Association of serum annexin A1 with treatment response and prognosis in patients with esophageal squamous cell carcinoma.

OBJECTIVE: Annexin A1 (ANXA1), a calcium-dependent phospholipid binding protein, is known to be regulated by microRNA-196a (miR-196a) in esophageal adenocarcinoma, and its high expression in tumor tissue is correlated with the poor prognosis of esophageal squamous cell carcinoma (ESCC). However, the role of ANXA1 in the serum of patients with ESCC remains unclear. MATERIALS AND METHODS: In this study, we used enzyme-linked immunosorbent assay to evaluate the levels of ANXA1 and real-time polymerase chain reaction to detect the expression of miR-196a in the serum of ESCC patients (healthy donors as controls) and evaluated the relationship between ANXA1 and clinical outcomes. RESULTS: The results showed that the level of serum ANXA1 in ESCC patients was significantly lower than that in controls (P = 0.001) but increased after chemoradiotherapy (P = 0.001). There was no correlation between the baseline level of serum ANXA1 and the short-term efficacy of treatment (P = 0.26) as well as the 1-year progression-free survival (PFS) (P = 0.094). However, there existed a significant correlation between the increases of serum ANXA1 expression and the 1-year PFS (P = 0.04). A higher increase (>2-fold of baseline) in the serum ANXA1 levels was correlated with a poorer PFS (hazard ratio = 3.096, 95% confidence interval 1.239-7.861). There was an inverse correlation between the expressions of miR-196a and ANXA1 in serum (Pearson's correlation of -0.54, P = 0.021). CONCLUSION: Our data revealed that the expression of serum ANXA1 in ESCC patients increases after chemoradiotherapy and the increased fold change in serum ANXA1 confers independent negative prognostic impact in ESCC. The higher the increase in serum ANXA1 levels, the poorer the outcome.

LncRNA-ECM is overexpressed in esophageal squamous cell carcinoma and promotes tumor metastasis.

The aim of the present study was to investigate the expression of long non-coding(lnc) RNA-extracellular matrix (ECM) in esophageal squamous cell carcinoma (ESCC) and its effect on ESCC metastasis. Using reverse transcription-quantitative polymerase chain reaction (RT-qPCR), the expression of lncRNA-ECM in ESCC tissues was investigated and compared with that in corresponding adjacent tissues. In addition, the expression of lncRNA-ECM in the human ESCC cell lines TE-1, EC9706, KYSE150, Eca109 and KYSE30 was also detected and compared with that in the normal esophageal mucosal epithelial cell line HET-1A. The clinicopathological association between lncRNA-ECM and ESCC was assessed. Silencing and overexpression of lncRNA-ECM in ESCC TE-1 and Eca109 cells determined the correlation between lncRNA-ECM expression and ESCC invasion and metastasis. The possible target genes of lncRNA-ECM were predicted and verified by bioinformatics analysis and experimental results. The expression level of intercellular adhesion molecule 1 (ICAM1) was detected in ESCC tissues by RT-qPCR and the correlation between the expression of ICAM1 and lncRNA-ECM was analyzed. Changes in the expression of ICAM1 in ESCC TE-1 and Eca109 cell lines were evaluated after knocking down lncRNA-ECM and transfection of lncRNA-ECM overexpression plasmids. The expression level of lncRNA-ECM in the tissues of ESCC with lymph node metastasis were significantly increased compared with ESCC with no lymph metastasis (P<0.05). LncRNA-ECM silencing notably reduced the invasion and metastasis of TE-1 and Eca109 cells, while lncRNA-ECM overexpression promoted the invasion and metastasis of the two cell lines. The expression level of ICAMI was directly correlated with the expression of lncRNA-ECM, suggesting that ICAM1 may be the downstream target gene of lncRNA-ECM. LncRNA-ECM was revealed as being overexpressed in ESCC. LncRNA-ECM expression was positively correlated with metastasis and may affect the metastasis of ESCC through ICAMI regulation. These findings indicate that lncRNA-ECM may be promising as a novel biomarker for the diagnosis and prediction of prognosis for ESCC, and it may also serve as a novel therapeutic target for ESCC.

An early superficial non-ampullary duodenal tumor cured with endoscopic submucosal dissection: A case report.

