Circular RNA circTMEM59 inhibits progression of pancreatic ductal adenocarcinoma by targeting miR-147b/SOCS1: An in vitro study.

Purpose: This study aimed to detect the role and mechanism of circTMEM59 in pancreatic ductal adenocarcinoma (PDAC). Methods: 66 paired PDAC tissues and normal samples were harvested from patients diagnosed and undergoing pancreatic cancer surgery in our hospital. The expression of circTMEM59 in PDAC tissues and cell lines was detected. Based on bioinformatics information, the circTMEM59 mimics, miR-147b mimics, miR-147b inhibitor and si-suppressor of cytokine signaling 1 (SOCS1) were transfected into PDAC cells. The expression levels of circTMEM59, miR-147b and SOCS1 were detected by quantitative real-time polymerase chain reaction (qRT-PCR). RNA interaction was confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Cell invasion and proliferation were evaluated by Transwell and Cell Counting Kit-8 (CCK-8) assays. The protein expression was detected by Western blot. Results: CircTMEM59 was confirmed to be downregulated in PDAC tumor tissues and cells. Low expression of circTMEM59 was closely correlated with the short survival time and poor clinicopathological characteristics. By up-regulating the expression of circTMEM59 in PDAC cells, cell proliferation, invasion and epithelial-mesenchymal transition (EMT) were inhibited. More importantly, miR-147b could be sponged by circTMEM59, and knockdown of miR-147b inhibited progression of PDAC cells. Further study revealed that SOCS1 was targeted by miR-147b. SOCS1 expression was negatively related to miR-147b expression and positively related to circTMEM59 expression in PDAC tissues. Upregulated miR-147b and downregulated SOCS1 could rescue the effects of circTMEM59 on cell proliferation, EMT and invasion. Conclusion: Our data indicated that circTMEM59 inhibited cell proliferation, invasion and EMT of PDAC by regulating miR-147b/SOCS1 axis.

Receptor Plants Alleviated Allelopathic Stress from Invasive Chenopodium ambrosioides L. by Upregulating the Production and Autophagy of Their Root Border Cells.

Chenopodium ambrosioides L. is an invasive plant native to the Neotropics that has seriously threatened the ecological security of China, and allelopathy is one of the mechanisms underlying its successful invasion. Maize (Zea mays L.) and soybean (Glycine max (L.) Merr.), as the main food crops, are usually affected by C. ambrosioides in their planting areas. The purpose of this study was to investigate the ultrastructure, autophagy, and release-related gene expression of receptor plant root border cells (RBCs) after exposure to volatile oil from C. ambrosioides and its main component α-terpene, which were studied using maize and soybean as receptor plants. The volatiles inhibited root growth and promoted a brief increase in the number of RBCs. As the volatile concentration increased, the organelles in RBCs were gradually destroyed, and intracellular autophagosomes were produced and continuously increased in number. Transcriptomic analysis revealed that genes involved in the synthesis of the plasma membrane and cell wall components in receptor root cells were significantly up-regulated, particularly those related to cell wall polysaccharide synthesis. Meanwhile, polygalacturonase and pectin methylesterases (PME) exhibited up-regulated expression, and PME activity also increased. The contribution of α-terpene to this allelopathic effect of C. ambrosioides volatile oil exceeded 70%. Based on these results, receptor plant root tips may increase the synthesis of cell wall substances while degrading the intercellular layer, accelerating the generation and release of RBCs. Meanwhile, their cells survived through autophagy of RBCs, indicating the key role of RBCs in alleviating allelopathic stress from C. ambrosioides volatiles.

KDOAM-25 Overcomes Resistance to MEK Inhibitors by Targeting KDM5B in Uveal Melanoma.

