, which causes severe side effects. Additionally, cervical tumors often become drug resistant. These problems could possibly be addressed by the use of liposome nanoparticles to encapsulate drugs and deliver them to the target. The aim of this study was to prepare liposome nanoparticles that co-encapsulate cisplatin and mifepristone, evaluate their cytotoxicity against HeLa cells and in vivo with subcutaneous inoculations of xenografts in nu/nu mice, and examine some plausible mechanisms of action. The liposomes were elaborated by the reverse-phase method and characterized by physicochemical tests. The nanoparticles had a mean particle size of 109 ± 5.4 nm and a Zeta potential of −38.7 ± 1.2 mV, the latter parameter indicating a stable formulation. These drug-loaded liposomes significantly decreased cell viability in vitro and tumor size in vivo, without generating systemic toxicity in the animals. There was evidence of cell cycle arrest and increased apoptosis. The promising results with the co-encapsulation of cisplatin/mifepristone warrant further research.

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Meta-analysis of clinical trials comparing the efficacy and safety of liposomal cisplatin versus conventional nonliposomal cisplatin in nonsmall cell lung cancer (NSCLC) and squamous cell carcinoma of the head and neck (SCCHN)

Abstract: Supplemental Digital Content is available in the text

Cited by 28 publications

References 21 publications

Platinum‐induced peripheral neurotoxicity: From pathogenesis to treatment

Platinum‐induced peripheral neurotoxicity: From pathogenesis to treatment

Treatment with catalpol protects against cisplatin‑induced renal injury through Nrf2 and NF‑κB signaling pathways

Liposomes Co-Encapsulating Cisplatin/Mifepristone Improve the Effect on Cervical Cancer: In Vitro and In Vivo Assessment

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