Early superficial non-ampullary duodenal tumors are particularly rare, the clinical manifestations, including typical endoscopic or imaging features, and treatment methods are not well-characterized. The present case report describes a case of an asymptomatic 74-year-old male who presented to the Taizhou People's Hospital (Taizhou, China) for a regular health screening, where a primary superficial non-ampullary duodenal tumor was identified. Upper endoscopy revealed ~1.2 cm lesion in the second portion of the duodenum. Chromoscopy and magnification endoscopy indicated an early cancer characteristic. Subsequent endoscopic submucosal dissection was performed to remove the lesion. Histopathology validated that the lesion was a high-grade intro-epithelial neoplasm without lymph node or blood vessel invasion.

TCN, an AKT inhibitor, exhibits potent antitumor activity and enhances radiosensitivity in hypoxic esophageal squamous cell carcinoma in vitro and in vivo.

The aim of the present study was to investigate the radiosensitization effect of triciribine (TCN) on human esophageal squamous cell carcinoma (ESCC) in normoxia or hypoxia and its mechanism. The cytotoxicity and radiosensitization mechanism of TCN were investigated by Cell Counting Kit 8, clonogenic assay, flow cytometry, western blotting (WB) and immunofluorescence staining of phospho-histone H2A.X, Ser139 (γ-H2AX) in ESCC in vitro, while the protein expression levels of AKT, phosphorylated (p)-AKT, hypoxia-inducible factor (HIF)-1α and vascular endothelial growth factor (VEGF) were evaluated by WB in vivo. The cytotoxicity of TCN was dose dependent. Upon exposure to TCN, ESCC cells in hypoxia treated with 4-Gy radiotherapy exhibited an evidently higher apoptotic rate than cells subjected to other treatments. TCN could significantly inhibit the protein expression of p-AKT, HIF-1α and VEGF in vitro and in vivo. The present results suggested that TCN can effectively inhibit AKT, p-AKT, HIF-1α and VEGF, thus conferring radiosensitivity to ESCC in vitro and vivo. TCN is considered as an adjuvant in radiotherapy of ESCC in clinical application.

Prognostic significance of preoperative platelet-lymphocyte ratio in a Chinese cohort patient with colorectal cancer.

Cancer-related systemic inflammation affects many aspects of malignancy. The platelet-to-lymphocyte ratio (PLR), an easily applicable inflammatory marker based on platelet and lymphocyte counts, is associated with the clinical outcome of some cancers. The present study aimed to investigate the prognostic significance of the preoperative PLR in a cohort of colorectal cancer (CRC) patients. A total of 138 patients with CRC were enrolled in this retrospective study. The optimal cutoff value for the PLR was calculated using receiver operating curve (ROC) analysis. The correlation of PLR with the clinicopathological characteristics of patients was explored. Cox proportional hazard analysis was applied to determine the independent prognostic effect of PLR. PLR of 248 yielded the most optimal predictive value for the prognosis of CRC [area under the curve (AUC) = 0.820]. High level of PLR was significantly associated with lymph node and distance metastasis (P<0.001 and = 0.003, respectively), vascular and perinural invasion (P<0.001), advanced TNM stage (P<0.001), and poor differentiation (P = 0.037). Furthermore, the univariable analysis showed a significant impact of increased PLR on OS (HR = 4.326, 95% CI: 2.903-6.445, P<0.001), while this association remained significant in multivariable analysis (adjusted HR = 4.605, 95% CI: 2.786-7.611, P<0.001). Our findings indicated that elevated preoperative PLR might have potential value in predicting poor outcome in patients with CRC.

Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma.

