A randomised study comparing the effectiveness of acupuncture or morphine versus the combination for the relief of dyspnoea in patients with advanced non-small cell lung cancer and mesothelioma

Minchom, Anna; Punwani, R.; Filshie, Jacqueline; Bhosle, Jaishree; Nimako, Kofi; Myerson, James S.; Gunapala, R.; Popat, Sanjay; O’Brien, Mary

doi:10.1016/j.ejca.2016.03.078

Cited by 36 publications

(34 citation statements)

References 22 publications

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“…A few, mostly small RCTs have examined the role of acupressure or acupuncture in patients with cancer and reported short-term benefit on breathlessness. [54][55][56] One open-label trial involving 152 patients with lung cancer compared prolonged acupuncture (with indwelling studs) with morphine or a combination of both and found similar reduction on breathlessness but fewer side-effects in the acupuncture group. 55 A recent systematic review of 12 clinical trials involving 190 patients with cancer and 347 patients with COPD found overall benefit from acupuncture on breathlessness severity.…”

Section: Complementary Therapiesmentioning

confidence: 99%

“…[54][55][56] One open-label trial involving 152 patients with lung cancer compared prolonged acupuncture (with indwelling studs) with morphine or a combination of both and found similar reduction on breathlessness but fewer side-effects in the acupuncture group. 55 A recent systematic review of 12 clinical trials involving 190 patients with cancer and 347 patients with COPD found overall benefit from acupuncture on breathlessness severity. 57 Additional therapies, including aromatherapy massage, hypnotherapy, meditation, reflexology and reiki, may provide limited short-term benefit.…”

Section: Complementary Therapiesmentioning

confidence: 99%

See 1 more Smart Citation

Management of breathlessness in patients with cancer: ESMO Clinical Practice Guidelines

et al. 2020

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Section: Complementary Therapiesmentioning

confidence: 99%

Section: Complementary Therapiesmentioning

confidence: 99%

Management of breathlessness in patients with cancer: ESMO Clinical Practice Guidelines

et al. 2020

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“…However, none of these drugs have been reported to be related to the treatment of lung cancer through interactions with TBXA2R. Nevertheless, there is much evidence indicating that iloprost [40], acetaminophen [41], morphine [42], furosemide [43], and vinblastine [44] are broadly applied in chemotherapy for lung cancer patients. Nevertheless, this study still provides novel insights into LUAD pathogenesis and treatment.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of the putative competing endogenous RNA network in human lung adenocarcinoma

