Screening of gene markers related to the prognosis of metastatic skin cutaneous melanoma based on Logit regression and survival analysis.

BACKGROUND: Bioinformatics was used to analyze the skin cutaneous melanoma (SKCM) gene expression profile to provide a theoretical basis for further studying the mechanism underlying metastatic SKCM and the clinical prognosis. METHODS: We downloaded the gene expression profiles of 358 metastatic and 102 primary (nonmetastatic) CM samples from The Cancer Genome Atlas (TCGA) database as a training dataset and the GSE65904 dataset from the National Center for Biotechnology Information database as a validation dataset. Differentially expressed genes (DEGs) were screened using the limma package of R3.4.1, and prognosis-related feature DEGs were screened using Logit regression (LR) and survival analyses. We also used the STRING online database, Cytoscape software, and Database for Annotation, Visualization and Integrated Discovery software for protein-protein interaction network, Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses based on the screened DEGs. RESULTS: Of the 876 DEGs selected, 11 (ZNF750, NLRP6, TGM3, KRTDAP, CAMSAP3, KRT6C, CALML5, SPRR2E, CD3G, RTP5, and FAM83C) were screened using LR analysis. The survival prognosis of nonmetastatic group was better compared to the metastatic group between the TCGA training and validation datasets. The 11 DEGs were involved in 9 KEGG signaling pathways, and of these 11 DEGs, CALML5 was a feature DEG involved in the melanogenesis pathway, 12 targets of which were collected. CONCLUSION: The feature DEGs screened, such as CALML5, are related to the prognosis of metastatic CM according to LR. Our results provide new ideas for exploring the molecular mechanism underlying CM metastasis and finding new diagnostic prognostic markers.

Aberrantly Methylated and Expressed Genes as Prognostic Epigenetic Biomarkers for Colon Cancer.

This study aimed to identify prognostic epigenetic biomarkers for colon cancer (CC). Methylation and mRNA expression in CC samples with clinical characteristics that corresponded to those in The Cancer Genome Atlas were analyzed. Differentially methylated genes (DMGs) and differentially expressed genes (DEGs) were screened between matched tumor and nontumor tissues. Among the 415 DEGs and DMGs that significantly correlated between cytosine-phosphate-guanine (CpG) methylation and gene expression, unc-5 netrin receptor C (UNC5C), solute carrier family 35 member F (SLC35F)1, Ly6/Neurotoxin (LYNX)1, stathmin (STMN)2, slit guidance ligand (SLIT)3, cell adhesion molecule L1 like (CHL1), CAP-Gly domain containing linker protein family member 4 (CLIP4), transmembrane protein (TMEM) 255A, granzyme B (GZMB), and brain expressed X-Linked (BEX)1 were promising epigenetic biomarkers. Prediction was more accurate when models were based on the expression and/or methylation of GZMB rather than clinical stage. Comparisons of tissues with high or low GZMB expression significantly associated the DEGs with natural killer-mediated cytotoxicity, cytokine-cytokine receptor interactions, and chemokine signaling pathways. From among the 10 epigenetic biomarkers, GZMB might serve as a tumor suppressor and function in several immune-related pathways in CC. Prognostic models based on GZMB expression and/or methylation would be significant for patients with CC.

MicroRNA-621 inhibits the growth of gastric cancer cells by targeting SYF2.

Increasing evidence indicates that aberrantly expressed microRNAs play a role in tumorigenesis and progression of gastric cancer. Recently, a novel cancer-related microRNA, miR-621, was found to be involved in cancer pathogenesis. However, the precise molecular mechanisms underlying the oncogenic activity of miR-621 remain unclear and require further investigation. In the current study, we demonstrate that miR-621 expression is downregulated in gastric cancer tissues and cell lines, and its reduction is associated with malignant clinical features including tumor size, lymph node metastasis, tumor-node-metastasis stage and poor prognosis. Functional studies involving gain- and loss-of-function experiments revealed that miR-621 represses cell viability, colony formation, cell cycle progression and proliferation in vitro, and miR-621 overexpression inhibited tumor growth in a gastric cancer xenograft model. SYF2 was identified as a direct target gene of miR-621 in gastric cancer. MiR-621 directly interacts with the SYF2 3'-UTR and post-transcriptionally repressed SYF2 expression in gastric cancer cells. SYF2 was significantly overexpressed in gastric cancer tissues and negatively correlated with miR-621 expression. Moreover, inhibition of SYF2 expression reversed the effects of miR-621 loss in gastric cancer cells. SYF2 overexpression was similar to that induced by miR-621 loss in gastric cancer. Taken together, these studies suggest that miR-621 may be a viable therapeutic target in gastric cancer.