Increasing evidence indicates that long non-coding RNA (lncRNA) plays an important role in tumorigenesis. However, the function and regulatory mechanism of lncRNAs are still unclear in esophageal squamous cell carcinoma (ESCC). To address this challenge, we screened lncRNAs expression profiles in 3 pairs of ESCC and matched non-cancerous tissues by microarray assay and identified the relationship between lncRNAs expression in ESCC tissue and clinicopathological characteristics and prognosis of patients with ESCC. We found 182 lncRNAs that were significantly differently expressed in ESCC tissues versus the matched non-cancerous tissues. Gene ontology and pathway analysis results suggested that the primary biological processes of these genes were involved in extracellular matrix, immune responses, cell differentiation and cell proliferation. Through cis and trans analyzing, we found 4 lncRNAs (ENST00000480669, NONHSAT104436, NONHSAT126998 and NONHSAT112918) may play important roles in tumorigenesis of ESCC. The four lncRNAs were checked in 73 patients with ESCC. The results showed that they mainly related to tumor metastasis. Kaplan-Meier survival analysis showed that high expression of NONHSAT104436, NONHSAT126998 and low expression of ENST00000480669 were related to poor 3-year overall survival (P=0.003, 0.032 and 0.040, respectively). Multivariate analysis showed that NONHSAT104436 was an independent prognostic factor (P=0.017). Thus we concluded that, lncRNAs showed differently expression patterns in ESCC versus matched non-cancerous tissues, and aberrantly expressed lncRNA may play important roles in ESCC development and progression. Interestingly, the overexpression of NONHSAT104436 was tightly correlated with distant metastasis and, poor survival rate, which might indicate that NONHSAT104436 might play a very important part in ESCC tumor progression.

Evaluation of tumor metastasis-associated markers for molecular classification in patients with esophageal squamous cell carcinoma.

This study aims to ascertain the relationship of tumor metastasis-associated markers cyclin D1, connective tissue growth factor (CTGF) and vascular endothelial growth factor (VEGF) with the clinicopathologic features and prognosis of patients with esophageal squamous cell carcinoma (ESCC), and to investigate their value in ESCC molecular classification. The expression of cyclin D1, CTGF and VEGF in 100 specimens from patients and 20 from normal esophageal mucosa were detected by immunohistochemistry. The relationship of their expression with prognosis of the patients with ESCC was evaluated by Cox regression model and Kaplan-Meier survival curve analysis. High levels of expression of cyclin D1, CTGF, and VEGF were observed in 61 (61%), 53 (53%), 49 (49%) cases, respectively. Univariate survival analysis indicated that the levels of expression of cyclin D1, CTGF and VEGF were associated with survival (all P-value < 0.05). Multivariate analysis indicated that cyclin D1 and VEGF were independent prognostic factors affecting the three-year survival rate of patients (P = 0.001, 0.017, respectively). Furthermore, high level expression of cyclin D1, CTGF and VEGF in stage I patients was found associated with poor three-year survival rate (all P-value < 0.05). The prognosis probably was favorable for patients with low expression of cyclin D1 even in stage III, or VEGF even in stage IV. Tumor metastasis-associated markers such as cyclin D1 and VEGF may be independent prognostic factors affecting survival rate of postoperative ESCC patients. It is possible to judge prognosis better and tailor treatments to each individual patient when these markers were applied to ESCC molecular classification.

Celastrol induces cell cycle arrest by MicroRNA-21-mTOR-mediated inhibition p27 protein degradation in gastric cancer.

OBJECTIVE: Celastrol has anti-cancer effects by increase of apoptosis of gastric cancer cells. However, its role in gastric cancer cell cycle is still unclear. The aim of this study was to investigate the effect and mechanism of celastrol on gastric cancer cell cycle. METHODS: The effects of celastrol on cell cycle in BGC-823 and MGC-803 cells were assayed via flow cytometry analysis. The expression of p27 and mTOR was detected by real-time PCR and western blot. The activity of mTOR and mTORC2 was measured by mTOR and mTORC2 kinase assays. miR-21 mimic was used to up-regulate miR-21 expression and mTOR expression plasmid was used to increase mTOR level in gastric cancer cells. RESULTS: Celastrol caused G2/M cell-cycle arrest that was accompanied by the down-regulation of miR-21 expression. In particular, miR-21 overexpression reversed cell cycle arrest effects of celastrol. Further study showed that celastrol increased levels of the p27 protein by inhibiting its degradation. miR-21 and mTOR signaling pathway was involved in the increase of p27 protein expression in BGC-823 and MGC-803 cells treated with celastrol. Significantly, miR-21 overexpression restored the decrease of mTOR activity in cells exposed celastrol. CONCLUSIONS: The effect of celastrol on cell cycle arrest of gastric cancer cells was due to an increase of p27 protein level via inhibiting miR-21-mTOR signaling pathway.

Prognostic significance of Glasgow prognostic score in patients with stage II colorectal cancer.