Background: Uveal Melanoma (UM) is a potentially lethal cancer, and epigenetics may participate in the regulation of MEK resistance. This study is aimed at targeting the epigenetic kinase to overcome the resistance to MEK inhibitor. Method: We developed the 92.1 and OMM1 MEK-inhibitor resistant cell lines by culturing them in the trametinib (Tra) mixed medium. We utilized CCK8 analysis for detecting the viability of the cell. Western blot was used to determine the ERK1/2 and Akt phosphorylation. Small compound library screening assays were carried out by CCK8 analysis. To test the apoptosis, we employed flow cytometric analysis with Annexin-V/PI. Western blot and CCK8 were used to explore the epigenetic regulation of KDM5B in MEK-resistance cell lines. To knock out the expression level of KDM5B, we used the CRISPR/Cas9 by lentivirus delivering well-validated shRNAs in pLKO.1 vector. The directly binding affinity of KDOAM-25 to KDM5B was determined by drug affinity responsive target stability (DARTS) and microscale thermophoresis (MST). Results: The phosphorylation of ERK1/2 and Akt (T308) was inhibited in OMM1 cell lines. However, inhibition of Tra was abolished in OMM1-R cell lines. From a compound screening assay, we identified that KDOAM-25 robustly inhibited the viability and colony formation of MEK-resistance cell lines. Furthermore, KDOAM-25 significantly promoted cell death in OMM1-R cells. H3K4me3 (tri-methylation of lysine 4 on histone H3) and H3K27ac (acetyl of lysine 27 on histone H3) were both upregulated in OMM1-R cells. Tra significantly inhibited the expression of KDM5B in OMM1-P cells. However, the effect on KDM5B was abolished in OMM1-R cells. Knockdown of KDM5B robustly suppressed the cell viability in OMM1-R cells. KDOAM-25 directly interacted with KDM5B. Conclusion: KDOAM-25 inhibited the viability and colony formation and promoted cell death of MEK-resistance cell lines through H3K4me3 and H3K27ac, indicating that KDOAM-25 may be a potential therapeutic agent for MEK resistance in UM patients.

Efficacy of erzhu jiedu recipe on hepatitis B cirrhosis with hyperalphafetoproteinemia: A randomized, double-blind, placebo-controlled clinical trial.

BACKGROUND: Hepatitis B cirrhosis with hyperalphafetoproteinemia is the intermediate stage of liver cirrhosis progressing to hepatocellular carcinoma (HCC), there is no effective way to treat precancerous lesions of liver in modern medicine. In recent decades, clinical and experimental evidence shows that Chinese medicine (CM) has a certain beneficial effect on Hepatitis B Cirrhosis. Therefore, this trial aims to evaluate the efficacy and safety of a CM erzhu jiedu recipe (EZJDR) for the treatment of Hepatitis B Cirrhosis with Hyperalphafetoproteinemia. METHODS: We designed a randomized, double blind, placebo-controlled clinical trial. A total of 72 patients of Hepatitis B Cirrhosis with hyperalphafetoproteinemia were randomized in 2 parallel groups. Patients in the control group received placebo granules similar to the EZJDR. In the EZJDR group, patients received EZJDR twice a day, after meals, for 48 weeks. The primary efficacy measures were changes in serum alpha-fetoprotein (AFP) and alpha-fetoprotein alloplasm (AFP-L3); The secondary indicators of efficacy are changes in liver function indicators, HBV-DNA level; Liver stiffness measurement (LSM); Hepatic portal vein diameter; T lymphocyte subgroup indexes during treatment. All data will be recorded in case report forms and analyzed by Statistical Analysis System software. Adverse events will also be evaluated. RESULTS: The results showed that EZJDR can significantly inhibit the levels of AFP and AFP-L3 in patients with hepatitis B cirrhosis and hyperalphafetoproteinemia and have good security. ETHICS AND DISSEMINATION: The study protocol was approved by the Medical Ethics Committee of Shuguang Hospital, affiliated with University of Traditional Chinese Medicine, Shanghai (NO.2018-579-08-01). TRIAL REGISTRATION: This trial was registered on Chinese Clinical Trial Center (NO.ChiCTR1800017165).

Preparation of Epidermal Growth Factor-Modified Targeted Doxorubicin Nanoliposomes and Therapy of Liver Cancer.

The objective of this study was to prepare doxorubicin-loaded EGF modified PEG-nanoparticles and evaluate its targeting capability and therapeutic effects with EGFR-expressing hepatocellular carcinoma cells. The morphology, particle size distribution, and doxorubicin content of the nanoparticles were measured, and the drug loading and encapsulation efficiency were calculated. The doxorubicin nanoparticles prepared were regular circular, with good dispersibility, no adhesion, and the average particle size was (136.7±9.3) nm. The average encapsulation efficiency was (76.67±8.63)%, the average drug loading was (3.86±0.55)%; the drug release rate of doxorubicin was 100% for 12 h, and the doxorubicin nanometer was loaded. The drug release rate of the granules was 52.9% at 24 h and 81.2% at 144 h. The inhibition rate of the proliferation of hepatocarcinoma cells by the doxorubicin-containing nanoparticles was slower than that of doxorubicin, and the IC50 of the two cells was 1.844 and 0.345 µg/mL, respectively. At the same time, apoptosis and cycle analysis showed that the doxorubicin nanoparticles could significantly inhibit the cell cycle of hepatoma cells and promote the apoptosis of hepatoma cells. This study successfully produced nanoparticles loaded with doxorubicin targeting EGFR, which has a good sustained release effect, and its antitumor effect is stronger than free doxorubicin.