MicroRNA-143 suppresses the proliferation and metastasis of human gastric cancer cells via modulation of STAT3 expression.

Accumulating evidences suggest that miRNAs may prove essential therapeutic targets for the treatment of cancer. Herein, the role and therapeutic implications of miRNA-143 was investigated in gastric cancer. The results revealed miRNA-143 to be aberrantly downregulated in gastric cancer cell lines. Ectopic expression of miRNA-143 resulted in a significant (P<0.05) inhibition of AGS gastric cancer cell proliferation suggestive of the tumor suppressive role of miRNA-143. The inhibition of AGS cell proliferation was mainly via activation of apoptotic cell death as evident from the AO/EB and annexin V/PI staining. Additionally, miR-143 overexpression also caused a significant (P<0.05) decline in the migration and invasion of AGS cells. TargetScan analysis and the dual luciferase assay revealed STAT3 to be the potential target of miRNA-143 in AGS cells. Analysis of STAT3 expression in gastric cancer cell lines showed upto 3.5 fold upregulation of STAT3. However, miRNA-143 overexpression resulted in considerable downregulation of STAT3 expression. Silencing of STAT3 also resulted in the inhibition of cell proliferation, migration and invasion of the AGS cells. Moreover, overexpression of STAT3 could nullify the tumor suppressive effects of miRNA-143 in AGS cells. Taken together, miRNA-143 has a tumor suppressive role in gastric cancer and may prove essential in gastric cancer treatment.

Long non-coding RNA OIP5-AS1 promotes the growth of gastric cancer through the miR-367-3p/HMGA2 axis.

Increasing evidence shows that aberrant lncRNAs expression contributes to the progression of gastric cancer (GC). The role of the novel lncRNA OIP5-AS1 and its underlying mechanisms in the growth of GC is largely unknown. Here we demonstrate for the first time that OIP5-AS1 expression was up-regulated in GC tissues and cell lines, which significantly correlated with unfavorable clinical characteristics and shorter survival. The results of in vitro and in vivo gain- and loss-of-function experiments indicate that OIP5-AS1 promoted cell proliferation and colony formation while inhibiting apoptosis of GC cells. OIP5-AS1 functioned as an endogenous sponge for miR-367-3p in GC cells. Restoration of miR-367-3p expression abolished the biological effects of OIP5-AS1 on GC cells. Moreover, we show that HMGA2 was a downstream target of miR-367-3p and mediated the effects of OIP5-AS1 on GC cells. OIP5-AS1 regulated the activities of the PI3K/AKT and Wnt/ß-catenin pathways through HMGA2. In conclusion, OIP5-AS1 functions as an oncogenic lncRNA that promotes the progression of GC and may serve as a therapeutic target for managing GC.

LncRNA HOXA11-AS accumulation-induced microRNA-761 downregulation regulates cell growth by targeting TRIM29 in papillary thyroid cancer.