Glasgow prognostic score (GPS), one information based prognostic score, has been previously shown to be a prognostic factor in varieties cancers mostly in advanced tumors. This study aimed to explore its value in patients with relatively early stage colorectal cancer (CRC). A total of 99 CRC patients with stage II from 2005 to 2010 operated in our hospital were enrolled in this study. C-reactive protein (CRP), albumin (ALB), Karnofsky Performance Status (KPS) score as well as a variety of biochemical variables before the operation was acquired from the database retrospectively. The value of GPS was calculated and its association with the clinical factors was further investigated. The prognostic significance was analyzed by univariate and multivariate analyses. Increased preoperative GPS was found associated with elevated carcinoembryonic antigen (CEA) and decreasing of KPS. Kaplan-Meier analysis and log-rank test revealed that a higher GPS predicted a higher risk of postoperative mortality in stage II CRC (P < 0.001). Furthermore, multivariate analysis demonstrated the GPS to be a risk factor for postoperative mortality (HR 3.215; P=0.025). The preoperative GPS might be a potential useful indicator for postoperative survival in patients with stage II CRC.

Hypertriglyceridemia and hyperglycemia induced by capecitabine: a report of two cases and review of the literature.

BACKGROUND: Capecitabine is a tumor-activated oral fluoropyrimidine used in breast and colorectal cancer. Hypertriglyceridemia associated with this drug has rarely been reported in the literature. METHODS: Two patients with colorectal carcinoma who developed capecitabine-induced hypertriglyceridemia (including a patient who developed hyperglycemia concurrently) were described, treatment modalities were discussed, and the literatures were reviewed. RESULTS: The first patient, a 43-year-old man, developed hyperlipidemia and hyperglycemia after two cycles of XELOX regimen chemotherapy for colorectal cancer. His triglyceride was 2.47 mmol/L (normal range 0.34-1.7 mmol/L) and total cholesterol was 6.93 mmol/L (normal range 3.12-5.9 mmol/L), while blood glucose was abnormal (fasting blood glucose was 10.58-11.9 mmol/L and 2 h postprandial glucose was 14.5-17.2 mmol/L) and glucose was positive in the urine(3+). The second patient, a 47-year-old woman, developed abnormalities in the lipid profile after the sixth cycle of XELOX regimen chemotherapy for colorectal cancer. Her serum triglyceride was 2.41 mmol/L (normal range 0.34-1.7 mmol/L), while the cholesterol level was 7.73 mmol/L (normal range 3.12-5.9 mmol/L). The profile of lipid improved gradually with reduced doses of capecitabine and was well restored after chemotherapy without any lipid-lowering agents. The Naranjo score for capecitabine-induced hypertriglyceridemia was 9 (definite). An analysis of the underlying pathogenic mechanisms was provided. CONCLUSION: It is important of physicians and pharmacists to be aware of the possibility of dyslipidemia, particularly hypertriglyceridemia induced by capecitabine.

Association of the expression of unc-51-Like kinase 1 with lymph node metastasis and survival in patients with esophageal squamous cell carcinoma.

Unc-51-Like Kinase 1 (ULK1) is regarded as a central role in autophagy. Although the details of how ULK1 triggers autophagy are obscure, the relationship between ULK1 expression and the diagnosis and prognosis of cancer patients may guide the clinical practice and scientific research. The aim of this study was to investigate and compare the expression level of ULK1 in 86 paired esophageal squamous cell carcinoma (ESCC) and paracancerous tissues, and to examine the effect of ULK1 expression on the prognosis of ESCC patients. ULK1 was primarily expressed in cytoplasm, but was rarely seen in nucleus. The levels of cytoplasmic ULK1 in ESCC tissues were higher than those in paracancerous tissue (P < 0.01) and significantly associated with lymph node metastasis (LNM) (P = 0.025). Survival analysis showed that patients with low expression of cytoplasmic ULK1 had worse survival time than those with high expression of cytoplasmic ULK1 (hazard ratio = 1.754, 95% confidence interval: 1.022-3.010, P = 0.041), which disappeared after adjustment for TNM stages and LNM (P = 0.319). In conclusion, ULK1 might play an important role in the occurrence and development of ESCC and represent a potential prognostic biomarker for ESCC patients. However, the precise impact of ULK1 on predicting the prognosis of patients with ESCC requires further investigation.

Elevated serum level of carbohydrate antigen 19-9 in benign biliary stricture diseases can reduce its value as a tumor marker.

