CFHR1 involvement in bile duct carcinoma: Insights from a data mining study.

The aim of this study is to investigate the role of CFHR1 in bile duct carcinoma (BDC) and its mechanism of action, and we hope that our analysis and research will contribute to a better understanding of cholangiocarcinoma (BDC) disease genesis, progression and the development of new therapeutic strategies. The prognostic receiver operating characteristic curve of CFHR1 was generated using survival ROC. The ROC curve for CFHR1 showed that there is a correlation between CFHR1 expression and clinicopathological parameters and has an impact on poor prognosis. STRING was used to predict the protein-protein interaction network of the identified genes, and the Microenvironment Cell Populations counter algorithm was used to analyze immune cell infiltration within the BDC. The combined analysis showed that CFHR1 was found to be upregulated in BDC tissues, along with a total of 20 related differentially expressed genes (DEGs) (8 downregulated and 12 upregulated genes). Also, the results showed that the expression of CFHR1 is correlated with immune cell infiltration in tumor and immune cell markers in BDC (P < 0.05). In addition, we have verified experimentally the biological function of CFHR1. These findings suggest that CFHR1 may be a prognostic marker and a potential therapeutic target for BDC. Information regarding the detailed roles of CFHR1 in BDC could be valuable for improving the diagnosis and treatment of this rare cancer.

E2F2 promotes lung adenocarcinoma progression through B-Myb- and FOXM1-facilitated core transcription regulatory circuitry.

Lung adenocarcinoma (LUAD) causes severe cancer death worldwide. E2F2 is a canonical transcription factor implicated in transcription regulation, cell cycle and tumorigenesis. The role of E2F2 as well as its transcription regulatory network in LUAD remains obscure. In this study, we constructed a weighted gene co-expression network and identified several key modules and networks overrepresented in LUAD, including the E2F2-centered transcription regulatory network. Function analysis revealed that E2F2 overexpression accelerated cell growth, cell cycle progression and cell motility in LUAD cells whereas E2F2 knockdown inhibited these malignant phenotypes. Mechanistic investigations uncovered various E2F2-regulated downstream genes and oncogenic signaling pathways. Notably, three core transcription factors of E2F2, B-Myb and FOXM1 from the LUAD transcription regulatory network exhibited positive expression correlation, associated with each other, mutually transactivated each other, and regulated similar downstream gene cascades, hence constituting a consolidated core transcription regulatory circuitry. Moreover, E2F2 could promote and was essentially required for LUAD growth in orthotopic mouse models. Prognosis modeling revealed that a two-gene signature of E2F2 and PLK1 from the transcription regulatory circuitry remarkably stratified patients into low- and high-risk groups. Collectively, our results clarified the critical roles of E2F2 and the exquisite core transcription regulatory circuitry of E2F2/B-Myb/FOXM1 in LUAD progression.

B-Myb accelerates colorectal cancer progression through reciprocal feed-forward transactivation of E2F2.

B-Myb is an important transcription factor that plays a critical role in gene expression regulation and tumorigenesis. However, its functional implication in colorectal cancer remains elusive. In this study, we found that B-Myb was significantly upregulated at both mRNA and protein levels in colorectal cancer samples compared to non-tumor counterparts. B-Myb overexpression accelerated cell proliferation, cell cycle progression and cell motility in colorectal cancer cells, and promoted tumor growth in orthotopic nude mouse models in vivo. In contrast, B-Myb depletion inhibited these malignant phenotypes. Mechanistic investigations revealed that E2F2 was a novel transcriptional target of B-Myb and is essential to B-Myb-induced malignant phenotypes. Notably, B-Myb and E2F2 exhibited positive expression correlation, and interacted with each other in colorectal cancer cells. In addition to their autoregulatory mechanisms, B-Myb and E2F2 can also directly transactivate each other, thus constituting consolidated reciprocal feed-forward transactivation loops. Moreover, both B-Myb and E2F2 are required for the activation of ERK and AKT signaling pathways in colorectal cancer cells. Taken together, our data clarified a critical role for B-Myb in colorectal cancer and unraveled an exquisite mutual collaboration and reciprocal cross regulation between B-Myb and E2F2 that contribute to the malignant progression of human colorectal cancer.