Protein liposomes-mediated targeted acetylcholinesterase gene delivery for effective liver cancer therapy.

BACKGROUND: Effective methods to deliver therapeutic genes to solid tumors and improve their bioavailability are the main challenges of current medical research on gene therapy. The development of efficient non-viral gene vector with tumor-targeting has very important application value in the field of cancer therapy. Proteolipid integrated with tumor-targeting potential of functional protein and excellent gene delivery performance has shown potential for targeted gene therapy. RESULTS: Herein, we prepared transferrin-modified liposomes (Tf-PL) for the targeted delivery of acetylcholinesterase (AChE) therapeutic gene to liver cancer. We found that the derived Tf-PL/AChE liposomes exhibited much higher transfection efficiency than the commercial product Lipo 2000 and shown premium targeting efficacy to liver cancer SMMC-7721 cells in vitro. In vivo, the Tf-PL/AChE could effectively target liver cancer, and significantly inhibit the growth of liver cancer xenografts grafted in nude mice by subcutaneous administration. CONCLUSIONS: This study proposed a transferrin-modified proteolipid-mediated gene delivery strategy for targeted liver cancer treatment, which has a promising potential for precise personalized cancer therapy.

LncRNA XIST promotes pancreatic cancer migration, invasion and EMT by sponging miR-429 to modulate ZEB1 expression.

Pancreatic cancer (PC) has become a worldwide malignancy accompanied by high metastasis and extremely poor prognosis. The critical roles of long non-coding RNAs (lncRNAs) in PC are generally summarized as molecular sponges of microRNAs (miRNAs). We intended to investigate the biological function and mechanism of lncRNA X-inactive specific transcript (XIST) in PC progression, especially in PC cell migration and invasion. qPCR was applied to detect the expression levels of XIST and miR-429 in PC tissues and cell lines. The roles of XIST and miR-429 on PC cell migration, invasion and epithelial-mesenchymal transition (EMT) were assessed by wound healing, transwell, qPCR and Western blot assays, respectively. The regulating relationship among XIST, miR-429 and zinc finger E-box binding homeobox 1 (ZEB1) was investigated in PC cells. XIST was frequently upregulated while miR-429 was commonly downregulated in PC tissues, especially in metastatic PC tissues. Knockdown of XIST in two PC cell lines caused inhibition of migration, invasion and EMT capacities. Forced expression of miR-429 exerted the similar tumor suppressing effects. XIST repressed miR-429 expression thus upregulated ZEB1, one of the targets of miR-429. ZEB1 mediated the tumor suppressing roles of XIST knockdown in PC cells. We identified the critical axis of XIST/miR-429/ZEB1 in PC cell migration, invasion and EMT, which may aid in developing new therapeutic strategies for PC.

DKK4 enhances resistance to chemotherapeutics 5-Fu and YN968D1 in colorectal cancer cells.

Dickkopf-related protein 4 (DKK4) is a target of the ß-catenin/transcription factor 4 complex in colorectal cancer. Previous research has demonstrated that its expression level may vary and has indicated that it may have a role in the development of resistance to chemotherapy in colorectal cancer cells. In the present study, DKK4 was over expressed in several colorectal cancer cell lines. The DKK4 over-expressing cell lines were screened using reverse transcription quantitative polymerase chain reaction analysis and western blotting. Analysis of cell viability in the control and DKK4 over-expressing cell lines, following treatment with 5-fluorouracil (5-Fu), YN968D1 or both, indicated that DKK4 over-expressing cells exhibit increased drug resistance. The results of Transwell chamber assays suggested that DKK4 had an effect on cell migration. Furthermore, the results from flow cytometric analysis showed that the percentage of apoptotic cells was reduced in the DKK4 over-expressing cell lines, following drug treatment, compared with the control. The present data suggested that DKK4 may enhance the resistance of colorectal cancer cells to 5-Fu and YN968D1 treatment, when used alone or in combination.