Increasing evidence demonstrate that dysregulated microRNAs (miRNAs) are involved in carcinogenesis and tumor progression in papillary thyroid cancer (PTC). However, the specific miR-761 in cancer remains largely unknown. In this study, we reported for the first that miR-761 expression was down-regulated in PTC tissues and cell lines, and its decrease was associated with tumor size and TNM stage. Gain- and loss-of function experiments revealed that miR-761 inhibited cell proliferation, colony formation and cell cycle progression in vitro and in vivo. Moreover, TRIM29 was identified as a direct downstream target of miR-761 in PTC cells and mediated the functional effects of miR-761 in PTC. Restoration of TRIM29 expression at least partially abolished the biological effects of miR-761 on PTC cells. Furthermore, overexpression of lncRNA HOXA11-AS was inversely correlated with miR-761 expression in PTC tissues. LncRNA HOXA11-AS could modulate the miR-761 expression and regulate cellular behaviors. Taken together, this research supports the first evidence that lncRNA HOXA11-AS-reguated miR-761 plays a functional role in inhibiting PTC progression by targeting TRIM29 and represent a promising therapeutic strategy for patients with PTC.

MicroRNA-1296 Facilitates Proliferation, Migration And Invasion Of Colorectal Cancer Cells By Targeting SFPQ.

MicroRNAs (miRNAs) are involved in cancer genesis and progression via acting as tumor suppressors or oncogenes. Previous studies report that miR-1296 shows upregulation in both colorectal cancer (CRC) tissues and plasma samples. However, the accurate clinical significance of miR-1296 and its role in CRC have not been well investigated. The aim of the present study was to disclose the aberrant expression, clinical significance, and the relevant biological function of miR-1296 in CRC. We found a marked upregulation of miR-1296 expression in CRC tissues compared to tumor-adjacent tissues. MiR-1296 overexpression was detected in five CRC cell lines (HCT116, Caco2, HT29, SW620 and SW480). High miR-1296 level was remarkably correlated with tumor size (>5cm), lymph node metastasis and TNM stage (III+IV). Notably. High miR-1296 expression was identified as a predictive factor for poor prognosis of CRC patients by survival analysis. MiR-1296 knockdown inhibited proliferation, migration, invasion capacities of HCT116 and SW480 cells in vitro. Moreover, miR-1296 silencing restrained the growth of CRC cells in vivo. Splicing factor proline and glutamine rich (SFPQ), a novel RNA binding protein, was identified as a direct target gene of miR-1296 in CRC. Downregulation of SFPQ expression was inversely associated with miR-1296 expression in CRC tissues. The Cancer Genome Atlas (TCGA) data revealed the prognostic value of dysregulated SFPQ in CRC patients. Interestingly, our findings established that the oncogenic role of miR-1296 was at least partially mediated by SFPQ in CRC cells. Collectively, these data indicate that miR-1296 accelerates CRC progression possibly by targeting SFPQ and may serve as a potential predictive factor and therapeutic target for CRC.

Forkhead box D1 promotes proliferation and suppresses apoptosis via regulating polo-like kinase 2 in colorectal cancer.

Transcription factor forkhead box D1 (FOXD1), a member of forkhead box family, has been recognized as a caner-related gene. Aberrant expression of FOXD1 is observed in glioma, lung cancer and breast cancer. However, the clinical significance of FOXD1 and its role in colorectal cancer (CRC) are unknown. Here, we found that FOXD1 displayed a higher expression in CRC tissues compared to tumor-adjacent tissues. Upregulation of FOXD1 was further confirmed in CRC tissues compared to normal tissues based on data from three GSE cohorts. Our clinical data indicated that high FOXD1 level was associated with tumor size (≥5 cm) and TNM tumor stage (III + IV). Moreover, both our data and TCGA data found that high expression of FOXD1 predicted poor prognosis of CRC patients. Next, we revealed that FOXD1 knockdown suppressed proliferation, cell cycle progression and induced apoptosis of SW480 cells in vitro. In accordance, FOXD1 overexpression promoted proliferation and reduced apoptosis of HT29 cells. Interestingly, polo-like kinase 2 (Plk2) expression was elevated and it positively correlated with FOXD1 expression in CRC tissues. FOXD1 promoted the expression of Plk2 mRNA and protein in CRC cells. Notably, Plk2 restoration abolished the effect of FOXD1 knockdown on proliferation and apoptosis of SW480 cells. Plk2 knockdown resulted in decreased proliferation and increased apoptosis of FOXD1-overexpressing HT29 cells. Altogether, we demonstrate for the first time that FOXD1 functions as an oncoprotein and a potential prognostic biomarker in CRC.

