Efficacy and safety of pulmonary rehabilitation training on lung function, quality of life, and T cell immune function in patients with stable chronic obstructive pulmonary disease: a randomized controlled trial.

BACKGROUND: Pulmonary rehabilitation training is an important means of stable chronic obstructive pulmonary disease (COPD). However, some people think that its effect is not satisfactory, and there is a lack of understanding of the effect of pulmonary rehabilitation training on T cell immune function. This study investigated the efficacy and safety of pulmonary rehabilitation training on lung function, quality of life and T cell immune function in stable COPD patients. METHODS: Seventy-two stable COPD patients recruited from the Outpatient department of Affiliated Hospital of Jiangnan University and Wuxi Huishan Rehabilitation Hospital, and divided them into experimental group (39 cases) and control group (33 cases) by random number table method. Both groups were received routine drug therapy, COPD knowledge education, and smoking cessation treatment. On this basis, the experimental group received daily pulmonary rehabilitation training, including pursed-lip breathing (PLB) training, abdominal breathing training, skeletal muscle training, and coughing and expectoration training. Lung function [percentage of forced expiratory volume in 1 second (FEV1%) and the percentage of FEV1/forced vital capacity (FEV1/FVC%)], quality of life [6-minute walk test (6MWT), COPD assessment test (CAT score)], and T lymphocyte subsets (CD3+%, CD4+%, CD8+%, and CD4+%/CD8+%) levels were compared by independent sample t-test or paired t-test between the 2 groups before and after 12 weeks of treatment in a double-blind method. RESULTS: There were no remarkable differences in lung function indexes, 6MWT, CAT score, and T cell immune function between the 2 groups before treatment. After 12 weeks, all indexes in the experimental group (all P<0.01) and T lymphocyte subsets in the control group (CD3+%, CD4+%, CD8+% and CD4+%/CD8+% were 0.010, 0.037, 0.021 and 0.016, respectively) were significantly better than before treatment, and there were no significant differences in lung function,6MWT, and CAT scores in the control group. After 12 weeks, all indexes in the experimental group were significantly better than those in the control group except CD8+% (FEV1%, FEV1/FVC%, 6MWT, CAT score, CD3+%, CD4+% and CD4+%/CD8+% were 0.002, 0.009, <0.001, 0.007, 0.037, 0.046 and <0.001, respectively). CONCLUSIONS: Pulmonary rehabilitation training can improve the lung function, quality of life, and T cell immune function of stable-phase COPD patients. Perhaps the recovery of T-cell immune function is the root of the patient's improvement. TRIAL REGISTRATION: Chinese Clinical Trial Registry ChiCTR2100048419.

Combination of platelet to lymphocyte ratio and neutrophil to lymphocyte ratio is a useful prognostic factor in advanced non-small cell lung cancer patients.

BACKGROUND: The neutrophil to lymphocyte ratio (NLR) was recently shown to be a remarkable prognostic factor in tumors. Moreover, some studies have indicated that the combination of NLR and platelet to lymphocyte ratio (PLR) could be a better prognostic factor. As the combined prognostic value of NLR and PLR in non-small cell lung cancer (NSCLC) is not clear, we conducted this study to explore this further. METHODS: A total of 366 primary NSCLC patients with stage III or IV were finally included. The neutrophil, platelet, and lymphocyte counts were recorded before treatment was initiated. NLR and PLR were calculated and NLR > 2.68 or PLR > 119.50 was defined as elevated. Univariate and multivariate survival analyses were conducted to test their prognostic value. RESULTS: The median of NLR and PLR were 3.14 and 152.63, respectively, in all patients. It was indicated that PLR is linearly associated with NLR. PLR is associated with survival, but is not an independent prognostic factor. Removing NLR, PLR is an independent prognostic factor (overall survival [OS]: hazard ratio [HR] = 1.918, P = 0.003; progression-free survival [PFS]: HR = 1.822, P = 0.007 in condition of NLR ≤ 2.68). It was also indicated that elevated NLR is an independent prognostic factor (OS: HR = 1.778, P = 0.009; PFS: HR = 1.535, P = 0.022) in all patients. CONCLUSIONS: PLR is a useful complement of NLR, thus, advanced NSCLC patients could be divided into three prognostic groups prior to treatment: poor: NLR > 2.68; moderate: NLR ≤ 2.68 and PLR > 119.50; and good: NLR ≤ 2.68 and PLR ≤ 119.50.

