Non-steroidal anti-inflammatory drugs, tumour immunity and immunotherapy

Hussain, Muzammal; Javeed, Aqeel; Ashraf, Muhammad; Al-Zaubai, Nuha; Stewart, Alastair G.; Mukhtar, Muhammad Mahmood

doi:10.1016/j.phrs.2012.02.003

Cited by 70 publications

(54 citation statements)

References 133 publications

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“…In addition, COX2/PGE2 signaling induces regulatory T cell (Treg) activity, which could impede the development of antitumor immune responses. 27 …”

Section: Tumor-derived Immunosuppressionmentioning

confidence: 99%

“…When used in combination, these treatments synergistically/additively enhanced the efficacy of vaccines including DC-based vaccines. 112 Histamine type-2 receptor antagonists Cimetidine is the oldest H2 receptor antagonist. An accumulating body of evidence suggests that this drug may improve the survival of patients with different malignancies, and its antitumor effect is mediated at least in part by immune mechanisms.…”

Section: Inhibitors Of Indoleamine 23-dioxygenase (Ido)mentioning

confidence: 99%

See 1 more Smart Citation

Clinically feasible approaches to potentiating cancer cell-based immunotherapies

Селедцов

Гончаров

Селедцова

2015

Human Vaccines & Immunotherapeutics

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“…In addition, COX2/PGE2 signaling induces regulatory T cell (Treg) activity, which could impede the development of antitumor immune responses. 27 …”

Section: Tumor-derived Immunosuppressionmentioning

confidence: 99%

Section: Inhibitors Of Indoleamine 23-dioxygenase (Ido)mentioning

confidence: 99%

Clinically feasible approaches to potentiating cancer cell-based immunotherapies

Селедцов

Гончаров

Селедцова

2015

Human Vaccines & Immunotherapeutics

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“…NSAIDs act by inhibiting inflammatory mediators, namely cyclo-oxygenase (COX) enzymes, which are responsible for producing prostaglandins (1). The COX-1 isoform is implicated in homeostasis while COX-2 is particularly associated with inflammatory reactions (2,3). Nimesulide (4-nitro-2-phenoxymethanesulfonanilide) is the first marketed NSAID that act through selective inhibition of COX-2 (1,4,5).…”

Section: Introductionmentioning

confidence: 99%

Applying response surface methodology to optimize nimesulide permeation from topical formulation

Shahzad¹,

Afreen²,

Shah³

et al. 2012

Pharmaceutical Development and Technology

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Nimesulide is a non-steroidal anti-inflammatory drug that acts through selective inhibition of COX-2 enzyme. Poor bioavailability of this drug may leads to local toxicity at the site of aggregation and hinders reaching desired therapeutic effects. This study aimed at formulating and optimizing topically applied lotions of nimesulide using an experimental design approach, namely response surface methodology. The formulated lotions were evaluated for pH, viscosity, spreadability, homogeneity and in vitro permeation studies through rabbit skin using Franz diffusion cells. Data were fitted to linear, quadratic and cubic models and best fit model was selected to investigate the influence of permeation enhancers, namely propylene glycol and polyethylene glycol on percutaneous absorption of nimesulide from lotion formulations. The best fit quadratic model explained that the enhancer combination at equal levels significantly increased the flux and permeability coefficient. The model was validated by comparing the permeation profile of optimized formulations' predicted and experimental response values, thus, endorsing the prognostic ability of response surface methodology.

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“…1 Some anti-inflammatory drugs show antitumor activities through affecting pathways such as nuclear factor (NF) kappa-B (NF-κB), cyclooxygenase-2 (COX2), Wnt/B-catenin, Protein Kinase B (known as Akt or PkB), reactive oxygen and nitrogen species (RONS) production, and angiogenic vascular endothelial growth factor (VEGF), which function in cellular mechanisms such as proliferation, apoptosis, angiogenesis, and migration/ invasion. [2][3][4][5][6][7] In addition, inflammation-related alterations of the androgen receptor (AR), NKX3.1, and Akt, which regulate cell proliferation in co-operation, have a significant role in prostate tumorigenesis. [8][9][10] The negative correlation between the use of anti-inflammatory drugs and cancer incidence proves that active inflammation supports carcinogenesis, and anti-inflammatory drugs can prevent inflammation-related tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%

