Establishing and Externally Validating a Hemoglobin, Albumin, Lymphocyte, and Platelet (HALP) Score-Based Nomogram for Predicting Early Recurrence in BCLC Stage 0/A Hepatocellular Carcinoma Patients After Radical Liver Resection: A Multi-Center Study.

Purpose: Early recurrence (ER) is associated with poor prognosis in hepatocellular carcinoma (HCC). In this study, we developed and externally validated a nomogram based on the hemoglobin, albumin, lymphocytes, and platelets (HALP) score to predict ER for patients with BCLC stage 0/A HCC who underwent radical liver resection. Patients and Methods: A total of 808 BCLC stage 0/A HCC patients from six hospitals were included in this study, and they were assigned to a training cohort (n = 500) and an external validation cohort (n = 308). We used univariate and multivariate Cox regression analysis to identify the independent risk factors for disease-free survival (DFS). We also established and externally validated a nomogram based on these risk predictors. The nomogram was evaluated using the area under the receiver operating characteristic curve (AUC), the concordance index (C-index), the calibration curve, decision curve analysis (DCA), and Kaplan‒Meier analysis. Results: Multivariate COX regression showed that HBV DNA ≥10,000 IU/mL (P < 0.001), HALP score ≤38.20 (P < 0.001), tumor size (P = 0.003), clinically significant portal hypertension (P = 0.001), Edmondson-Steiner grade (III-IV) (P = 0.007), satellite nodules (P < 0.001), and MVI (P = 0.001) were independent risk factors for post-operative tumor recurrence. The AUC of our nomogram for predicting the 2-year and 5-year DFS was 0.756 and 0.750, respectively, in the training cohort and 0.764 and 0.705, respectively, in the external validation cohort. We divided the patients into low-, intermediate- and high-risk groups according to the risk score calculated by the nomogram. There were statistically significant differences in the DFS and overall survival (OS) among the three groups of patients (P < 0.001). Conclusion: We developed and externally validated a new nomogram, which is accurate and can predict ER in BCLC stage 0/A HCC patients after curative liver resection.

Transforming growth factor-ß and bone morphogenetic protein signaling pathways in pathological cardiac hypertrophy.

Pathological cardiac hypertrophy (referred to as cardiac hypertrophy) is a maladaptive response of the heart to a variety of pathological stimuli, and cardiac hypertrophy is an independent risk factor for heart failure and sudden death. Currently, the treatments for cardiac hypertrophy are limited to improving symptoms and have little effect. Elucidation of the developmental process of cardiac hypertrophy at the molecular level and the identification of new targets for the treatment of cardiac hypertrophy are crucial. In this review, we summarize the research on multiple active substances related to the pathogenesis of cardiac hypertrophy and the signaling pathways involved and focus on the role of transforming growth factor-ß (TGF-ß) and bone morphogenetic protein (BMP) signaling in the development of cardiac hypertrophy and the identification of potential targets for molecular intervention. We aim to identify important signaling molecules with clinical value and hope to help promote the precise treatment of cardiac hypertrophy and thus improve patient outcomes.

Application of circulating genetically abnormal cells in the diagnosis of early-stage lung cancer.

PURPOSE: Lung cancer is the leading cause of cancer-related death worldwide. The early detection of lung cancer is crucial for the diagnosis of this disease. Therefore, an effective and noninvasive method for the early diagnosis of lung cancer is urgently needed. METHODS: To evaluate the diagnostic performance of circulating genetically abnormal cells (CACs) in early lung cancer, a total of 63 participants who completed CAC detection by Zhuhai SanMed Biotech Inc. and obtained pathological results from January to December 2020 were included in our study; 50 patients had lung cancer and 13 patients had benign lung disease. The levels of lung cancer-related markers in peripheral blood and the chest computed tomography (CT) imaging characteristics of these patients were collected before pathological acquisition. RESULTS: The positive rate of CAC was 90.0% in the lung cancer group and 23.1% in the benign lung disease group, and the difference was statistically significant (P < 0.01). The area under the receiver operating characteristic (ROC) curve of CAC was 0.837, the sensitivity was 90%, and the specificity was 76.9%. The area under the ROC curve and sensitivity were both higher than those of the combined or single serum tumor marker test. CONCLUSIONS: This study preliminarily concludes that the CAC test, as a noninvasive test, has high sensitivity and specificity for the early diagnosis of lung cancer. This test is expected to help with the early detection of disease in lung cancer patients.