Clinical verification of vimentin/EpCAM immunolipid magnetic sorting system in monitoring CTCs in arterial and venous blood of advanced tumor.

BACKGROUND: Circulating tumor cells (CTCs) are the dominant factor leading to tumor metastasis. This study aims to investigate the effect of disparate sources of CTCs on the treatment and prognosis of patients with advanced tumors by analyzing the number and gene mutations change of CTCs in arterial and venous blood in patients with advanced tumors. RESULTS: A CTCs sorting system was constructed based on Vimentin-immunolipid magnetic balls (Vi-IMB) and EpCAM immunolipid magnetic balls (Ep-IMB). Results showed that the prepared Ep-IMB and Vi-IMB had lower cytotoxicity, better specificity and sensitivity. The number of arterial CTCs was higher than that of venous CTCs, with a statistically significant difference (P < 0.05). Moreover, the prognosis of the low positive group of total CTCs in arterial blood and venous blood was higher than that of the high positive group, with a statistical significance (P < 0.05). The genetic testing results showed that the targeted drug gene mutations in tissues, arterial CTCs and venous CTCs showed a complementary trend, indicating that there was heterogeneity among different tumor samples. CONCLUSIONS: CTCs in blood can be efficiently captured by the CTCs sorting system based on Vi-LMB/Ep-LMB, and CTCs detection in arterial blood can be utilized to more accurately evaluate the prognosis and predict postoperative progress. It is further confirmed that tumor samples from disparate sources are heterogeneous, providing a reference basis for gene mutation detection before clinical targeted drug treatment, and the detection of CTCs in arterial blood has more potential clinical application value. TRIAL REGISTRATION: The Ethics Committee of Putuo Hospital, PTEC-A-2019-18-1. Registered 24 September 2019.

miR-532-3p Inhibits Proliferation and Promotes Apoptosis of Lymphoma Cells by Targeting ß-Catenin.

Background: Dysregulated expression of miR-532-3p has been observed in several types of cancer and plays a key role in tumor progression and metastasis. In this study, we analyzed the role and molecular mechanism of miR-532-3p in lymphoma progression. Methods: The expression of miR-532-3p in lymphoma sample tissues was analyzed using the GEO database and in cell lines by quantitative reverse transcription (qRT)-PCR. The functions of miR-532-3p in lymphoma cell proliferation and apoptosis were analyzed by CCK-8 assay and Annexin V-FITC/propidium iodide staining, respectively. In vivo, the tumor weight and volume were measured. The target gene of miR-532-3p was predicted using miRanda software, and then luciferase, qRT-PCR, and western blot assays were performed to verify that ß-catenin was the downstream target gene of miR-532-3p. Results: miR-532-3p was decreased in lymphoma tissues and cell lines. In vitro and in vivo experiments showed that overexpression of miR-532-3p inhibited lymphoma cell proliferation and promoted apoptosis. Mechanistic studies demonstrated that ß-catenin was a functional target gene of miR-532-3p. Furthermore, we found that overexpression of ß-catenin reversed the tumor-suppression activities caused by overexpression of miR-532-3p in lymphoma proliferation and apoptosis. Conclusion: This study demonstrates that miR-532-3p functions as a tumor inhibitor in lymphoma progression by targeting ß-catenin, suggesting miR-532-3p/ß-catenin as a new diagnosis marker or potential therapeutic target in lymphoma.

BTG4 is A Novel p53 Target Gene That Inhibits Cell Growth and Induces Apoptosis.

BTG4 is the last cloned and poorly studied member of BTG/Tob family. Studies have suggested that BTG4 is critical for the degradation of maternal mRNAs in mice during the process of maternal-to-zygotic transition, and downregulated in cancers, such as gastric cancer. However, the regulatory mechanism of BTG4 and its function in cancers remain elusive. In this study, we have for the first time identified the promoter region of the human BTG4 gene. Serial luciferase reporter assay demonstrated that the core promoter of BTG4 is mainly located within the 388 bp region near its transcription initiation site. Transcription factor binding site analysis revealed that the BTG4 promoter contains binding sites for canonical transcription factors, such as Sp1, whereas its first intron contains two overlapped consensus p53 binding sites. However, overexpression of Sp1 has negligible effects on BTG4 promoter activity, and site-directed mutagenesis assay further suggested that Sp1 is not a critical transcription factor for the transcriptional regulation of BTG4. Of note, luciferase assay revealed that one of the intronic p53 binding sites is highly responsive to p53. Both exogenous p53 overexpression and adriamycin-mediated endogenous p53 activation result in the transcriptional upregulation of BTG4. In addition, BTG4 is downregulated in lung and colorectal cancers, and overexpression of BTG4 inhibits cell growth and induces apoptosis in cancer cells. Taken together, our results strongly suggest that BTG4 is a novel p53-regulated gene and probably functions as a tumor suppressor in lung and colorectal cancers.