Sonic Hedgehog-GLI Family Zinc Finger 1 Signaling Pathway Promotes the Growth and Migration of Pancreatic Cancer Cells by Regulating the Transcription of Eukaryotic Translation Initiation Factor 5A2.

OBJECTIVES: The Hh (hedgehog) signaling pathway is still waiting for further studies because its downstream molecular mechanism remains elusive. Because EIF5A2 (eukaryotic translation initiation factor 5A2) gene was up-regulated upon Gli1 (GLI family zinc finger 1) in pancreatic cancer (PC) cells, we speculated that this pathway might promote tumor progression through regulating EIF5A2. METHODS: We investigated regulation effect of Hh signaling pathway to EIF5A2 gene transcription by Gli1 knockdown or overexpression in PC cell lines first. Then, the regulation mechanism of Gli1 to EIF5A2 gene was studied at transcription level. Finally, we studied cancer-promoting effects of Gli1-dependent EIF5A2 in PC cells. RESULTS: The data showed that Gli1 up-regulated expression of EIF5A2 by promoting transcription via cis-acting elements in PC cells. Moreover, vimentin gene was up-regulated significantly by sonic hedgehog (SHh)/Gli1 expression increasing, and E-cadherin was significantly reduced. The EIF5A2 knockdown partially reversed cell proliferation and migration induced by artificial SHh overexpression and inhibited epithelial mesenchymal transition process in PC cells with SHh overexpression (P < 0.05). CONCLUSIONS: Our data establish a novel transcription mechanism of Gli1 to EIF5A2 gene in cis-regulatory manner in PC cells. Thus, EIF5A2 oncogene effect could be incorporated into cancer-promoting molecular network upon Hh signaling pathway.

High prevalence of hepatitis B virus infection in primary central nervous system lymphoma.

Primary central nervous system lymphoma (PCNSL) is a rare extranodal form of non-Hodgkin lymphoma (NHL). The present study aimed to investigate the potential association between infection with the Hepatitis B virus (HBV) and PCNSL. The prevalence of HBV infection in 199 patients with PCNSL was compared in our hospital with that of an age-and sex-matched group of patients with other cancers (except liver cancer), and with a national population-based control group. Enzyme-linked immunosorbent assays were used to test blood samples for HBV markers. It was found that the prevalence of HBV infection in PCNSL was 16.1%, which was higher as compared with patients with other non-hematologic cancers and the national population-based control group. In conclusion, the present study demonstrated that PCNSL patients had a higher prevalence of HBV infection and suggested a potential association between infection with HBV and PCNSL.

A phase II FOLFOX-4 regimen as second-line treatment in advanced biliary tract cancer refractory to gemcitabine/cisplatin.

OBJECTIVE: We aimed to evaluate the efficacy and safety of oxaliplatin, 5-fluorouracil (5-FU), and leucovorin (LV) (FOLFOX-4) as second-line treatment in patients with advanced biliary tract cancer (BTC) failing gemcitabine/cisplatin first-line chemotherapy. METHODS: Thirty-seven patients with advanced BTC refractory to gemcitabine/cisplatin chemotherapy were included in the study. FOLFOX-4 regimen consisted of oxaliplatin (85 mg/m(2)) as a 2-hour infusion on day 1 and 2-hour infusion of LV (200 mg/m(2)/day) followed by a 5-FU bolus (400 mg/m(2)/day) and 22-hour infusion of 5-FU (600 mg/m(2)/day) for two consecutive days every 2 weeks. The primary end point was the time to progression (TTP). RESULTS: Between January 2009 and January 2012, a total of 37 patients were enrolled. The median age was 57 years (range 32-70) and male to female ratio was 21:16. Median TTP was 3·1 months (95% CI 2·3-3·6). The objective response rate was 21·6% (eight partial responses), and disease control rate was 62·2% (15 stable disease). Grade 3-4 toxicities were observed in 37·8% of the patients with neutropenia and fatigue being the most frequent (21·6%). CONCLUSIONS: FOLFOX-4 regimen is a feasible and moderately efficacious second-line chemotherapy for advanced BTC.

Efficacy of capecitabine and oxaliplatin regimen for extrahepatic metastasis of hepatocellular carcinoma following local treatments.