Clinical efficacy of treatment for primary tracheal tumors by flexible bronchoscopy: Airway stenosis recanalization and quality of life.

The aim of the present study was to evaluate the effectiveness of interventional treatment of primary tracheal tumors through flexible bronchoscopy. The clinical data of 38 patients with primary tracheal tumours who underwent flexible bronchoscopy intervention therapy between January 2011 and January 2017 were retrospectively analyzed. The average time interval from onset of symptoms to the appearance of actual clinical manifestations in the 38 patients ranged from 0 to 60 months, with an average of 8.1±11.6 months and a median of 4.2 months. The rate of misdiagnosis at the first visit was 36.8% (14/38). After interventional treatment, the overall efficiency (complete + partial response) of airway stenosis recanalization in the 38 patients was 89.5%. In 3 patients with benign tumors, the anhelation score was reduced following treatment (1.00±0.77 vs. 3.13±1.21 at the pre-treatment stage; P<0.001). The overall survival rates of the 35 patients at 1, 3 and 5 years were 69.3, 48.7 and 20.3%, respectively. Therefore, flexible bronchoscopic intervention may effectively smoothen the airways of patients and relieve the symptoms of anhelation. Combining radiotherapy and chemotherapy may improve patient prognosis and safety.

The lncRNA NORAD/miR-520a-3p Facilitates Malignancy in Non-Small Cell Lung Cancer via PI3k/Akt/mTOR Signaling Pathway.

BACKGROUND/AIMS: The effects of lncRNA-NORAD/mir-520a-3p on proliferation and invasion of non-small cell lung cancer (NSCLC) were studied, and its potential molecular mechanism was discussed. METHODS: qRT-PCR was used to detect the expression of lncRNA NORAD and miR-520a-3p in non-small cell lung cancer tissues and cell lines. CCK-8 method and Transwell test were used to identify the effects of lncRNA NORAD on the proliferation and invasion in NSCLC. Target gene prediction and screening and luciferase reporter assay was used to verify downstream target genes of lncRNA NORAD. The expressions of PI3K, AKT, and mTOR proteins were detected by Western blot. RESULTS: Compared with normal tissues and cells, the expressions of lncRNA NORAD in cancer tissues and cells were significantly higher. Compared with normal cells, the expression of miR-520a-3p in cells was considerably lower. LncRNA NORAD could accelerate the growth and metastasis of NSCLC in vitro and in vivo. Luciferase reporter assay results indicated that miR-520a-3p was a downstream target gene of lncRNA NORAD. Further findings showed that lncRNA NORAD might bind to miR-520a-3p, thereby affecting the PI3k/Akt/mTOR signaling pathway. CONCLUSION: LncRNA NORAD can regulate the proliferation of NSCLC by regulating miR-520a-3p/PI3k/Akt/mTOR signaling pathway, thus promoting the occurrence and development of NSCLC.

Safety and complications of medical thoracoscopy in the management of pleural diseases.

BACKGROUND: Medical thoracoscopy is considered an overall safe procedure, whereas numbers of studies focus on complications of diagnostic thoracoscopy and talc poudrage pleurodesis. We conduct this study to evaluate the safety of medical thoracoscopy in the management of pleural diseases and to compare complications in different therapeutic thoracoscopic procedures. METHODS: A retrospective study was performed in 1926 patients, 662 of whom underwent medical thoracoscopy for diagnosis and 1264 of whom for therapeutic interventions of pleural diseases. Data on complications were obtained from the patients, notes on computer system, laboratory and radiographic findings. Chi-square test was performed to compare categorical variables and Fisher's exact test was used for small samples. RESULTS: The mean age was 51 ± 8.4 (range 21-86) years and 1117 (58%) were males. Diagnostic procedure was taken in 662 (34.4%) patients, whereas therapeutic procedure was taken in 1264 (65.6%) patients. Malignant histology was reported in 860 (44.6%) and 986 (51.2%) revealed benign pleural diseases. Eighty patients (4.2%) were not definitely diagnosed and they were considered as unidentified pleural effusion. One patient died during the creation of artificial pneumothorax, and the causes of death were supposed as air embolism or an inhibition of phrenic motoneurons and circulatory system. Complication of lung laceration was found in six patients (0.3%) and reexpansion pulmonary edema was observed in two patients (0.1%). Higher incidence of prolonged air leak was observed in bulla electrocoagulation group, in comparison with pleurodesis group. Moreover, pain and fever were the most frequently complications in pleurodesis group and cutaneous infection in entry site was the most frequently reported complication in pleural decortication of empyema group. CONCLUSIONS: Medical thoracoscopy is generally a safe and effective method, not only in the diagnosis of undiagnosed pleural effusions, but also in the management of pleural diseases. Mastering medical thoracoscopy well, improving patient management after the procedure and attempts to reduce the occurrence of post-procedural complications are the targets that physicians are supposed to achieve in the future.