The tumor suppressive miR-26a regulation of FBXO11 inhibits proliferation, migration and invasion of hepatocellular carcinoma cells.

Accumulating researches identify microRNA-26a (miR-26a) as a tumor suppressor in hepatocellular carcinoma (HCC). F-box protein 11 (FBXO11), a predicted target gene of miR-26a, is an E3 ubiquitin ligase and a type II methyltransferase, and functions as a key regulator of tumor initiation and progression. This study was aimed to investigate the regulatory role of miR-26a in FBXO11 expression and explored the clinical significance as well as functional role of FBXO11 in HCC. The expression levels of miR-26a were prominently downregulated in HCC tissues compared to matched tumor-adjacent tissues. MiR-26a inversely regulated FBXO11 abundance in HCC cells. Hereby, miR-26a could directly target 3'UTR of FBXO11 mRNA to suppress its expression. Gene Expression Omnibus (GEO) database (GSE54236 and GSE45436) and our data demonstrated that the expression of FBXO11 was up-regulated in HCC tissues. The level of FBXO11 mRNA was inversely correlated with miR-26a expression in HCC specimens. High FBXO11 expression was positively correlated with large tumor size, venous infiltration and advanced tumor stage of HCC patients. Clinical prognostic analysis illustrated that high FBXO11 expression predicted a poor survival of HCC patients. In vitro, FBXO11 knockdown inhibited cell proliferation, colony formation, migration and invasion of HCC cells. Additionally, miR-26a overexpression showed a consistent effect with FBXO11 knockdown on these malignant behaviors of HCC cells. Notably, FBXO11 restoration reversed the inhibitory effect of miR-26a on HCC cell proliferation, colony formation, migration and invasion. In summary, these results indicated that miR-26a regulation of FBXO11 exhibited an oncogenic role in HCC. Inhibition of FBXO11 might serve as a therapeutic target for HCC.

F-box protein 11 promotes the growth and metastasis of gastric cancer via PI3K/AKT pathway-mediated EMT.

F-box protein 11 (FBXO11) has both the E3 ubiquitin ligase activity and the methyltrasferase activity, and regulates metastasis, apoptosis and chemosensitivity in human cancer. However, the clinical significance and biological function of FBXO11 in gastric cancer (GC) are rarely known. Here, we demonstrated up-regulated expression of FBXO11 in GC tissues in comparison with that in tumor-adjacent tissues. Clinical analysis based on our specimens and the TCGA database revealed that FBXO11 overexpression was associated with large tumor size, lymph node metastasis and advanced TNM stage. Notably, GC patients with high FBXO11 expression showed a significant shorter overall survival. Cell proliferation and mobility were measured by CCK-8 and Transwell assays. FBXO11 silencing by transfection with two specific shRNAs attenuated proliferation, migration and invasion of MGC-803 cells. In accordance, FBXO11 overexpression promoted these cellular processes in SGC-7901 cells. Mechanistically, FBXO11 obviously facilitated epithelial-mesenchymal transition (EMT) process as suggested by immunoblotting and immunofluorescence data. Moreover, we found that FBXO11 promoted the activation of AKT pathway with increased phosphorylated AKT level in SGC-7901 cells. LY294002 and Wortmannin, phosphotidylinsitol-3-kinase (PI3K) inhibitors, blocked FBXO11 induced EMT, proliferation, migration and invasion of SGC-7901 cells. Phosphatase and tensin homolog (PTEN), which played a crucial role in regulating PI3K/AKT pathway, was negatively modulated by FBXO11 in GC cells. Taken together, our findings contribute to current understanding of the functions of FBXO11 and suggest a mechanism by which FBXO11 plays an oncogenic role in the development of GC possibly by inhibiting PTEN and subsequently promoting PI3K/AKT pathway activation.

MicroRNA-216a inhibits the metastasis of gastric cancer cells by targeting JAK2/STAT3-mediated EMT process.