Yang

et al. 2020

Preprint

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Background Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer worldwide. Until now, the molecular mechanisms underlying LUAD progression have not been fully explained. This study aimed to identify a competing endogenous RNA (ceRNA) network in LUAD. Methods Differentially expressed lncRNAs (DELs), miRNAs (DEMs), and mRNAs (DEGs) were identified from The Cancer Genome Atlas (TCGA) database with a |log2FC| > 1.0 and a false discovery rate (FDR) < 0.05. Then, these DELs, DEMs, and DEGs were used to construct the initial ceRNA network. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), protein-protein interaction (PPI) network, and survival analyses were performed to analyse these DEGs involved in the ceRNA network. Subsequently, the drug-gene interaction database (DGIdb) was utilized to select candidate LUAD drugs interacting with significant DEGs. Then, lasso-penalized Cox regression and multivariate Cox regression models were used to construct the risk score system. Kaplan-Meier (K-M) survival curves and receiver operating characteristic (ROC) curves were utilized to validate the reliability of the risk score system. Finally, based on the correlations between DELs and DEGs involved in the risk score system, the final ceRNA network was identified. Results A total of 340 DELs, 29 DEMs, and 218 DEGs were selected to construct the initial ceRNA network. Functional enrichment analyses indicated that 218 DEGs were significantly enriched in the GO terms “nucleoplasm”, “transcription factor complex”, “protein binding”, and “metal ion binding”, whereas these DEGs were associated with the KEGG pathway terms “microRNAs in cancer”, “pathways in cancer”, “cell cycle”, “HTLV-1 infection”, and the “PI3K-Akt signalling pathway”. K-M survival analysis of all differentially expressed genes involved in the ceRNA network identified 24 DELs, 4 DEMs, and 29 DEGs, all of which were significantly correlated with LUAD progression (P < 0.05). Furthermore, 15 LUAD drugs interacting with 29 DEGs were selected. After lasso-penalized Cox regression and multivariate Cox regression modelling, 4 DEGs, PRKCE, DLC1, LATS2, and DPY19L1, were incorporated into the risk score system. The area under the curve (AUC) values of the time-dependent ROC curves at 3 years and 5 years were both higher than 0.5. Finally, the correlation coefficients between these 4 DEGs and their corresponding DELs involved in the ceRNA network suggested that there were 2 DEL-DEG pairs, NAV2-AS2 – PRKCE (r = 0.430, P < 0.001) and NAV2-AS2 – LATS2 (r = 0.338, P < 0.001). Considering the previously constructed ceRNA network, NAV2-AS2 – mir-31 – PRKCE and NAV2-SA2 – mir-31 – LATS2 were identified. Conclusions The lncRNA-miRNA-mRNA ceRNA network plays an essential role in LUAD. These results may improve our understanding and provide novel mechanistic insights to explore diagnostics, tumourigenesis, prognosis, and therapeutic drugs for LUAD patients.

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“…Morphine is an opiate‐based drug by stimulating opioid receptor signalling in neurons, which is served as an analgesic to alleviate persistent pain caused by cancer all over the world . Based on many experiments of cancer cell lines and mouse models, some studies reported that morphine might even change cancer progression.…”

Section: Introductionmentioning

confidence: 99%

Morphine contributed to the deterioration of cancer via miR-543/MARCKS/FcγR-mediated phagocytosis pathway

Luo

Chen

et al. 2019

Journal of Pharmacy and Pharmacology

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Objectives It has been confirmed that morphine was detrimental to patients with cancers. Hence, we aimed to reveal a certain mechanism of morphine in cancer development. Methods Microarray and GSEA analysis were utilized to seek for differently expressed genes and pathway. Key findings Bioinformatics analysis identified that downregulation of MARCKS and upregulation of miR‐543 in samples treated with morphine. FcγR‐mediated phagocytosis pathway was illustrated to be upregulated in the control. PANC‐1 and DU145 cell viability was increased but apoptosis was declined as morphine concentration went up from 10−8 to 10−6 mol/l. On the other curve, the viability was reduced and apoptosis was elevated from 10−6 to 10−5 mol/l. The expression of miR‐543 ran the same trend as cell viability. Assays in vivo and in vitro validated that miR‐543 facilitated cell viability, tumour growth, levels of CA199 and PSA, whereas inhibited apoptosis. MARCKS could target and inhibit miR‐543 expression, which exhibited an opposite effect on cancer progression. MiR‐543 blocked but MARCKS activated FcγR‐mediated phagocytosis pathway. Conclusions Morphine at 10−6 mol/l could benefit miR‐543 expression to inhibit MARCKS expression, consequently, blocking FcγR‐mediated phagocytosis pathway, which contributed to the cancer progression in vitro and in vivo.

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A randomised study comparing the effectiveness of acupuncture or morphine versus the combination for the relief of dyspnoea in patients with advanced non-small cell lung cancer and mesothelioma

Cited by 36 publications

References 22 publications

Management of breathlessness in patients with cancer: ESMO Clinical Practice Guidelines

Management of breathlessness in patients with cancer: ESMO Clinical Practice Guidelines

Comprehensive analysis of the putative competing endogenous RNA network in human lung adenocarcinoma

Morphine contributed to the deterioration of cancer via miR-543/MARCKS/FcγR-mediated phagocytosis pathway

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