Berberine induces mitochondrial­mediated apoptosis and protective autophagy in human malignant pleural mesothelioma NCI­H2452 cells.

Increasing evidence shows that berberine has antitumor effects against a number of tumor cells. In the present study, we evaluated the effect of berberine on the proliferation of the human malignant pleural mesothelioma (MPM) cell line NCI­H2452, and explored the therapeutic potential and underlying mechanisms of this agent. Our results showed that berberine inhibited the proliferation of NCI­H2452 cells in a dose­ and time­dependent manner and could induce apoptosis, possibly through a caspase­9­dependent intrinsic mitochondrial pathway. In addition, autophagy was induced by berberine, which was characterized by the accumulation of LC3­II and decreased p62 expression. We used inhibitors of apoptosis and autophagy, and an inducer of autophagy, to evaluate the significance of autophagy in berberine­induced cell death. The results demonstrated that apoptosis is the primary route through which berberine induces NCI­H2452 cell death. Berberine­induced autophagy may be an adaptive response to antitumor agents and have a protective role in MPM cells. Inhibition of autophagy enhanced berberine­induced apoptosis. Therefore, inhibition of autophagy may be an effective treatment strategy in the management of MPM. In conclusion, berberine is a potent antitumor agent for treating MPM, and it induces mitochondrial­mediated apoptosis and protective autophagy in human NCI­H2452 MPM cells.

Screening key candidate genes and pathways involved in insulinoma by microarray analysis.

Insulinoma is a rare type tumor and its genetic features remain largely unknown. This study aimed to search for potential key genes and relevant enriched pathways of insulinoma.The gene expression data from GSE73338 were downloaded from Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified between insulinoma tissues and normal pancreas tissues, followed by pathway enrichment analysis, protein-protein interaction (PPI) network construction, and module analysis. The expressions of candidate key genes were validated by quantitative real-time polymerase chain reaction (RT-PCR) in insulinoma tissues.A total of 1632 DEGs were obtained, including 1117 upregulated genes and 514 downregulated genes. Pathway enrichment results showed that upregulated DEGs were significantly implicated in insulin secretion, and downregulated DEGs were mainly enriched in pancreatic secretion. PPI network analysis revealed 7 hub genes with degrees more than 10, including GCG (glucagon), GCGR (glucagon receptor), PLCB1 (phospholipase C, beta 1), CASR (calcium sensing receptor), F2R (coagulation factor II thrombin receptor), GRM1 (glutamate metabotropic receptor 1), and GRM5 (glutamate metabotropic receptor 5). DEGs involved in the significant modules were enriched in calcium signaling pathway, protein ubiquitination, and platelet degranulation. Quantitative RT-PCR data confirmed that the expression trends of these hub genes were similar to the results of bioinformatic analysis.The present study demonstrated that candidate DEGs and enriched pathways were the potential critical molecule events involved in the development of insulinoma, and these findings were useful for better understanding of insulinoma genesis.

Erythromycin poudrage versus erythromycin slurry in the treatment of refractory spontaneous pneumothorax.

BACKGROUND: Refractory (recurrent or persistent) spontaneous pneumothorax with high recurrence rates required treatment either by continuous chest drainage or interventional approaches. Pleurodesis by sclerosing agents has become a significant therapy in the treatment of refractory spontaneous pneumothorax (RSP) on account of its high efficiency and safety. However, the efficacy, safety and appropriate mode of administration of intrapleural erythromycin for pleurodesis have not yet been realized in the treatment of RSP. METHODS: The trial was performed to compare thoracoscopic erythromycin poudrage with erythromycin slurry via a chest tube for patients with documented RSP. Fifty-seven patients with RSP were enrolled in this study with 30 patients for erythromycin poudrage and 27 patients for erythromycin slurry. Response to pleurodesis, complications and recurrences were recorded. Continuous variables were compared with t-test. Chi-square test was performed to compare categorical variables and Fisher's exact test was used for small samples. RESULTS: Twenty-four patients in the erythromycin poudrage group (80%) and sixteen in the erythromycin slurry (ES) group (59.26%) had an immediately successful pleurodesis within 5 days (P=0.087). Patients in erythromycin poudrage had shorter duration of postprocedural chest tube drainage (6.23±3.04 days) than patients in ES (10.67±9.81 days) (P=0.032). During the follow-up, there was no significant statistical difference in recurrence rates between the two groups. Common adverse reactions included fever and chest pain with no significant difference between the two groups. CONCLUSIONS: Erythromycin is an effective and safe sclerosing agent for pleurodesis in management of RSP. Both methods are safe but erythromycin poudrage is more effective than ES.