AIM: To investigate the efficacy and safety of capecitabine and oxaliplatin (CapeOx) for extrahepatic metastasis after local treatment of hepatocellular carcinoma (HCC). METHODS: Thirty-two patients with extrahepatic metastasis of HCC after local treatment were prospectively enrolled. The CapeOx regimen consisted of capecitabine 1000 mg/m(2) taken orally twice daily on days 1-14, and oxaliplatin was administered at a total dose of 100 mg/m(2) on day 1. The treatment was repeated every 3 wk until disease progression or unaccetablle toxicity. Efficacy and safety were assessable for all enrolled patients. The primary objective of this study was to assess the overall response rate. The secondary objectives were to evaluate the overall survival (OS), the time to tumor progression (TTP) and the toxicity profile of the combined strategy. TTP and OS were assessed by the Kaplan-Meier method and differences between the curves were analyzed using the log-rank test. The statistical software SPSS version 15.0 for Windows (SPSS Inc., Chicago, IL, United States) was used for statistical analysis. All P values were 2-tailed, with statistical significance defined by P ≤ 0.05. RESULTS: Thirty-two patients were assessable for efficacy and toxicity. The median follow-up duration was 15 mo (range, 12-20 mo). At the cut-off date of March 31, 2012, 27 patients died due to tumor progression and one patient died of myocardial infarction. Four patients were still alive (three patients with disease progression). OR was 21.9% (n = 7), the stabilization rate was 40.6% (n = 13), and the disease control rate was 62.5%. The responses lasted from 4 to 19 mo (median, 6 mo). Median TTP was 4.2 mo (95%CI: 2.5-7.4), and the median OS time was 9.2 mo (95%CI: 6.5-17.8). The 1-year survival rate was 43.6% (95%CI: 29.0-66.0). In a multivariate analysis, OS was significantly longer in patients with a Child-Pugh class A compared with class B patients (P = 0.014), with a median OS of 10.1 mo vs 5.4 mo, and there were trends towards longer OS (P = 0.065) in patients without portal vein tumor thrombosis. There were no significant effects of age, gender, performance status, cirrhosis, metastatic sites, and level of alpha fetoprotein (AFP) or hepatitis B virus-DNA on OS. Among the 22 patients with elevated AFP levels at baseline (≥ 400 ng/mL), the level fell by more than 50% during treatment in 6 patients (27.3%). The most frequent treatment-related grade 3 to 4 toxicities included leucopenia/neutropenia, transient elevation of aminotransferases, hand-foot syndrome and fatigue. CONCLUSION: CapeOx showed modest anti-tumor activity in metastatic HCC. However, the manageable toxicity profile and the encouraging disease control rate deserve further study for these patients.

Genome-wide screening reveals an EMT molecular network mediated by Sonic hedgehog-Gli1 signaling in pancreatic cancer cells.

AIMS: The role of sonic hedgehog (SHH) in epithelial mesenchymal transition (EMT) of pancreatic cancer (PC) is known, however, its mechanism is unclear. Because SHH promotes tumor development predominantly through Gli1, we sought to understand its mechanism by identifying Gli1 targets in pancreatic cancer cells. METHODS: First, we investigated invasion, migration, and EMT in PC cells transfected with lentiviral Gli1 interference vectors or SHH over-expression vectors in vitro and in vivo. Next, we determined the target gene profiles of Gli1 in PC cells using cDNA microarray assays. Finally, the primary regulatory networks downstream of SHH-Gli1 signaling in PC cells were studied through functional analyses of these targets. RESULTS: Our results indicate there is decreased E-cadherin expression upon increased expression of SHH/Gli1. Migration of PC cells increased significantly in a dose-dependent manner within 24 hours of Gli1 expression (P<0.05). The ratio of liver metastasis and intrasplenic miniature metastasis increased markedly upon activation of SHH-Gli1 signals in nude mice. Using cDNA microarray, we identified 278 upregulated and 59 downregulated genes upon Gli1 expression in AsPC-1 cells. The data indicate that SHH-Gli1 signals promote EMT by mediating a complex signaling network including TGFß, Ras, Wnt, growth factors, PI3K/AKT, integrins, transmembrane 4 superfamily (TM4SF), and S100A4. CONCLUSION: Our results suggest that targeting the molecular connections established between SHH-Gli1 signaling and EMT could provide effective therapies for PC.

Capecitabine "metronomic" chemotherapy for palliative treatment of elderly patients with advanced gastric cancer after fluoropyrimidine-based chemotherapy.