Video-assisted thoracoscopic surgery and thoracotomy during lobectomy for clinical stage I non-small-cell lung cancer have equivalent oncological outcomes: A single-center experience of 212 consecutive resections.

The aim of the present study was to compare the oncological outcomes following lobectomy using either video-assisted thoracoscopic surgery (VATS) or thoracotomy in clinical stage I non-small cell lung cancer (NSCLC) patients. Short- and long-term data from 212 consecutive patients who underwent lobectomy for clinical stage I NSCLC via VATS or thoracotomy between February 2003 and July 2013 were retrospectively reviewed. The primary endpoints were mediastinal lymph node staging, disease-free survival time and overall survival time. A total of 212 lobectomies for clinical stage I NSCLC were performed, 123 by VATS and 89 by thoracotomy. Patients' demographic data, pathological stage and residual tumor were similar in the two groups. Reduced blood loss, less post-operative analgesia required and earlier hospital discharge were recorded for the VATS group, as compared with the thoracotomy group. The overall morbidity was similar in the two groups. However, the rate of major complications was higher following thoracotomy than following VATS. No 30-day mortality occurred subsequent to either thoracotomy or VATS lobectomy. The overall survival and disease-free survival times were comparable between the two groups. In the univariate analysis, the treatment approach was not associated with the overall five-year survival or the disease-free survival times. Multivariate Cox regression analysis of survival times revealed that significant predictors of shorter survival times were advanced pathological T3 stage, pathological N1 or N2 disease and poor cancer differentiation. In conclusion, it is reasonable to conclude from the present study that VATS lobectomy performed by specialist thoracic surgeons is safe and may achieve similar long-term survival times to the open surgery approach. However, further prospective randomized multi-center trials are warranted prior to incorporating VATS into clinical routine.

Prognostic value of FGFR1 gene copy number in patients with non-small cell lung cancer: a meta-analysis.

BACKGROUND: A number of studies have investigated the relationship between fibroblast growth factor receptor1 (FGFR1) gene copy number and survival in non-small cell lung cancer (NSCLC) patients. However, conclusions reported by different parties seem to be inconsistent, especially regarding the differences among different histopathologic subtypes. To derive a more precise estimate of the prognostic significance of FGFR1 gene copy number, we have reviewed published studies and carried out a meta-analysis. METHODS: The meta-analysis was conducted in accordance with PRISMA guidelines. The required data for estimation of individual hazard ratios (HRs) for survival were extracted from the publications and an overall HR was calculated. RESULTS: We identified 6 eligible studies, all dealing with NSCLC. The global quality score ranged 32.5-80%, with a median of 53.33%. For FGFR1 amplification in three studies including differed according to histological type, the overall RR was 0.86 which 95% confidence interval (CI) was 0.75 to 0.99 and P value was 0.048. Combined HR for the six evaluable studies was 1.17 (95% CI: 0.95 to 1.43). In the subgroup of squamous cell lung cancer (SQCC), the combined HR was 1.24 (95% CI: 0.89 to 1.73). For the Asian populations' studies, the combined HR was 1.67 (95% CI: 1.1 to 2.52). CONCLUSIONS: FGFR1 amplification significantly was more frequent in SQCC. FGFR1 was not associated with poorer survival in patients with NSCLC. Furthermore studies will be needed in terms of survival implications.

Diagnostic and prognostic significance of lysophosphatidic acid in malignant pleural effusions.