MicroRNAs (miRNAs), a group of small, non-protein coding, endogenous RNAs, play critical roles in the tumorigenesis and progression of human cancer. miR-216a has recently been reported to play an oncogenic role in human cancer. While, the expression of miR-216a, its biological function and underlying molecular mechanisms in gastric cancer (GC) are largely unknown. In this study, we revealed that miR-216a was underexpressed in GC tissues compared to matched noncancerous tissues. Decreased levels of miR-216a were confirmed in GC cell lines compared with a normal gastric epithelium cell line. miR-216a underexpression was associated with malignant prognostic features including lymph node metastasis, venous infiltration, invasive depth and advanced TNM stage. GC patients with low miR-216a level showed an obvious shorter overall survival. miR-216a overexpression restrained migration and invasion of MGC-803 cells, while its knockdown exerted opposite effects on metastatic behaviors of SGC-7901 cells. In vivo experiments found that miR-216a restoration reduced metastatic nodes of GC cells in nude mice liver. miR-216a notably suppressed epithelial-mesenchymal transition (EMT) of GC cells. Janus kinase 2 (JAK2) was recognized as a direct target and downstream mediator of miR-216a in GC cells. Interestingly, JAK2/signal transducer and activator of transcription 3 (STAT3) pathway was prominently inactivated by miR-216a and probably mediated the role of miR-216a in the regulation of migration, invasion and EMT process of GC cells. In conclusion, these data suggest that miR-216a functions as a tumor suppressive miRNA in the development of GC possibly by targeting JAK2/STAT3-mediated EMT.

miR-205 regulation of ICT1 has an oncogenic potential via promoting the migration and invasion of gastric cancer cells.

Immature colon carcinoma transcript-1 (ICT1) is a newly identified oncogene, which regulates mobility, apoptosis, cell cycle progression and proliferation of cancer cells. Nevertheless, the role of ICT1 and its clinical significance in gastric cancer (GC) is largely uncovered. Here, we found that ICT1 displayed higher expression in GC tissues compared to corresponding tumor-adjacent tissues. Further investigation confirmed ICT1 overexpression in GC cell lines. Clinical data disclosed that high ICT1 expression correlated with distant metastasis and advanced tumor-node-metastasis (TNM) stage. The Cancer Genome Atlas (TCGA) data further demonstrated that GC tissues with metastasis showed a significant higher level of ICT1 compared to those without metastasis. Furthermore, ICT1 overexpression notably predicted poor prognosis of GC patients. Functionally, we demonstrated that ICT1 knockdown suppressed invasion and migration of MGC-803 and BGC-823 cells in vitro. ICT1 overexpression promoted the mobility of SGC-7901 cells. Mechanistically, microRNA-205 (miR-205) was recognized as a direct down-regulator and inversely modulated ICT1 abundance in GC cells. miR-205 expression was down-regulated and negatively associated with ICT1 level in GC tissues. Underexpression of miR-205 indicated an obvious shorter survival of GC patients. miR-205 overexpression inhibited migration and invasion of MGC-803 cells, while these inhibitory effects were reversed by ICT1 restoration. Taken together, we have the earliest evidence that miR-205 regulation of ICT1 functions as an oncogene and prognostic biomarker in GC.

SMURF1 promotes the proliferation, migration and invasion of gastric cancer cells.