Identification and characterization of the promoter of cancer-related gene LOXL2.

Lysyl oxidase like 2, LOXL2, as a member of the lysyl oxidase (LOX) family, has been shown to function similarly to LOX in the extracellular matrix (ECM) by promoting crosslinking of collagen and elastin. LOXL2 is also engaged to transcription regulation, cell signaling transduction and cell adhesion regulation. It has been reported that LOXL2 is highly expressed in several types of tumors and promotes cell proliferation and migration in various cancer cells. However, the regulatory mechanism of LOXL2 expression remains largely unknown. To further investigate its transcriptional regulatory mechanism, LOXL2 promoter region has been cloned and identified in the present study. Chromatin state analysis revealed that LOXL2 gene locus contained an active promoter near its first exon. We then constructed five different LOXL2 gene promoter luciferase reporter constructs covering 1.7 kb upstream of LOXL2 gene transcription initiation site. Series luciferase reporter assay demonstrated that all the five constructs showed notable promoter activity, and LOXL2 core promoter was located in a region of 185 bp near the transcription initiation site. Transcriptional factor binding analysis indicated that, LOXL2 promoter lacked classical TATA box, but contained putative binding sites for classic transcriptional factors such as Sp1 and NF-κB. Ectopic overexpression of Sp1 significantly enhanced LOXL2 promoter activity as well as its endogenous expression in cells. In contrast, mithramycin A (a selective Sp1 inhibitor) treatment repressed LOXL2 promoter as well as its endogenous transcription. Site directed mutagenesis assay further confirmed that the Sp1 binding sites were essential for proximal prompter activity of LOXL2 gene. Chromatin immunoprecipitation (ChIP) assay revealed that Sp1 bound LOXL2 promoter in vivo. Of note, the expression of Sp1 and LOXL2 are positively correlated, and the higher expression of LOXL2 is associated with poor prognosis in colorectal cancer, strongly suggesting the implication of Sp1-mediated LOXL2 transactivation in the pathogenesis of colorectal cancer.

B-Myb Mediates Proliferation and Migration of Non-Small-Cell Lung Cancer via Suppressing IGFBP3.

B-Myb has been shown to play an important oncogenic role in several types of human cancers, including non-small-cell lung cancer (NSCLC). We previously found that B-Myb is aberrantly upregulated in NSCLC, and overexpression of B-Myb can significantly promote NSCLC cell growth and motility. In the present study, we have further investigated the therapeutic potential of B-Myb in NSCLC. Kaplan⁻Meier and Cox proportional hazards analysis indicated that high expression of B-Myb is significantly associated with poor prognosis in NSCLC patients. A loss-of-function study demonstrated that depletion of B-Myb resulted in significant inhibition of cell growth and delayed cell cycle progression in NSCLC cells. Notably, B-Myb depletion also decreased NSCLC cell migration and invasion ability as well as colony-forming ability. Moreover, an in vivo study demonstrated that B-Myb depletion caused significant inhibition of tumor growth in a NSCLC xenograft nude mouse model. A molecular mechanistic study by RNA-seq analysis revealed that B-Myb depletion led to deregulation of various downstream genes, including insulin-like growth factor binding protein 3 (IGFBP3). Overexpression of IGFBP3 suppressed the B-Myb-induced proliferation and migration, whereas knockdown of IGFBP3 significantly rescued the inhibited cell proliferation and motility caused by B-Myb siRNA (small interfering RNA). Expression and luciferase reporter assays revealed that B-Myb could directly suppress the expression of IGFBP3. Taken together, our results suggest that B-Myb functions as a tumor-promoting gene via suppressing IGFBP3 and could serve as a novel therapeutic target in NSCLC.