BACKGROUND: Lysophosphatidic acid (LPA) is an important extracellular signal transmitter and intracellular second messenger in body fluids. It can be detected in the ascitic fluid of patients with ovarian cancer. Increasing evidence shows that LPA can stimulate cancer cell proliferation and promote tumor invasion and metastasis. Our study aimed to evaluate the diagnostic value of LPA in differentiating between malignant pleural effusions (MPEs) and benign pleural effusions (BPEs) and to evaluate the association between the level of LPA in MPE and the prognosis of lung cancer patients. PATIENTS AND METHODS: The level of LPA in the pleural effusions (PEs) of 123 patients (94 MPE, 29 BPE) with lung cancer was evaluated using an enzyme-linked immunosorbent assay. The performance of LPA was analyzed by standard Receiver operator characteristic curve (ROC) analysis methods, using the area under the curve (AUC) as a measure of accuracy. Overall survival (OS) curves and progression-free survival (PFS) curves were based on the Kaplan-Meier method, and the survival differences between subgroups were analyzed using the log-rank or Breslow test (SPSS software). A multivariate Cox proportional hazards model was used to assess whether LPA independently predicted lung cancer survival. RESULTS: The levels of LPA differed significantly between MPE (22.08±8.72 µg/L) and BPE (14.61±5.12 µg/L) (P<0.05). Using a cutoff point of 18.93 µg/L, LPA had a sensitivity of 60% and a specificity of 83% to distinguish MPEs from BPEs with an AUC of 0.769±0.045 (SE) (P=0.000) (95% CI, 0.68-0.857). In the three pathological types of lung cancer patients with MPE, there were no significant associations between LPA levels and the length of PFS and OS (P=0.58 and 0.186, respectively). Interestingly, in the patients with MPE caused by lung adenocarcinoma there were significant associations between the LPA levels and the PFS and OS (P=0.018 and 0.026, respectively). Multivariate analysis showed that the LPA level was an independent prognostic factor for PFS in lung adenocarcinoma. CONCLUSIONS: Our results indicate that LPA can be used as a new biomarker for the diagnosis of MPE caused by lung cancer and that higher levels of LPA are related to shorter PFS in adenocarcinoma of the lung.

SUZ12 is involved in progression of non-small cell lung cancer by promoting cell proliferation and metastasis.

The suppressor of zeste-12 protein (SUZ12), a core component of Polycomb repressive complex 2 (PRC2), is implicated in transcriptional silencing by generating di- and tri-methylation of lysine 27 on histone H3 (H3K27Me3). Although SUZ12 is known to be of great importance in several human cancer tumorigenesis, limited data are available on the expression profile and functional role of SUZ12 in non-small cell lung cancer (NSCLC). Here, we determined the expression level of SUZ12 in 40 paired clinical NSCLC tissues and adjacent normal tissues by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The results showed that SUZ12 was anomalously expressed in NSCLC tissues compared to adjacent noncancerous tissues (P<0.05) and was highly correlated to tumor size, lymph node metastasis, and clinical stages (P<0.05). Additionally, siRNA-mediated knockdown of SUZ12 could inhibit tumor cell growth, migration, and invasion, indicating that SUZ12 might function as an oncogene in NSCLC initiation and progression. Furthermore, we found that SUZ12 silencing significantly reduced the expression levels of transcription factor transcription factor E2F1 (E2F1) as well as potential metastasis promoters Rho-associated, coiled-coil-containing protein kinase 1 (ROCK1) and roundabout homolog 1 (ROBO1) through Western blot analysis. Altogether, we provide evidences suggesting that SUZ12 is an oncogene in NSCLC and can regulate NSCLC cells proliferation and metastasis partly via reducing E2F1, ROCK1, and ROBO1. Thus, SUZ12 may represent a new potential diagnostic marker for NSCLC and may be a novel therapeutic target for NSCLC intervention.