“…[8][9][10] The negative correlation between the use of anti-inflammatory drugs and cancer incidence proves that active inflammation supports carcinogenesis, and anti-inflammatory drugs can prevent inflammation-related tumorigenesis. 4,5 Inflammation leads to neoplastic transformation by altering gene expression levels of oncogenes and tumor suppressors. In addition, these genetic changes influence the expression patterns of many inflammation-related genes and result in the recruitment of inflammatory cells in the tumor microenvironment.…”

Section: Introductionmentioning

confidence: 99%

Use of Non-steroidal Anti-inflammatory Drugs for Chemoprevention of Inflammation-induced Prostate Cancer

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Öztürk

2017

tjps

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Amaç: Kronik enflamasyonun kanser gelişiminin önemli nedenlerinden biri olduğu ve epidemiyolojik verilere göre kanser olgularının %25'inin kronik inflamasyona bağlı olarak geliştiği bilinmektedir. Kronik inflamasyon, hücre proliferasyonu, apoptoz, anjiyogenez gibi mekanizmalarda bozukluklara yol açarak tümörleşmeyi tetiklemektedir. Bu nedenle kanseri önleyici ilaç geliştirme çalışmalarında, inflamasyon ile tetiklenen mekanizmaların inhibisyonununda etkin bir terapötik strateji olduğu düşünülmektedir. Klinik çalışmalarda da, birçok kanser tipinde anti-inflamatuvar ilaçların kanser insidansını azaltıcı etkisi belirlenmiş ve prostat kanserinde de düzenli aspirin veya non-streoidal anti-inflamatuvar ilaç (NSAID) kullananların prostat kanserine yakalanma riskinin yaklaşık %15-20 azaldığı saptanmıştır. Gereç ve Yöntemler: Bu çalışma kapsamında, klinik kullanımdaki NSAID'lerden indometazin, sulindak, ibuprofen, naproksen, selekoksib ve nimesulidin inflamasyona bağlı prostat kanserleşmesinde rol oynayan moleküler mekanizmalardan bazıları üzerindeki etkileri araştırılmıştır. Tümörijenik mekanizmaları aktifleştiren nükleer faktör kappa B sinyal yolağı üzerindeki inhibisyon etkileri ve prostat hücrelerinin proliferasyonunu düzenleyen androjen reseptörü sinyal yolağı üzerindeki etkileri araştırılmıştır. Ayrıca inflamatuvar mikroçevrede etkinleşerek tümörleşmeye neden olan protein kinaz B (Akt) aktivitesindeki değişim de incelenmiştir. Bulgular: Elde edilen sonuçlar, anti-inflamatuvar ajanların, androjen reseptörü ve tümör baskılayıcı NKX3.1'in protein seviyelerinde konsantrasyona bağlı bir değişime neden olduğu, ayrıca tümörleşmeyi tetikleyen Akt (S473) düzeyinde de beklenmedik bir aktivasyonu tetikleyebildiğini göstermiştir. Sonuç: Anti-inflamatuvar ajanların, prostat inflamasyonu ile tetiklenen kanserleşme sürecini önleme amacıyla kullanımlarında yalnızca inflamatuvar yolakların değil prostat kanserleşmesine özgün mekanizmaların da dikkate alınması gereği ortaya konmuştur. Anahtar kelimeler: NSAID, prostat kanseri, inflamasyon, androjen reseptörü, NKX3.1 Objectives: Chronic inflammation has been known as one of the major causes of cancer progression and 25% of cancer cases initiate due to chronic inflammation according to epidemiologic data. It has been determined that chronic inflammation induces carcinogenesis through the abrogation of cell proliferation, apoptosis, and angiogenesis mechanisms. Therefore, it is believed that inhibition of inflammation-induced carcinogenic mechanisms is an efficient therapeutic strategy in drug development studies of cancer chemoprevention. It has also been observed that use of anti-inflammatory drugs reduces the incidence of cancer, and the risk of developing prostate cancer decreases 15-20% with regular use of aspirin and non-steroidal anti-inflammatory drugs (NSAID). Materials and Methods:In this study, we investigated the effects of some clinically used NSAIDs on cellular mechanisms that play a role in inflammation-induced prostate carcinogenesis. Inhibition activities on the...

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Non-steroidal anti-inflammatory drugs, tumour immunity and immunotherapy

Cited by 70 publications

References 133 publications

Clinically feasible approaches to potentiating cancer cell-based immunotherapies

Clinically feasible approaches to potentiating cancer cell-based immunotherapies

Applying response surface methodology to optimize nimesulide permeation from topical formulation

Use of Non-steroidal Anti-inflammatory Drugs for Chemoprevention of Inflammation-induced Prostate Cancer

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