Immunomagnetic Lipid Separation and Plastin Identification for Pancreatic Cancer Cells and Its Clinical Application.

Circulating tumour cells isolated from the peripheral blood of patients have the advantage of being non-invasive. The aim of this study was to develop an effective method for detecting pancreatic cancer micrometastasis from peripheral blood and explore the clinical application value of the separation of circulating pancreatic cancer cells using epithelial cell adhesion molecule (EpCAM) lipid magnetic spheres (ELMS) and plastin monoclonal antibody for identification. The pancreatic cancer PANC-1 cells were respectively added to phosphate-buffered saline (PBS) and fresh blood provided by healthy volunteers to detect cell recovery using ELMS. Moreover, trials were conducted using nude mice with tumour and samples from patients with pancreatic cancer to evaluate the effect of CTC isolation and identification. The prepared ELMS captured PANC-1 cells from blood with high efficiency, which was similar to the efficiency obtained with nude mice with tumour and the samples from patients with pancreatic cancer, in agreement with the clinical test results. This study is based on the high efficiency of the EpCAM magnetic nanolipid sphere separation system capturing CTC of pancreatic cancer, which provides a strong support for investigating pancreatic cancer, in terms of its early diagnosis, preoperative and post-operative analysis and analysing the treatment effects.

Icariin inhibits LPS-induced cell inflammatory response by promoting GRα nuclear translocation and upregulating GRα expression.

AIMS: Icariin (ICA) is a flavonoid isolated from certain plant species in the genus Epimedium, especially Epimedium brevicornum. Previous studies indicated that ICA has certain regulatory effects on some inflammatory diseases, and that ICA regulates the activity of glucocorticoid receptor (GR) and NF-κB. But the causal link between GR and NF-κB and other downstream pathways in effects of ICA remained elusive, therefore here we have investigated whether ICA could promote GR function, in turn, to regulate NF-κB and/or other factors to achieve its anti-inflammatory effect. MAIN METHODS: Inflammatory cell models were induced by lipopolysaccharide (LPS) in RAW 264.7 and HeLa cell line. Observation of GRα nuclear translocation by confocal laser scanning microscopy. GRα and inflammatory cytokines expression was detected by RT-qPCR, Western Blotting and ELISA. Co-immunoprecipitation technique was used to detect the binding of GRα to downstream transcription factors. GRα activity was blocked by GRα antagonist RU486, and GR downstream transcription factors including NF-κB, c-Jun, and Stat3 were silenced by corresponding RNA interference. KEY FINDINGS: In both inflammatory cell models, ICA decreased LPS-induced production of inflammatory cytokines (IL-6 and TNF-α). While ICA up-regulated the amount of GRα and promoted its nucleus translocation. The increased GRα in the nucleus by ICA bound more NF-κB, c-Jun, and Stat3. Blockade GRα and silence of NF-κB, c-Jun, and Stat3 expression partially abolished the anti-inflammatory effects of ICA. SIGNIFICANCE: Promoted GR function and the consequent inhibition of pro-inflammatory transcription factors contribute a main mechanism by which ICA exerts its anti-inflammatory effect.

MicroRNA-98-5p Inhibits Cell Proliferation and Induces Cell Apoptosis in Hepatocellular Carcinoma via Targeting IGF2BP1.

Some microRNAs (miRs) have been demonstrated to play promoting or tumor-suppressing roles in the development and progression of hepatocellular carcinoma (HCC). However, the regulatory mechanism of miR-98-5p in HCC still remains largely unclear. In the present study, our data showed that miR-98-5p was significantly downregulated in 84 cases of HCC tissues compared to the matched adjacent nontumor tissues. In addition, downregulation of miR-98-5p was associated with tumor size, portal vein tumor embolus, node metastasis, and clinical stage in HCC. HCC patients with low expression of miR-98-5p showed a shorter survival time compared with those with high miR-98-5p levels. Moreover, the expression of miR-98-5p was also reduced in HCC cell lines (HepG2, Hep3B, LM3, and SMCC7721) compared to the normal liver cell line THLE-3. Overexpression of miR-98-5p significantly decreased LM3 cell growth by inducing cell cycle arrest at the G1 stage and cell apoptosis. Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) was then identified as a novel target gene of miR-98-5p, and its protein expression was negatively regulated by miR-98-5p in LM3 cells. Overexpression of IGF2BP1 eliminated the effects of miR-98-5p overexpression on the proliferation, cell cycle, and apoptosis of LM3 cells. Finally, we found that IGF2BP1 was upregulated in HCC, and its expression was negatively correlated to miR-98-5p levels. In summary, we demonstrate that miR-98-5p could inhibit HCC cell proliferation while inducing cell apoptosis, partly at least, via inhibition of its target gene IGF2BP1, and we suggest that miR-98-5p may become a promising therapeutic candidate for HCC treatment.

