Herbal medicine on cancer-related fatigue of lung cancer survivors: Protocol for a systematic review.
- 作者列表："Kwon CY","Lee B","Kim KI","Lee BJ
BACKGROUND:Lung cancer is one of the most common cancers worldwide, and approximately half of the patients with lung cancer receiving chemotherapy suffer from cancer-related fatigue (CRF). Herbal medicines (HMs) have been used in Oriental countries for centuries as tonics. Various beneficial effects of HM on fatigue and cancer have been reported. However, the effectiveness and safety of HM for CRF in lung cancer patients have not been synthesized. The purpose of this systematic review is to evaluate the effectiveness and safety of HM for CRF in patients with lung cancer, regardless of their cancer type or stage. METHODS AND ANALYSIS:A comprehensive search will be conducted in 12 electronic medical databases including 5 English-language databases (Medline via PubMed, EMBASE via Elsevier, the Cochrane Central Register of Controlled Trials [CENTRAL], the Allied and Complementary Medicine Database [AMED] via EBSCO, and the Cumulative Index to Nursing and Allied Health Literature [CINAHL] via EBSCO), 4 Korean-language databases (Oriental Medicine Advanced Searching Integrated System [OASIS], Koreanstudies Information Service System [KISS], Research Information Service System [RISS], and Korea Citation Index [KCI]), 2 Chinese-language databases (China National Knowledge Infrastructure [CNKI] and Wanfang Data), and 1 Japanese-language database (CiNii). Only randomized controlled trials (RCTs) and quasi-RCTs on HM for CRF will be allowed. The severity of fatigue assessed using a validated tool will be considered as theprimary outcome. The secondary outcomes will include the patients' quality of life, activities of daily life, incidence of adverse events, and total effective rate. Two independent researchers will perform the study selection, data extraction, and quality assessment. RevMan version 5.3 will be used for data synthesis. The methodological quality of the included RCTs will be assessed using the Cochrane Collaboration's risk of bias tool. In the meta-analysis, for dichotomous data and continuous data, risk ratio and mean difference, respectively, will be estimated with their 95% confidence intervals. According to the heterogeneity, either a fixed-effects or a random-effects model will be used. ETHICS AND DISSEMINATION:Ethical approval is not required because individual patient data are not included. The findings of this systematic review will be disseminated through a peer-reviewed publication or conference presentation. PROSPERO REGISTRATION NUMBER:CRD42019141660.
背景: 肺癌是世界范围内最常见的癌症之一，接受化疗的肺癌患者中约一半患有癌症乏力 (CRF)。几个世纪以来，草药 (HMs) 一直作为滋补品在东方国家使用。已经报道了HM对乏力和癌症的各种有益作用。然而，HM对肺癌患者CRF的有效性和安全性尚未合成。本系统综述的目的是评估HM对肺癌患者CRF的有效性和安全性，无论其癌症类型或分期如何。 方法和分析: 将在 12 个电子医学数据库中进行全面搜索，包括 5 个英语数据库 (Medline通过PubMed，EMBASE通过Elsevier，控制试验的Cochrane中心注册 [中心]，通过EBSCO的联合和补充医学数据库 [AMED]，以及护理和联合健康文献的累积索引[CINAHL] via EBSCO)，4 个韩文数据库 (东方医学高级搜索集成系统 [OASIS]，Koreanstudies信息服务系统 [KISS]，研究信息服务系统 [RISS]，和韩国引文索引 [KCI]) 、 2 个中文数据库 (中国国家知识基础设施 [CNKI] 和万方数据) 、 1 个日语数据库(CiNii)。仅允许关于CRF的HM的随机对照试验 (rct) 和准rct。严重乏力评估用一种有效的工具，将被视为首要结局.次要结局包括患者的生活质量、日常生活活动能力、不良事件发生率和总有效率。两名独立的研究人员将进行研究选择，数据提取和质量评估。将使用RevMan 5.3 版本进行数据合成。将使用Cochrane协作的偏倚风险工具评估纳入的rct的方法学质量。在荟萃分析中，对于二分类数据和连续数据，将分别用其 95% 置信区间估计风险比和平均差。根据异质性，将使用固定效应或随机效应模型。 伦理和传播: 不需要伦理批准，因为不包括个体患者数据。本系统综述的结果将通过同行评审的出版物或会议介绍传播。 普洛斯彼罗注册号: crd42019141660。
METHODS::Pulmonary artery sling is a rare congenital anomaly of the origin and course of the left pulmonary artery. Patients with this condition typically present with respiratory failure in young infancy, and asymptomatic cases are uncommon. We describe the case of an adult patient with a lung adenocarcinoma of the right upper lobe, extending into the hilum and superior mediastinum, and with a previously unknown pulmonary artery sling anomaly. The local invasiveness of the tumor and the peculiar vascular anatomy contributed to a unique surgical scenario, wherein multiple reconstructive procedures were required.