Overexpression of OCT4 is associated with gefitinib resistance in non-small cell lung cancer.

Epidermal growth factor receptor (EGFR)-targeted tyrosine kinase inhibitors (TKIs) have emerged as first-line drugs for non-small cell lung cancers (NSCLCs). However, the resistance to TKIs represents the key limitation for their therapeutic efficacy. We found that the difference of OCT4 expression between NSCLC and the adjacent non-tumourous tissues was statistically significant. Knockdown of OCT4 in NSCLC cells could decrease cell proliferation, and potentiate apoptosis induced by gefitinib, suggesting OCT4 may contribute to gefitinib resistance in NSCLC.

Serum albumin as a significant prognostic factor in patients with malignant pleural mesothelioma.

Our aim was to evaluate the prognostic role of the pretreatment serum albumin level in patients with malignant pleural mesothelioma (MPM) receiving platinum-based systemic chemotherapy. From 1995 to 2013, a total of 97 patients receiving platinum-based systemic chemotherapy for newly diagnosed MPM were enrolled. All clinical information and laboratory results were retrospectively collected from the medical records. The Kaplan-Meier method was used to calculate survival. The Cox proportional hazards model was used to identify significant independent prognostic factors for predicting survival. In total, 34 of the 97 patients (35.1 %) had hypoalbuminaemia (albumin ≤ 35 g/l). The 1-year overall survival rate was 44.1 % for patients with hypoalbuminaemia and 72.0 % for patients with a normal albumin level. Multivariate analysis indicated that pretreatment albumin was an independent prognostic factor in MPM. Patients with hypoalbuminaemia had a greater risk of death than those with a normal albumin level [hazard ratio (HR) 1.778; 95 % confidence interval (CI) 1.504-2.998; P = 0.031]. When albumin was entered as a continuous variable in the Cox regression model, the HR of death was significantly decreased by 9.8 % (95 % CI 0.851-0.956) for each 1-g/l increment. The pretreatment serum albumin level is a simple, inexpensive and easily measurable marker with prognostic significance in MPM patients treated with platinum-based systemic chemotherapy.

Prognostic nutritional index predicts outcomes of malignant pleural mesothelioma.

PURPOSE: Nutritional status has been associated with long-time outcomes in cancer patients. We investigated whether the prognostic nutritional index (PNI), an indicator of nutritional status, affects overall survival in patients with malignant pleural mesothelioma (MPM). METHODS: We enrolled 121 patients with histologically confirmed MPM, who had successfully undergone biopsy by medical thoracoscopy in this study. Demographic, clinical and laboratory data were collected retrospectively. The PNI was calculated as 10× serum albumin value (g/dl) + 0.005 × total lymphocyte count (per mm(3)) in peripheral blood. Univariate and multivariate analyses were used to identify prognostic factors. RESULTS: Mean pretreatment PNI was 44.6. PNI was significantly associated with age (P = 0.031), smoking habits (P = 0.039) and weight loss (P = 0.029). Survival analysis showed PNI to be an independent prognostic factor in MPM. Patients with lower PNIs (PNI < 44.6) had greater risk of death than those with higher PNIs (PNI ≥ 44.6; hazard ratio: 2.290; 95 % confidence interval: 1.415-3.706; P = 0.001). These analyses were adjusted for patient age, gender, smoking habits, dyspnea, chest pain, weight loss, primary site of tumor, histology, platinum-based systemic chemotherapy, hospital and stage. CONCLUSIONS: Pretreatment PNI is a novel independent prognostic factor in MPM.

Endostatin, an angiogenesis inhibitor, ameliorates bleomycin-induced pulmonary fibrosis in rats.