Although carbohydrate antigen (CA19-9) level is frequently upregulated in pancreatobiliary cancer, it is also elevated in some benign diseases. This study aimed to determine whether CA19-9 levels could be used to distinguish between benign obstructive jaundice and pancreatobiliary cancer. Fifty-seven patients with obstructive jaundice were studied retrospectively. Endoscopic retrograde cholangiopancreatography (ERCP), sphincterotomy, stone extraction, or stent placement were used to treat patients with benign bile duct stricture or inoperable malignant biliopancreatic diseases, whilst surgery was performed in suitable cases. Serum CA19-9 levels and some additional biochemical parameters were evaluated before and after treatment. CA19-9 levels were elevated in most patients, along with levels of total bilirubin, alkaline phosphatase (ALP), and gamma glutamyl transpeptidase (GGT), and 10 patients with benign disorders had extraordinarily high levels of these markers (> 1000 U/mL). The mean CA19-9 level in the malignant group was greater than that in the benign group (826.83 ± 557.34 vs. 401.92 ± 483.92 U/mL, P = 0.005), and the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) for CA19-9 were 100%, 7.69%, 33.33% and 47.47%, respectively. CA19-9 levels in the whole cohort were correlated with ALP (r = 0.77, P < 0.001), GGT (r = 0.83, P < 0.001), bilirubin (r = 0.69, P < 0.001), and CRP (r = 0.37, P = 0.004). The reduction in serum level of CA19-9 after treatment in the malignant group was remarkably less than that observed in the benign group (97.26 ± 123.24 U/mL vs. 352.71 ± 397.29 U/mL, P < 0.001). CA19-9 levels may not be sufficient to distinguish between malignant and benign obstructive jaundice diseases.

VEGF +405G/C (rs2010963) polymorphisms and digestive system cancer risk: a meta-analysis.

Vascular endothelial growth factor (VEGF) polymorphisms, specifically +405G/C (rs2010963), reportedly influence the risk for various digestive cancers. However, the consequences of these polymorphisms remain controversial and ambiguous. Therefore, we performed a meta-analysis of 11 studies with VEGF +405G/C genotyping on 2,862 patients and 3,028 controls using the random effects model. We obtained a pooled odds ratio (OR) of 1.04 (95% confidence interval (CI) = 0.86-1.26) for the recessive genetic model, 1.07 (95% CI = 0.81-1.42) for the dominant genetic model, 1.09 (95% CI = 0.81-1.47) for the homozygote comparison, and 1.03 (95% CI = 0.83-1.27) for the heterozygote comparison. In the subgroup analysis of the recessive model, the OR was 1.20 (95% CI = 1.02-1.40) in colorectal cancer. These results show that VEGF +405G/C polymorphisms are unlikely to be a major determinant of susceptibility to digestive cancer. Furthermore, the subgroup analysis of recessive model indicates that VEGF +405G/C polymorphisms increase the risk for colorectal cancer.

Celastrol induces apoptosis of gastric cancer cells by miR-21 inhibiting PI3K/Akt-NF-κB signaling pathway.

OBJECTIVE: Celastrol, a plant triterpene, has anticancer effects by increase of apoptosis. In the present study, the mechanism of celastrol on gastric cancer cell apoptosis was examined. METHODS: The effect of celastrol on PI3K/Akt and the NF-κB signaling pathway was evaluated with Western blot and luciferase reporter assay. miR-21 expression was determined using real-time PCR. miR-21 inhibitor and miR-21 mimic were used to downregulate and upregulate miR-21 expression, respectively. RESULTS: It was identified that celastrol was capable of inducing apoptosis of gastric cancer cells, which was mediated via inhibiting the activation of PI3K/Akt and NF-κB. A strong activator of Akt, IGF-1 restored NF-κB activity in cells treated with celastrol. Celastrol could also significantly suppress miR-21 expression. Furthermore, miR-21 inhibitor could decrease phospho-Akt expression and NF-κB activity. Notably, upregulation of miR-21 expression can increase PI3K/Akt and NF-κB activity and decrease apoptosis of gastric cancer cells treated with celastrol, which could be reversed by PI3K inhibitor. CONCLUSIONS: Our data revealed that the effect of celastrol on apoptosis was due to miR-21 inhibiting the PI3K/Akt-dependent NF-κB pathway.