METHODS::Patients with idiopathic pulmonary fibrosis (IPF) have higher risk of developing lung cancer, for example, squamous cell carcinoma (SCC), and show poor prognosis, while the molecular basis has not been fully investigated. Here we conducted DNA methylome analysis of lung SCC using 20 SCC samples with/without IPF, and noncancerous lung tissue samples from smokers/nonsmokers, using Infinium HumanMethylation 450K array. SCC was clustered into low- and high-methylation epigenotypes by hierarchical clustering analysis. Genes hypermethylated in SCC significantly included genes targeted by polycomb repressive complex in embryonic stem cells, and genes associated with Gene Ontology terms, for example, "transcription" and "cell adhesion," while genes hypermethylated specifically in high-methylation subgroup significantly included genes associated with "negative regulation of growth." Low-methylation subgroup significantly correlated with IPF (78%, vs. 17% in high-methylation subgroup, p = 0.04), and the correlation was validated by additional Infinium analysis of SCC samples (n = 44 in total), and data from The Cancer Genome Atlas (n = 390). The correlation between low-methylation subgroup and IPF was further validated by quantitative methylation analysis of marker genes commonly hypermethylated in SCC (HOXA2, HOXA9 and PCDHGB6), and markers specifically hypermethylated in high-methylation subgroup (DLEC1, CFTR, MT1M, CRIP3 and ALDH7A1) in 77 SCC cases using pyrosequencing (p = 0.003). Furthermore, low-methylation epigenotype significantly correlated with poorer prognosis among all SCC patients, or among patients without IPF. Multivariate analysis showed that low-methylation epigenotype is an independent predictor of poor prognosis. These may suggest that lung SCC could be stratified into molecular subtypes with distinct prognosis, and low-methylation lung SCC that significantly correlates with IPF shows unfavorable outcome.
METHODS::The role of Fyn-related kinase (FRK) in malignant tumors remains controversial. Our study investigated the function of FRK in lung cancer. Immunohistochemistry staining and generating a knockout of FRK by CRISPR/Cas9 in H1299 (FRK-KO-H1299) cells were strategies used to explore the role of FRK. Immunohistochemistry staining indicated that FRK expression was elevated in 223 lung cancer tissues compared to 26 distant normal lung tissues. FRK contributed to poor survival status in lung cancer patients and acted as a predictor for poor prognosis of lung cancer. Knockout of FRK by CRISPR/Cas9 markedly inhibited proliferation, invasion, colony formation and epithelial-mesenchymal transition (EMT) process in the lung cancer cell line H1299. Further exploration indicated that FRK-KO damaged the stemness phenotype of H1299 by inhibiting CD44 and CD133 expression. Seahorse detection and a U-13 C flux assay revealed that FRK-KO induced metabolism reprogramming by inhibiting the Warburg effect and changing the energy type in H1299 cells. Epidermal growth factor stimulation recovered the expression of FRK and biological functions, metabolic reprogramming and stemness phenotype of H1299 cells. FRK plays an oncogenic role in lung cancer cells via a novel regulation mechanism of enhancing the stemness of H1299 cells by inducing metabolism reprogramming, which finally promotes EMT and metastasis. Our study also indicates that FRK could be used as a potential therapeutic target for drug development.