We aimed to study the efficacy and safety of metronomic capecitabine in pretreated elderly patients with advanced gastric cancer. Eligible patients with advanced gastric cancer were treated with capecitabine at a fixed dose 1,000 mg daily (days 1-28 continuously, every 5 weeks) until disease progression or significant toxicity. Tumor response was assessed every 10 weeks by computed tomography scan using Response Evaluation Criteria in solid tumors. In total, 45 patients were enrolled, of whom 43 were evaluated for efficacy and 45 for safety. A median of 3 cycles (range 1-12) were administered. Metronomic chemotherapy had a disease control rate (DCR) at 8 weeks of 51.1% (95% CI 25.7-67.8), and the objective response rate was 20.9% (95% CI 13.1-38.5, 9 of 43 assessable patients). The median time-to-progression and median overall survival were 3.6 months (95% CI: 3.2-4.0 months) and 7.6 months (95% CI 7.0-8.2 months), respectively. Grade II neutropenia and thrombocytopenia were observed in 13.3 and 2.2% of patients, respectively. Grade II/III nonhematological toxicities included diarrhea (4.4%), stomatitis (13.4%), and hand-foot syndrome (15.5%). No grade IV toxicity, neutropenic fever or treatment-related deaths occurred. Metronomic capecitabine was effective and well tolerated as palliative treatment in elderly patients with advanced gastric cancer after fluoropyrimidine-based chemotherapy.

[Vascular endothelial cells targeted Tyr-RGD-PEG-PEI nano-drug synthesis and its biological activity].

The study is designed to synthesize nano-carrier Tyr-RGD (cyclo-[Arg-Gly-Asp-d-Tyr-Lys]) and poly(ethylene glycol) modified polyethylenimine (Tyr-RGD-PEG-PEI) targeting vascular endothelial cells, then analyze its nanoparticle properties and the characteristics of drug carrying and targeting properties in vivo / in vitro tumor. The nano-carrier Tyr-RGD-PEG-PEI was synthesized with the method of chemical synthesis and the properties of this nanoparticle and drug carrying characteristics were identified. Its effect of targeting vascular endothelial cells in vitro was studied with the method of competitive binding assay. The fluorescent labeled nano-drug was injected into tumor-bearing nude mice to observe its tumor-targeting. The mean size of nano-carrier Tyr-RGD-PEG-PE was about 145 nm, good in encapsulation efficiency of siRNA. After incubation in plasma for half an hour, only about 3 percent of siRNA out. It was confirmed that it was a single spot with TLC analysis, the R(f) value was 0.65. Receptor competition experiments showed that the nano could effectively compete with RGD in binding the receptors on endothelial cells. Tumor-bearing nude mice experiments showed that when containing a fluorescent-labeled siRNA of Tyr-RGD-PEG-PEI nano-drug was injected into mice, after 24 hours this nano-drug mainly distributed within the tumor tissue. However, nano-drug without Tyr-RGD appeared in tumor tissue as well as other organs such as livers, lungs, etc. The Tyr-RGD-targeted gene vector Tyr-RGD-PEG-PEI synthesized in this study has good nanoparticle properties and high efficiency of gene-drug encapsulation. Study of nude mice shows that the ability of its tumor-targeting is significantly better than nano-drug without Tyr-RGD.

[Study on glucose metabolic rate in non-small cell lung cancer patients with blood stasis syndrome and non-blood stasis syndrome].

OBJECTIVE: To study the difference of glucose metabolic rate in non-small cell lung cancer (NSCLC) patients with blood stasis syndrome and with non-blood stasis syndrome. METHODS: Whole body positron emission tomography (PET) and functional agent 2-[fluorine-18] fluorine-2-deoxy-glucose (18FDG) were used to detect the 18FDG uptake value in regions of interest (ROI) in tumor tissue of patients. RESULTS: In patients with same pathologic type, the maximum and mean standardized uptake value (Max SUV and Mean SUV) were significantly higher in the blood stasis group than those in the non-blood stasis group (P < 0.01); it also showed the same in patients with NSCLC of phase I, II and III (P < 0.05), but the 18FDG uptake rate was obviously enhanced in patients of phase IV (P < 0.01). CONCLUSION: The glucose uptake in NSCLC patients of blood stasis syndrome was higher than that in those with of non-blood stasis syndrome.