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The role of patient-physician relationship on health-related quality of life and pain in cancer patients.

患者-医生关系对癌症患者健康相关生活质量和疼痛的作用。

  • 影响因子:2.83
  • DOI:10.1007/s00520-019-05070-y
  • 作者列表:"Samuel CA","Mbah O","Schaal J","Eng E","Black KZ","Baker S","Ellis KR","Guerrab F","Jordan L","Lightfoot AF","Robertson LB","Yongue CM","Cykert S
  • 发表时间:2020-06-01
Abstract

PURPOSE:Health-related quality of life (HRQOL) and pain are important supportive cancer care outcomes. The patient-provider relationship, a modifiable care experience, has been linked to healthcare outcomes; however, less is known about associations between patient-provider relationship and supportive care outcomes in cancer patients. We examined the role of multiple aspects of the patient-provider relationship in explaining patterns of HRQOL and pain among breast and lung cancer patients. METHODS:Our analysis included 283 breast and lung cancer patients from two cancer centers. Clinical data and survey data on patient sociodemographic factors, physical and mental HRQOL, pain, and patient-physician relationship (i.e., doctor's respectfulness, time spent with doctors, patient involvement in decision-making, satisfaction with care, and following doctor's advice/treatment plan) were collected at baseline and during treatment. We estimated adjusted modified Poisson regression models to assess associations between patient-physician relationship factors and physical and mental HRQOL and pain. RESULTS:Compared with patients reporting suboptimal respect from doctors, patients reporting optimal respect were less likely to report below average physical HRQOL (adjusted risk ratio (ARR), 0.73; 95%CI, 0.62-0.86), below average mental HRQOL (ARR, 0.71; 95%CI, 0.54-0.93), and moderate-to-severe pain (ARR, 0.53; 95%CI, 0.35-0.79). Patients reporting optimal involvement in care decision-making and patients who reported following their doctor's advice/treatment plan were less likely to report below average mental HRQOL than their respective counterparts (ARR, 0.64; 95%CI, 0.50-0.83; ARR, 0.65; 95%CI, 0.48-0.86). CONCLUSION:Multiple patient-physician relationship factors account for variations in HRQOL and pain in cancer patients. These findings provide insight into potential targets for improving the patient-provider relationship and supportive cancer care outcomes.

摘要

目的: 健康相关生活质量 (HRQOL) 和疼痛是重要的支持性癌症治疗结果。患者-提供者关系 (一种可改变的护理体验) 已经与医疗保健结果相关联; 然而,关于癌症患者中患者-提供者关系和支持性护理结果之间的关联知之甚少。我们研究了患者-提供者关系的多个方面在解释乳腺癌和肺癌患者HRQOL和疼痛模式中的作用。 方法: 我们的分析包括来自两个癌症中心的 283 名乳腺癌和肺癌患者。关于患者社会人口学因素、身体和精神HRQOL、疼痛和患者-医生关系的临床数据和调查数据 (i.e.,在基线和治疗期间收集医生的尊重、与医生相处的时间、患者参与决策、对护理的满意度以及遵循医生的建议/治疗计划)。我们估计了调整后的改良泊松回归模型,以评估患者-医生关系因素与身心HRQOL和疼痛之间的关联。 结果: 与报告来自医生的次优尊重的患者相比,报告最佳尊重的患者报告低于平均身体HRQOL的可能性较小 (校正风险比 (ARR),0.73; CI,0.62-0.86),低于平均精神HRQOL (ARR,0.71; 95% CI,0.54-0.93),和中重度疼痛 (ARR,0.53; 95% CI,0.35-0.79)。报告最佳参与护理决策的患者和报告遵循医生建议/治疗计划的患者报告低于平均精神HRQOL的可能性低于其各自的同行 (ARR,0.64; 95% CI,0.50-0.83; ARR,0.65; 95% CI,0.48-0.86)。 结论: 多种患者-医生关系因素导致了癌症患者HRQOL和疼痛的变化。这些发现提供了对改善患者-提供者关系和支持性癌症护理结果的潜在目标的洞察。

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影响因子:6.93
发表时间:2020-01-15
DOI:10.1002/ijc.32532
作者列表:["Hata A","Nakajima T","Matsusaka K","Fukuyo M","Morimoto J","Yamamoto T","Sakairi Y","Rahmutulla B","Ota S","Wada H","Suzuki H","Matsubara H","Yoshino I","Kaneda A"]

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.

翻译标题与摘要 下载文献
影响因子:6.93
发表时间:2020-01-01
DOI:10.1002/ijc.32530
作者列表:["Zhang L","Yang Y","Chai L","Bu H","Yang Y","Huang H","Ran J","Zhu Y","Li L","Chen F","Li W"]

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.

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