Smad ubiquitin regulatory factor 1 (SMURF1), a well-known E3 ubiquitin ligase, targets substrate proteins for ubiquitination and proteasomal degradation. Accumulating studies have shown that SMURF1 acts as an oncogenic factor in human malignancies. However, the clinical significance of SMURF1 and its role in gastric cancer (GC) remain unclear. The expression of SMURF1 was detected in 68 cases of GC and corresponding tumor-adjacent specimens. Our results revealed that SMURF1 was prominently overexpressed in GC specimens compared to corresponding tumor-adjacent tissues. Furthermore, increased levels of SMURF1 mRNA were also observed in GC cell lines. Clinicopathological detection ascertained that SMURF1-positive expression was associated with large tumor size, more lymph nodes and distant metastasis as well as advanced tumor-node-metastasis (TNM) stage of GC. Notably, GC patients with SMURF1 positive­expressing tumors exhibited a significant decreased survival. Further experiments illustrated that SMURF1 knockdown significantly inhibited proliferation, migration and invasion of MGC-803 cells, while SMURF1 overexpression prominently promoted these behaviors in SGC-7901 cells. In vivo studies revealed that SMURF1 knockdown markedly inhibited tumor growth and liver metastasis of GC. Mechanically, SMURF1 inversely regulated the expression of DOC-2/DAB2 interactive protein (DAB2IP) in GC tissues and cells. Furthermore, DAB2IP restoration revealed similar effects to SMURF1 knockdown on MGC-803 cells with decreased proliferation, migration and invasion. In addition, the PI3K/Akt pathway and its downstream targets including c-Myc and ZEB1 were potentially involved in the oncogenic role of the SMURF1/DABIP axis. Collectively, the present study revealed the first evidence that SMURF1 can be potentially used as a clinical biomarker and target for novel treatment of human GC.

LncRNA CHRF-induced miR-489 loss promotes metastasis of colorectal cancer via TWIST1/EMT signaling pathway.

microRNA-489 (miR-489) is a novel cancer-related miRNAs and functions as a tumor suppressor in human cancers. While, the clinical significance of miR-489 and its role in colorectal cancer (CRC) remain rarely known. Here, we found that the levels of miR-489 in CRC tissues were significantly lower than those in matched tumor-adjacent tissues. Furthermore, decreased levels of miR-489 also observed in CRC cell lines compared to HIEC cells. Clinicopathological analysis revealed that miR-489 underexpression was positively correlated with advanced pT stage, pN stage and AJCC stage. Moreover, miR-489 low expressing CRC patients showed a obvious shorter survival. Functionally, miR-489 restoration inhibited cell migration and invasion as well as epithelial-mesenchymal transition (EMT) in HCT116 cells, while miR-489 loss facilitated these cellular processes in SW480 cells. In vivo experiments revealed that miR-489 overexpression reduced the number of metastatic nodules in nude mice liver. Notably, TWIST1 was recognized as a direct downstream target of miR-489 in CRC cells. Interestingly, TWIST1 restoration abrogated the effects of miR-489 on CRC cells with enhanced cell migration, invasion and EMT process. Furthermore, overexpression of long noncoding RNA cardiac hypertrophy-related factor (lncRNA CHRF) was inversely correlated with miR-489 expression in CRC tissues. CHRF knockdown increased the expression of miR-489 and suppressed EMT events of HCT116 cells, while CHRF overexpression showed opposite effects on miR-489 expression and EMT in SW480 cells. Taken together, this work support the first evidence that lncRNA CHRF-induced miR-489 loss facilitates metastasis and EMT process of CRC cells probably via TWIST1/EMT signaling pathway.

Sulfatase-2 promotes the growth and metastasis of colorectal cancer by activating Akt and Erk1/2 pathways.

The molecular mechanisms underlying the growth and metastasis of colorectal cancer (CRC) remain largely unknown. Sulfatase-2 (SULF2) was found to play critical roles in human cancers. Recent study reported that SULF1/2 overexpression resulted in increased viability and proliferation, and augmented cell migration in CRC cells. However, the expression of SULF2 and its underlying molecular mechanisms in CRC remain unknown. In this study, we found that the expressions of SULF2 in CRC tissues and cell lines were significantly increased compared to control groups. Increased expression of SULF2 was associated with malignant clinical features and poor prognosis of CRC patients. Loss of SULF2 significantly prohibited the proliferation, cell cycle progression, migration and invasion of HT29 cells, while restoration of SULF2 significantly promoted these cellular functions of SW480 cells. In vivo tumorigenicity and liver metastasis assays confirmed that SULF2 knockdown significantly reduced the growth and metastatic abilities of HT29 cells in nude mice. Furthermore, SULF2 knockdown reduced the levels of p-Akt and p-Erk1/2 in HT29 cells, while SULF2 overexpression showed opposite effects on the expressions of these proteins in SW480 cells. In all, SULF2 promotes the growth and metastasis of CRC probably by activating Akt and Erk1/2 pathways. SULF2 potentially serves as a promising biomarker and therapeutic target in CRC.