Role of the tumor microenvironment in pancreatic adenocarcinoma.

Pancreatic cancer is a devastating disease with proclivity for early metastasis, which accounts for its poor prognosis. The clinical problem of pancreatic cancer is its resistance to conventional therapies, such as chemotherapy or radiation. Based upon these challenges, the focus of research on pancreatic cancer has shifted gradually towards the tumor microenvironment. The cancer microenvironment consists of various components, including fibroblasts, endothelial cells, immune cells, and endocrine cells, that interact with each other, and with the cancer cells in a complex fashion. Evidence is accumulating that the cancer microenvironment plays an active role in disease progression, and efforts are being made to target this interplay between cancer cells and host cells, to improve the prognosis of the disease. In the present review, we describe the cellular microenvironment of pancreatic ductal adenocarcinoma (PDA), the major type of pancreatic cancer. Our hope is that a better understanding of the cellular microenvironment of PDA will eventually lead to better treatments for this disease.

MicroRNA-29a Promotes Pancreatic Cancer Growth by Inhibiting Tristetraprolin.

BACKGROUND/AIMS: The microRNA (miR) 29 family has been studied extensively for its involvement in several diseases, and aberrant expression of its members is associated with tumorigenesis and cancer progression. Here, we examined the role of miR-29a in pancreatic cancer and the involvement of tristetraprolin (TTP). METHODS: We monitored miR-29a and TTP expression in pancreatic cancer by qRT-PCR and western blotting. The effect of miR-29a on pancreatic cancer was determined through MTT assay and migration assay. The results were validated in the tumorigenesis model. RESULTS: We found that miR-29a was up regulated in pancreatic tumor tissues and cell lines and positively correlated with metastasis. Ectopic expression of miR-29a increased the expression of pro-inflammatory factors and epithelial-mesenchymal transition (EMT) markers, through down regulating TTP. TTP was down regulated in tumor tissues, and its ectopic expression decreased cell viability and migration in vitro, inhibited tumor growth and the EMT phenotype in vivo, and reversed the effect of miR-29a on tumor cell proliferation and invasion in vitro and in vivo. CONCLUSION: Our results suggest that miR-29a acts as an oncogene by down regulating TTP and provide the basis for further studies exploring the potential of miR-29a and TTP as biomarkers and targets for the treatment of pancreatic cancer.

MicroRNA-340 Inhibits Esophageal Cancer Cell Growth and Invasion by Targeting Phosphoserine Aminotransferase 1.

BACKGROUND/AIMS: Emerging evidence indicates that microRNA (miR)-340 is downregulated in various human cancers, suggesting that it acts as a tumor suppressor. The aim of the present study was to evaluate the expression and role of miR-340 in human esophageal squamous cell carcinoma (ESCC). METHODS: The expression of miR-340 was examined in 64 paired ESCC and adjacent non-tumor tissues by quantitative real time PCR. The effects of miR-340 on ESCC cell proliferation and metastasis were examined by MTT and Matrigel invasion assays. Tumor growth was assessed by subcutaneous inoculation of cells into BALB/c nude mice. Targets of miR-340 were identified by bioinformatics and verified by luciferase reporter assays, quantitative real-time PCR, and western blotting. RESULTS: MiR-340 was significantly downregulated in ESCC tumor tissues compared to adjacent non-tumor tissues and in ESCC cell lines compared to esophageal endothelial cells. Overexpression of miR-340 inhibited ESCC cell growth, colony formation, and invasion, and tumor growth in a xenograft mouse model. PSAT1 was identified as a direct target of miR-340 and its ectopic expression partially reversed the miR-340 mediated inhibition of viability, invasion and EMT in ESCC cells. The expression of miR-340 was negatively correlated with that of PSAT1 in human ESCC samples. CONCLUSION: MiR-340 functions as a tumor suppressor by modulating the expression of PSAT1 and may contribute to the progression and invasiveness of ESCC.

