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Chen C.,Qingdao University | Qi X.J.,Peoples Hospital of Linzi District | Cao Y.W.,Qingdao University | Wang Y.H.,Qingdao University | And 3 more authors.
Urologia Internationalis

Bladder cancer relapse and treatment failure in most patients have often been attributed to chemoresistance in tumor cells and metastasis. Emerging evidence indicates that tumor heterogeneity may play an equally important role and extends to virtually all measurable properties of cancer cells. Although the idea of tumor heterogeneity is not new, little attention has been paid to applying it to understand and control bladder cancer progression. With the development of biotechnology, such as Gene sequencing, recent advances in understanding its generation model, original basis, consequent problems, and derived therapies provide great potential for tumor heterogeneity to be considered a new insight in the treatment of bladder cancers. © 2015 S. Karger AG, Basel. Source

Wang T.,Shandong Jiaotong Hospital | Dong A.-H.,Peoples Hospital of Linzi District | Cao H.-Y.,Peoples Hospital of Linzi District
Genetic Testing and Molecular Biomarkers

Context: Slow coronary flow (SCF) is a special coronary microvascular disorder associated with recurrent chest pain. The pathogenesis of SCF remain unclear. Objectives: We sought to assess whether serum salusin-β levels are correlated with SCF. Methods: We enrolled 76 patients with angiographically confirmed SCF and 108 age- and gender-matched controls. We measured serum salusin-β levels by enzyme-linked immunosorbent assay and coronary flow rate was assessed using thrombolysis in myocardial infarction frame count (TFC). Results: Serum salusin-β levels were elevated in SCF patients compared with controls (4.33 [range 3.52-5.87] nmol/L vs. 3.76 [range 2.98-4.67] nmol/L). Multivariate logistic regression analysis revealed that salusin-β in serum was the independent predictor of SCF (odds ratio = 1.814). Serum salusin-β levels were independently correlated with mean-TFC (r = 0.355, p = 0.002). Conclusions: Serum salusin-β levels were independently associated with SCF. Therefore, our findings implicate a potential role of salusin-β in the pathophysiology of SCF and provide insights on both risk stratification and modification in this patient population. © Copyright 2016, Mary Ann Liebert, Inc. Source

Sun Y.-Q.,Nantong University | Shi W.,Nantong University | Zheng G.-J.,Peoples Hospital of Linzi District
Journal of Practical Oncology

Objective: To evaluate the effect of refecoxib on angiogenesis and expression of vascular endothelial growth factor (VEGF) in human gastric carcinoma of nude mice. Methods: Human gastric carcinoma SGC-7901 cells were orthotopically transplanted in BALB/C nu/nu nude mice. The animals were randomly divided into 4 groups: in refecoxib group refecoxib (0.2 mL, 5 mg·kg-1·d-1) was given to tumor-transplanted nude mice by gastric gavage, in 5-FU group 5-FU (0.2 mL, 60 mg·kg -1·w-1) was given, in combination group refecoxib (0.2 mL, 5 mg·kg-1·d-1) + 5-FU (0.2 mL, 60 mg·kg-1·w-1) was given and in control group 0.2 mL normal saline was given. After 12 weeks, the animals were examined with color Doppler to observe the quantity of newborn vessels in tumor tissues. The expression of VEGF protein and VEGFmRNA in tumor tissue was detected by EnVision immunohistochemistry and semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) , respectively. Results: The vascular volumes in tumor tissue of refecoxib group(9.96 ± 3.58), 5-FU group(9.74 ± 2.83) and combination group(8.25 ± 3.14) were significantly lower than those in control group(13.10 ± 4.00)(P < 0.05). The expressions of VEGF protein and VEGFmRNA in tumor tissue of all therapeutic groups were lower than those in control group (P < 0.05). Conclusion: Refecoxib can down-regulate the expression of VEGF protein and VEGFmRNA, which is associated with the inhibition of angiogenesis in human gastric carcinoma transplanted of nude mice. Source

Guo H.,University of Houston | German P.,University of Houston | Bai S.,University of Houston | Barnes S.,University of Houston | And 7 more authors.
Journal of Genetics and Genomics

The phosphatidylinositol 3 kinase (PI3K)/AKT pathway is genetically targeted in more pathway components and in more tumor types than any other growth factor signaling pathway, and thus is frequently activated as a cancer driver. More importantly, the PI3K/AKT pathway is composed of multiple bifurcating and converging kinase cascades, providing many potential targets for cancer therapy. Renal cell carcinoma (RCC) is a high-risk and high-mortality cancer that is notoriously resistant to traditional chemotherapies or radiotherapies. The PI3K/AKT pathway is modestly mutated but highly activated in RCC, representing a promising drug target. Indeed, PI3K pathway inhibitors of the rapalog family are approved for use in RCC. Recent large-scale integrated analyses of a large number of patients have provided a molecular basis for RCC, reiterating the critical role of the PI3K/AKT pathway in this cancer. In this review, we summarize the genetic alterations of the PI3K/AKT pathway in RCC as indicated in the latest large-scale genome sequencing data, as well as treatments for RCC that target the aberrant activated PI3K/AKT pathway. © 2015 Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, and Genetics Society of China. Source

Shi H.,Qingdao University | Qi X.,Peoples Hospital of Linzi District | Ma B.,Qingdao University | Cao Y.,Qingdao University | And 3 more authors.
Chinese Journal of Cancer Research

In recent years, immunotherapy has been gradually established as the fourth frequently adopted antitumor therapy, following surgery, chemotherapy and radiotherapy, for advanced urologic malignancies with an improved understanding of theoretical basis, such as molecular biology and immunology. Thereinto, adoptive cellular immunotherapy (ACI) has become one of the hotspots, which comprises a variety of treatment approaches, such as TIL, CIK cell, γδ T cell, CAR-engineered T cell and Allogeneic stem cell transplantation (alloSCT). Although preclinical efficacy has been demonstrated remarkably, clinical trials could not consistently show the benefit due to multi-factors in complex immunosuppressive microenvironment in vivo compared to that of in vitro. Here we review some timely aspects of ACI for advanced urologic malignancies, and describe the current status and limitation of immunotherapy from the cellular level. It’s our expectation to provide prompting consideration of novel combinatorial ACI strategies and a resurgence of interest in ACI for advanced urologic malignancies. © Chinese Journal of Cancer Research. All rights reserved. Source

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