BACKGROUND: Recent evidence has demonstrated the role of angiogenesis in the pathogenesis of pulmonary fibrosis. Endostatin, a proteolytic fragment of collagen XVIII, is a potent inhibitor of angiogenesis. The aim of our study was to assess whether endostatin has beneficial effects on bleomycin (BLM)-induced pulmonary fibrosis in rats. METHODS: The rats were randomly divided into five experimental groups: (A) saline only, (B) BLM only, (C) BLM plus early endostatin treatment, (D) BLM plus late endostatin treatment, and (F) BLM plus whole-course endostatin treatment. We investigated the microvascular density (MVD), inflammatory response and alveolar epithelial cell apoptosis in rat lungs in each group at different phases of disease development. RESULTS: Early endostatin administration attenuated fibrotic changes in BLM-induced pulmonary fibrosis in rats. Endostatin treatment decreased MVD by inhibiting the expression of VEGF/VEGFR-2 (Flk-1) and the activation of extracellular signal-regulated protein kinase 1/2 (ERK1/2). Endostatin treatment also decreased the number of inflammatory cells infiltrating the bronchoalveolar lavage fluid during the early inflammatory phase of BLM-induced pulmonary fibrosis. In addition, the levels of tumour necrosis factor-α (TNF-α) and transforming growth factor ß1 (TGF-ß1) were reduced by endostatin treatment. Furthermore, endostatin decreased alveolar type II cell apoptosis and had an epithelium-protective effect. These might be the mechanism underlying the preventive effect of endostatin on pulmonary fibrosis. CONCLUSIONS: Our findings suggest that endostatin treatment inhibits the increased MVD, inflammation and alveolar epithelial cell apoptosis, consequently ameliorating BLM-induced pulmonary fibrosis in rats.

Overexpression of Numb suppresses tumor cell growth and enhances sensitivity to cisplatin in epithelioid malignant pleural mesothelioma.

Malignant pleural mesothelioma (MPM) is a highly aggressive and conventional treatment-resistant tumor with a dismal prognosis. Among the three histological subtypes of MPM, the epithelioid is the most common type. Numb is considered as a tumor suppressor playing a critical role in controlling asymmetric cell division, maintenance of stem cell compartments, ubiquitination of specific substrates and regulating Notch-, Hedgehog- and TP53-activated pathways. The present study was designed to analyze the role of Numb in epithelioid MPM. We investigated the expression of Numb in 39 epithelioid MPM and 22 normal pleural tissues by immunohistochemistry. Furthermore, we overexpressed Numb in NCI-H2452, an epithelioid human MPM cell line, and investigated the effect of Numb overexpression on the proliferation, apoptosis and sensitivity to cisplatin in cells. The expression of Numb was significantly lower in MPM compared to the control group and Numb had an inverse correlation with the ki-67 labeling index. Loss of Numb expression was associated with poor prognosis in epithelioid MPM. Overexpression of Numb in NCI-H2452 cells significantly inhibited proliferation, promoted apoptosis and enhanced sensitivity to cisplatin. Moreover, Numb overexpression activated caspase-9 and caspase-3 through release of cytochrome c as well as downregulation of XIAP and survivin. We speculate that cytochrome c/caspase signaling is a possible mechanism through which Numb enhances the apoptosis of NCI-H2452 cells. These results suggest that Numb may be involved in epithelioid MPM development, and its upregulation may confer sensitivity to cisplatin, suggesting potential therapeutic options for MPM.

Effects of partial portal vein arterialization on liver regeneration after hepatectomy in minipigs with obstructive jaundice.

BACKGROUND: Hilar cholangiocarcinoma is a malignant tumor that is difficult to cure. The aim of this study was to observe the effects of flow-controlled partial portal vein arterializations (PPVA) on liver regeneration after hepatectomy in minipigs with chronic obstructive jaundice. METHODS: Eight minipigs were made into chronic obstructive jaundice models. United semi-hepatectomy, which imitates extended radical surgery for treatment of hilar cholangiocarcinoma, was then performed. The eight minipigs were randomly divided into groups A and B (n = 4 minipigs each). PPVA was performed in Group A but not in Group B. The effects of flow-controlled PPVA on live regeneration after hepatectomy were observed for 30 days after hepatectomy. RESULTS: The portal vein PO(2) at the immediate time point and on postoperative day 30 was higher in Group A ((47.33 ± 2.43) and (48.50 ± 4.44) mmHg) than in Group B ((35.38 ± 4.06) and (35.55 ± 2.55) mmHg respectively, all P < 0.01). The mitotic index of liver cells on postoperative days 14 and 21 was higher in Group A (12.55% ± 2.85% and 15.25% ± 1.99% respectively) than in Group B (6.85% ± 2.10% and 11.88% ± 1.15% respectively, all P < 0.05). The regeneration rate of residual liver on postoperative days 14 and 21 was higher in Group A (24.56% ± 6.15% and 70.63% ± 9.83% respectively) than in Group B (11.96% ± 5.43% and 44.92% ± 7.42% respectively, P < 0.05 and P < 0.01 respectively). CONCLUSION: Flow-controlled PPVA can promote liver regeneration after hepatectomy and prevent liver failure in minipigs with chronic obstructive jaundice.