Application of chemokine receptor antagonist with stents reduces local inflammation and suppresses cancer growth.

Severe pain and obstructive jaundice resulting from invasive cholangiocarcinoma or pancreatic carcinoma can be alleviated by implantation of biliary and duodenal stents. However, stents may cause local inflammation to have an adverse effect on the patients' condition and survival. So far, no efficient approaches have been applied to prevent the occurrence of stents-related inflammation. Here, we reported significantly higher levels of serum stromal cell-derived factor 1 (SDF-1) in the patients that developed stents-associated inflammation. A higher number of inflammatory cells have been detected in the cancer close to stent in the patients with high serum SDF-1. Since chemokine plays a pivotal role in the development of inflammation, we implanted an Alzet osmotic pump with the stents to gradually release AMD3100, a specific inhibitor binding of SDF-1 and its receptor C-X-C chemokine receptor 4 (CXCR4), at the site of stents in mice that had developed pancreatic cancer. We found that AMD3100 significantly reduced local inflammation and significantly inhibited cancer cell growth, resulting in improved survival of the mice that bore cancer. Moreover, the suppression of cancer growth may be conducted through modulation of CyclinD1, p21, and p27 in the cancer cells. Together, these data suggest that inhibition of chemokine signaling at the site of stents may substantially improve survival through suppression of stent-related inflammation and tumor growth.

Percutaneous needle decompression in treatment of malignant small bowel obstruction.

AIM: To investigate the efficacy and safety of percutaneous needle decompression in the treatment of malignant small bowel obstruction (MSBO). METHODS: A prospective analysis of the clinical data of 52 MSBO patients undergoing percutaneous needle decompression was performed. RESULTS: Percutaneous needle decompression was successful in all 52 patients. Statistically significant differences were observed in symptoms such as vomiting, abdominal distension and abdominal pain before and after treatment (81.6% vs 26.5%, 100% vs 8.2%, and 85.7% vs 46.9%, respectively; all P < 0.05). The overall significantly improved rate was 19.2% (11/52) and the response rate was 94.2% (49/52) using decompression combined with nasal tube placement, local arterial infusion of chemotherapy and nutritional support. During the one-month follow-up period, puncture-related complications were acceptable. CONCLUSION: Percutaneous needle intestinal decompression is a safe and effective palliative treatment for MSBO.

Esophageal cancer stem cells express PLGF to increase cancer invasion through MMP9 activation.

Cancer stem cells (CSCs) are a distinct population in tumors and cause cancer relapse and metastasis. Thus, treating CSCs are believed to be potential to cure rapidly growing and highly metastatic cancers. To date, CSCs in esophageal cancer have not been characterized. In the current study, we detected significant higher levels of placental growth factor (PLGF) and matrix metalloproteinase 9 (MMP9) in the esophageal cancers with metastasis, compared to those without metastasis, in which the expression levels of PLGF and MMP9 strongly correlated with each other. Thus, we used a human esophageal cancer cell line, TE-1, to examine the cross talk of PLGF and MMP9. We found that the levels of PLGF in TE-1 cells positively affected the levels of MMP9, while the levels of MMP9 did not affected the levels of PLGF, suggesting that PLGF may activate MMP9 in esophageal cancer cells. Then, we separated PLGF-positive and PLGF-negative TE-1 cells that had been transfected with a GFP reporter under a PLGF promoter by flow cytometry. We found that PLGF-positive cells grew significantly faster than PLGF-negative cells both in vitro and in vivo in a stereotactical implantation model, suggesting that PLGF-positive cells are likely CSCs in esophageal cancer. Taken together, we demonstrate that PLGF-positive cells appear to be CSCs in esophageal cancer, and they may release PLGF to promote cancer metastasis through MMP9 activation.

[The study of clinical value of transarterial chemical perfusion as second-line therapy for late stage pancreatic cancer].