Artesunate exerts an anti-immunosuppressive effect on cervical cancer by inhibiting PGE2 production and Foxp3 expression.

Artesunate (ART), derived from a common traditional Chinese medicine, has beeen used an antimalarial for several years. In this study, the effect and mechanism of ART on anti-human cervical cancer cells was examined. The level of prostaglandin E2 (PGE2 ) and the population of CD4+CD25+Foxp3 regulatory T cells (Treg) in peripheral blood were detected by flow cytometry. In vivo antitumor activity was investigated in mice with cervical cancer by the subcutaneous injection of various concentrations of ART. The concentrations of PGE2 in the supernatants of CaSki cells were measured using an ELISA kit. Cyclooxygenase-2 (COX-2) and Foxp3 expression were determined using quantitative polymerase chain reaction (qPCR) and western blot analysis. The effect of ART on the viability of CaSki and Hela cells was evaluated with a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. It was identified that the level of PGE2 and the population of CD4+CD25+Foxp3 Treg cells in the peripheral blood were significantly higher in cervical cancer patients and mice with cervical cancer. ART was capable of inhibiting orthotopic tumor growth, which correlated with a decrease in the level of PGE2 and the percentage of Treg cells in mice with cervical cancer. Furthermore, ART decreased COX-2 expression and the production of PGE2 in CaSki and Hela cells. Notably, the supernatants of CaSki cells treated with ART lowered the expression of Foxp3 in Jurkat T cells, which was capable of being reversed by exogenous PGE2 . Our data revealed that ART may elicit an anti-tumor effect against cervical cancer by inhibition of PGE2 production in CaSki and Hela cells, which resulted in the decrease of Foxp3 expression in T cells. Therefore, ART may be an effective drug for immunotherapy of cervical cancer.

Aberrant expression of microRNAs in serum may identify individuals with pancreatic cancer.

Pancreatic cancer (PC) has the poorest survival rate among all types of human cancer due to the lack of sensitive and non-invasive diagnostic screen methods for PC screening. Our aim was to identify novel serum microRNA (miRNA) biomarkers for the early detection of PC. We used microarray to screen differential expression of miRNAs in two pooled serum samples (6 PC patients and 6 healthy controls). A panel of miRNAs (22 over-expression and 23 decreased) were deregulated in serum of PC patients in comparison to controls. The expressions of 8 selected miRNAs were further evaluated in sera from 49 PC patients and 27 controls using quantitative reverse transcription-polymerase chain reaction. The levels of serum miR-492 and miR-663a were significantly decreased in PC patients compared with controls (P < 0.05). ROC curve analysis showed that serum miR-492 and miR-663a yield an AUC of 0.787 with 75.5% sensitivity and 70.0% specificity and 0.870 with 85.7% sensitivity and 80.0% specificity, respectively, for discriminating between PC patients and healthy controls. In addition, the level of miR-663a was significantly and inversely associated with TNM stage (P = 0.027). These results suggested that serum miR-492 and miR-663a could have strong potential as novel non-invasive biomarkers for the early detection of PC.

HER2 gene amplification in esophageal squamous cell carcinoma is less than in gastroesophageal junction and gastric adenocarcinoma.

The aim of the present study was to detect the amplification of the human epidermal growth factor receptor 2 (HER2) gene in esophageal squamous cell carcinoma (ESCC), gastroesophageal junction adenocarcinoma (GEJAC) and gastric cancer (GC), as well as to understand the pathological meaning of HER2 gene amplification with regard to clinico-pathological parameters in these types of cancer. HER2 gene amplification was evaluated by fluorescence in situ hybridization (FISH) in surgically obtained specimens from 76 cases of ESCC, 50 of GEJAC and 48 of GC, as well as 21 specimens of tumor-adjacent normal epithelium as a control group. The HER2 gene amplification rates in ESCC, GEJAC and GC were 3.9 (3/76), 24.0 (12/50) and 18.8% (9/48), respectively. The rates of HER2 gene amplification in GEJAC and GC were significantly higher compared with ESCC (χ2=11.563, P<0.001 and χ2=7.375, P<0.007, respectively). HER2 gene amplification was not detected in the normal esophageal or gastric mucosa samples. In ESCC, HER2 gene amplification was correlated with the invasion of the ESCC cells, vascular invasion and lymph node metastasis (χ2=4.789, 3.858 and 5.354, respectively; all P<0.05). However, in GEJAC and GC, no correlations were observed between HER2 amplification and the gender, age, degree of differentiation, invasion, vascular invasion and lymph node metastases of the patients (all P>0.05). The rate of HER-2 gene amplification was low in ESCC, although the amplification of HER-2 was correlated with tumor metastasis in these patients. The rates of HER-2 gene amplification in GEJAC and GC were higher compared with ESCC. Therefore, compared with ESCC, GEJAC may be more similar to GC with regard to HER-2 gene amplification features.