Therapeutic effects of sequential chemoradiotherapy with pemetrexed and cisplatin on locally advanced laryngeal cancer.

OBJECTIVE: To explore the therapeutic effects of sequential chemoradiotherapy with pemetrexed and cisplatin on locally advanced laryngeal cancer (LALC). METHODS: Fifty LALC patients who were treated in our hospital between January 2010 and January 2012 were selected and randomly divided into an observation group and a control group (n=25). The two groups were given conventional radiotherapy in the same manner, before which two cycles of chemotherapy were performed. The observation group intravenously infused with 500 mg/m2 pemetrexed on d1 and 25 mg/m2 cisplatin on d1-3, with 28 days as a cycle. The control group was intravenously infused with 25 mg/m2 cisplatin on d1-3 and 400 mg/m2 fluorouracil, with 28 days as a cycle. The short-term effects and adverse reactions of both groups were observed after treatment, and their survival was observed by follow-up for five years. RESULTS: The response rate was 84% (21/25) in the observation group and 64% (16/25) in the control group, between which the difference was statistically significant (P<0.05). The differences in the incidence rates of short-term adverse reactions such as grade III-IV gastrointestinal reactions and bone marrow suppression were not statistically significant between PC regimen (pemetrexed combined with cisplatin) and PF regimen (cisplatin combined with fluorouracil) (P>0.05). The incidence of long-term adverse reactions such as grade III-IV laryngeal edemas, laryngeal cartilage inflammation and laryngeal cartilage necrosis showed no significant differences between the two groups (P>0.05). The median survival was 3.3 years after PC chemotherapy and 2.8 years after PF chemotherapy, between which the difference was not statistically significant (P>0.05). The levels of serum tumor markers significantly decreased after PC and PF treatments compared with those before (P<0.05). CONCLUSION: Combining PC chemotherapy with radiotherapy has satisfactory short-term therapeutic effects on LALC, and the resulting adverse effects can be tolerated. Therefore, this strategy is worthy of promotion and application in clinical practice.

[Comparative study of three-dimensional and two-dimensional laparoscopic-assisted D2 radical gastrectomy in short-term efficacy].

OBJECTIVE: To evaluate the advantage and short-term efficacy of three-dimensional (3D) laparoscopic-assisted D2 radical gastrectomy for gastric cancer. METHODS: Clinical data of 116 gastric cancer patients who underwent laparoscopic-assisted D2 radical gastrectomy in our department from January 2014 to August 2015 were analyzed retrospectively. Among 116 patients, 56 received 3D and 60 received two-dimensional(2D) technique respectively. All the surgeries were performed by the same team. The operative parameters, short-term efficacy and hospital expense were compared between the two groups. RESULTS: There were no significant differences between the two groups in baseline data(all P>0.05). All the operations were performed successfully without conversion. Compared with 2D group, 3D group had shorter operative time [(186.2±22.8) minutes vs. (198.1±26.4) minutes, t=2.589, P=0.011], less intraoperative blood loss [(73.6±28.5) ml vs. (88.1±32.3)ml, t=2.555, P=0.012]. Whereas no significant differences in dissected lymph nodes(36.5±6.6 vs. 34.5±5.4, P=0.073), time to first flatus[(3.1±1.5) days vs. (3.3±1.8) days, P=0.729], length of hospital stay[(11.7±2.9) days vs. (12.6±3.1) days, P=0.088], incidence of postoperative complications [8.9%(5/56) vs. 11.7%(7/60), P=0.628] and hospitalization cost [(8.6±1.4)×10(4) yuan vs. (8.1±1.2)×10(4) yuan, P=0.055] were found between two groups. CONCLUSION: Three-dimensional laparoscopic-assisted D2 radical gastrectomy may be advantageous over two-dimensional laparoscopic-assisted D2 radical gastrectomy.