OBJECTIVE: To discuss arterial infusion chemotherapy as second-line treatment for advanced pancreatic carcinoma salvage after failed vein chemotherapy. METHODS: 35 cases with IV stage pancreatic carcinoma, all cases are failed first-line chemotherapy of Gemcitabine. Via femoral artery puncture, gastroduodenal artery, the dorsal pancreatic artery, pancreatic artery, pancreatic tail artery, the rib waist artery, superior mesenteric artery and tumor related to blood supply artery intubation and chemical drug perfusion. Plan: Cisplatin 30 mg/m², Gemcitabine 1 000 mg/m². Treatment for every 3-4 weeks, there is no limit on the total number. RESULTS: 35 cases were local chemotherapy for 217 cycles, at least 1 cycle, a maximum of 9 cycles, 6.2 cycles on average. Among which: CR 1 case, PR 6 cases, SD 15 cases, effective rate (CR+PR) is 20%, disease control rate (DCR) is 68.75%. The median survival time was 9.6 months. The median TTP was 3.7 months. Total effective rate of CBR , the stability rate of CBR and inefficiency rate of CBR were 51.4%, 25.7% and 22.9% respectively. Pain score improvement 88.57% (31/35), 42.86% (15/35) Pain relief last for 3-20 days ( median time 11 days). 17.14% (6/35) Pain relief last for more than 20 days. Pain relief maintain the most elderly 160 days. Half of the patients have different degree of side reaction, III, IV degree leukopenia accounted for 17.14% (6/35), 8.57% (3/35). CONCLUSION: The arterial perfusion chemotherapy as second-line treatment of advanced pancreatic cancer salvage is of clinical value, with better disease control rate and the rate of pain relief.

Objective tongue inspection on 142 liver cancer patients with damp-heat syndrome.

OBJECTIVE: To establish the diagnosis evidence of objective tongue inspection for liver cancer (LC) patients with damp-heat syndrome (DHS) by dynamically observing their tongue figures using modern tongue image analytic apparatus, and to explore the effect of intervention on the tongue figures. METHODS: Tongue figures were collected from 142 LC patients with DHS by tongue image analytic apparatus. Red (R), green (G) and blue (B) values were analyzed. The r and g values were calculated requesting r=R/(R+G+B), g=G/(R+G+B), and b=1-r-g, and scored in combination with Chinese medical symptoms scale. The tongue figure and correlated scores were collected from 59 of them 3 days after transcatheter arterial chemoembolization intervention. RESULTS: The range of objective tongue inspection of LC patients with DHS was as follows: as for tongue fur, 0.360

Combined radiochemotherapy in patients with locally advanced pancreatic cancer: a meta-analysis.

AIM: To compare the long-term clinical efficacy of chemotherapy plus radiotherapy (CRT) with that of radiotherapy alone (RT) or chemotherapy alone (CT) for locally advanced pancreatic carcinoma (LAPC). METHODS: Using manual and computer-aided methods, we searched the data through the databases, including PubMed/EmBase/CNKI/CQVIP/China Journals Full Text Database and websites and proceedings of major annual meetings such as ASCO and CSCO. The methodological quality of the included studies was assessed using the Jadad scoring system. Both English and Chinese publications were searched. We collected data from controlled clinical trials on CRT vs RT or CT for LAPC, and conducted a meta-analysis of 15 included studies. Meta-analysis was performed using RevMan4.2 Software according to the method recommended by Cochrane Collaboration. RESULTS: Fifteen eligible randomized controlled trials including a total of 1128 patients were screened. Jadad score was 2 in only one article, and 3-4 in the remaining 14 studies. The meta-analysis showed that CRT was superior in the 6- and 12-mo survivals to the RT alone group or CT alone group (P = 0.0001 and P = 0.02, respectively), whereas the 18-mo survival showed no significant difference (P = 0.23). Subgroup analysis showed that the 6-, 12-, and 18-mo survivals were not significantly different between the CRT group and CT group (P = 0.07, P = 0.23, and P = 0.91, respectively). Notably, the CRT group had significantly better 6-, 12-, and 18-mo survivals than the RT group (all P < 0.01). CRT group had significantly more grade 3-4 treatment-related hematologic and non-hematologic toxicities than the CT group or RT group (all P < 0.01). CONCLUSION: Compared with CT or RT, CRT can benefit the long-term survival of LAPC patients, although it may also increase treatment-related toxicities.