Amplified in breast cancer 1 enhances human cholangiocarcinoma growth and chemoresistance by simultaneous activation of Akt and Nrf2 pathways.

UNLABELLED: Transcriptional coactivator amplified in breast cancer 1 (AIB1) plays important roles in the progression of several cancers such as prostate cancer, breast cancer, and hepatocellular carcinoma. However, its role in cholangiocarcinoma (CCA), a chemoresistant bile duct carcinoma with a poor prognosis, remains unclear. In this study we found that AIB1 protein was frequently overexpressed in human CCA specimens and CCA cell lines. Down-regulation of AIB1 induced the G2/M arrest and decreased the expression of mitosis-promoting factors including Cyclin A, Cyclin B, and Cdk1 through suppressing the Akt pathway, which resulted in inhibiting CCA cell proliferation. In addition, AIB1 enhanced the chemoresistance of CCA cells at least in part through up-regulating the expression of antiapoptotic protein Bcl-2. AIB1 regulated the expression of Bcl-2 in CCA cells through activating the Akt pathway as well as suppressing intracellular reactive oxygen species (ROS). AIB1 suppressed ROS by up-regulating antioxidants such as glutathione synthetase and glutathione peroxidase, which are targets of the NF-E2-related factor 2 (Nrf2), a critical transcription factor that regulates antioxidants, detoxification enzymes, and drug efflux proteins. AIB1 also increased the expression of another two Nrf2 targets, ABCC2 and ABCG2, to enhance drug efflux. AIB1 served as an essential coactivator for Nrf2 activation by physically interacting with Nrf2 to enhance its transcriptional activity. CONCLUSION: AIB1 plays an important role in proliferation and chemoresistance of CCA through simultaneous activation of Akt and Nrf2 pathways, suggesting that AIB1 is a potential molecular target for CCA treatment.

EGFR mutations predict a favorable outcome for malignant pleural effusion of lung adenocarcinoma with Tarceva therapy.

The aim of the present study was to evaluate the therapeutic effects and adverse reactions of Tarceva treatment for malignant pleural effusion (MPE) caused by metastatic lung adenocarcinomas. One hundred and twenty-eight patients who failed first-line chemotherapy drug treatment were divided into a mutation and a non-mutation group according to the presence or absence of epidermal growth factor receptor (EGFR) mutations. Each patient received closed drainage combined with simple negative pressure suction after thoracoscopic talc poudrage pleurodesis and oral Tarceva treatment. Short-term and long-term clinical therapeutic effects of Tarceva were evaluated. The EGFR mutation rate in pleural metastatic tissues of lung adenocarcinoma acquired through video-assisted thoracoscopic surgery was higher compared to that in surgical resection specimens, plasma specimens and pleural effusion specimens compared to previously reported results. There were significant statistical differences in the average extubation time (p<0.01), drainage volume of pleural effusion (p<0.05), Karnofsky score and formation of encapsulated pleural effusion 4 weeks after surgery (p<0.05) between these two groups. The number of patients with mild pleural hypertrophy in the mutation group was significantly higher compared to the non-mutation group (p<0.01), while the number of patients with severe pleural hypertrophy was significantly reduced (p<0.05). There was significant statistical discrepancy between these two groups in terms of improvement of peripheral blood carcinoembryonic antigen and tissue polypeptide antigen after 4 weeks of therapy. The complete remission rate and the efficacy rate were higher in the mutation group compared to that in the non-mutation group (p<0.05). There was a longer overall survival time after Tarceva treatment in patients with EGFR mutations than those without EGFR mutation. EGFR mutations predict a favorable outcome for malignant pleural effusion of lung adenocarcinoma with Tarceva therapy. Detection of EGFR mutations may determine the responsiveness of malignant pleural effusion to Tarceva treatment.