The effect of CD33 expression on inflammatory response in chronic obstructive pulmonary disease.

OBJECTIVE: In this article, the effects of CD33 expression from peripheral blood granulocytes and monocytes on inflammatory response in chronic obstructive pulmonary disease (COPD) were examined. METHODS: CD33 and CD64 expression on peripheral blood granulocytes and monocytes from patients with acute exacerbation of chronic obstructive pulmonary disease and healthy control were detected by flow cytometry. To evaluate the effect of CD33 on inflammation immunity in COPD, the correlation between CD33 expression and CD64 expression, as well as inflammatory indices were investigated. RESULTS: We found that the expression of CD64 on granulocytes and monocytes, as well as the levels of C-reacting protein (CRP) and myoglobin (MYO) or the proportion of neutrophils (N%) significantly increased in COPD patients compared to normal control group (p < 0.01). The expression of CD33 on granulocytes was significantly and negatively correlated with the level of CRP (r = -0.311, p = 0.012), as well as to the level of MYO (r = -0.295. p = 0.018). CONCLUSIONS: The granulocytes and monocytes in peripheral blood were activated in patients of acute exacerbation in COPD. CD33 on granulocytes had the potential to inhibit inflammation and prevent tissue damage.

Cyclin A overexpression is associated with chemosensitivity to paclitaxel-based chemotherapy in patients with esophageal squamous cell carcinoma.

The aim of this study was to investigate the correlation between cyclin A expression and efficacy of paclitaxel-based chemotherapy in patients with esophageal squamous cell carcinoma (ESCC). The expression of cyclin A was examined in 48 newly diagnosed ESCC patients prior to treatment using the MaxVision immunohistochemistry method. The patients received four cycles of paclitaxel-based chemotherapy, the short-term treatment efficacy was evaluated and a 3-year follow-up was conducted. The response rate was greater in patients with positive cyclin A expression compared with those with negative expression (54.8 vs. 23.5%; χ(2)=4.373; P<0.05). Univariate and multivariate Cox analysis revealed that clinicopathological stage, degree of differentiation and expression of cyclin A were independent prognosis factors in patients with ESCC following paclitaxel-based chemotherapy. ESCC patients with positive cyclin A expression demonstrated an increased sensitivity to paclitaxel-based chemotherapy, suggesting that cyclin A may be used as a marker to predict the treatment efficacy of paclitaxel in patients with ESCC.

Elevation of platelet count in patients with colorectal cancer predicts tendency to metastases and poor prognosis.

BACKGROUNDS/AIMS: Thrombocytosis had been found to be associated with tumor metastasis and poor prognosis in malignant tumors including colorectal cancer (CRC). In the present study, we investigated the relationship between the platelet and the biological features in patients with CRC in China. METHODOLOGY: The correlation of platelet counts of 150 cases with CRC with their clinicopathological characteristics was explored. Furthermore, the survival impact of preoperative platelet count was also investigated. RESULTS: Statistically significant correlations between the platelet count and the lymph node and distance metastasis (p=0.016 and 0.014), vascular and perinural invasion (p=0.025 and 0.016) as well as TNM clinical stages (p=0.014) except for the age, gender and grades (p=0.245, 0.276 and 0.324, respectively) were found. In addition, 5-year survival of patients with high platelet count and normal platelet count were 13.30% and 56.30%, respectively (p=0.000). Meanwhile, concurrent with lymph node and distance metastasis, perinural invasion and clinical stages (p=0.000, 0.022, 0.034 and 0.000), platelet count (p=0.010) was also found to be an independent prognostic factor in CRC in our study through multivariate analysis. CONCLUSIONS: Elevated platelet might play some role in the progress of CRC and preoperative platelet count might be a prognostic indicator in the CRC patients.