Sang Y.,National Clinical Research Center for Cancer |
Mei J.,National Clinical Research Center for Cancer |
Yu W.,National Clinical Research Center for Cancer |
Zhang X.,National Clinical Research Center for Cancer |
And 4 more authors.
Chinese Journal of Cancer Biotherapy
Objective: To analyze expressions of the mismatch repair proteins, MLH1, MSH2 and MSH6, and infiltration of T lymphocytes in tissues of non-small cell lung cancer (NSCLC) and to explore a relationship of microsatellite instability (MSI) with infiltration of T lymphocytes in NSCLC. Methods:One hundred samples of NSCLC tissues diagnosed in Cancer Institute and Hospital, Tianjin Medical University between 2004 and 2010 were collected. Expressions of the MLH1, MSH2 and MSH6, and infiltration of T lymphocytes in the carcinoma tissues were examined with immunohistochemical assay. The carcinoma tissues with one negative expression among the above proteins were determined as MSI, and clinical pathologic characteristics of MSI NSCLC were analyzed. Results: Petection rate of MSI in NSCLC tissues was 24%, that was lower than that in MSS. Infiltration of T lymphocytes in the tissues of MSI NSCLC was obviously higher than that in MSS. Results of the immunohistochemical assays showed that numbers of CD3+, CD4+ and CD8+ T lymphocytes infiltrated in the tissues of MSI NSCLC were significantly higher than those in the tissues of MSS NSCLC (P<0.05). MSI situation in the cases was related with their age (P<0.05) but not with their gender, pathological type of tumor, primary tumor size, involvement of regional lymph node and distant metastasis (P>0.05). Conclusion: MSI affects the tumor immune microenvironment of NSCLC, which might provide a novel predictive indicator for immunotherapy of NSCLC. © 2016, Editorial office of Chinese Journal of Cancer Biotherapy. All rights reserved. Source
Hui Z.,Tianjin Medical University |
Hui Z.,National Clinical Research Center for Cancer |
Hui Z.,Key Laboratory of Cancer Immunology and Biotherapy |
Hui Z.,Key Laboratory of Cancer Prevention and Therapy |
And 16 more authors.
Frontiers in Immunology
We present the first clinical evidence of advanced squamous non-small cell lung cancer with severe thrombocytopenia showing dramatic improvement after first-line treatment with pembrolizumab plus autologous cytokine-induced killer cells. © 2015 Hui, Zhang, Ren, Li and Ren. Source
Li F.-X.,Tianjin Medical University |
Li F.-X.,National Clinical Research Center for Cancer |
Li F.-X.,Key Laboratory of Cancer Prevention and Therapy |
Wei L.-J.,Tianjin Medical University |
And 11 more authors.
Asian Pacific Journal of Cancer Prevention
Purpose: We aimed to study the relationship between thrombocytosis and clinical features of gastric cancerfocussing on platelet counts and gastric cancer progression through different TNM stages. Methods: According to the normal range of platelet count in our institution, 1,596 patients were divided to two groups: a thrombocytosis group (120 patients, >400×1000/μL) and a control group (1,476 patients, ≤400×1000/μL). Results: The incidence of thrombocytosis was 7.5%. Higher platelet counts were observed in patients with older age, larger tumor size, deeper invasion, lymph node metastasis, distant metastasis and advanced TNM stage. In multivariate logistic regression, tumor size, depth of tumor invasion, lymph node metastasis and TNM stage were independent risk factors for thrombocytosis of gastric cancer patients. On prognostic analysis, age, tumor size, tumor location, histologic type, depth of tumor invasion, lymph node metastasis, distant metastasis and TNM stage and platelet count were important factors. Tumor size, invasion depth, lymph node metastasis, TNM stage and the platelet count were independent prognostic factors. Conclusion: Thrombocytosis is associated with clinical features of gastric cancer patients and correlates with a poor prognosis. Source
Li X.,Tianjin Medical University |
Li X.,National Clinical Research Center for Cancer |
Li X.,Key Laboratory of Cancer Prevention and Therapy |
Yu X.,Tianjin Medical University |
And 11 more authors.
Extracellular matrix metalloproteinase inducer, also knowns as cluster of differentiation 147 (CD147) or basigin, is a widely distributed cell surface glycoprotein that is involved in numerous physiological and pathological functions, especially in tumor invasion and metastasis. Monocarboxylate transporters (MCTs) catalyze the proton-linked transport of monocarboxylates such as L-lactate across the plasma membrane to preserve the intracellular pH and maintain cell homeostasis. As a chaperone to some MCT isoforms, CD147 overexpression significantly contributes to the metabolic transformation of tumor. This overexpression is characterized by accelerated aerobic glycolysis and lactate efflux, and it eventually provides the tumor cells with a metabolic advantage and an invasive phenotype in the acidic tumor microenvironment. This review highlights the roles of CD147 and MCTs in tumor cell metabolism and the associated molecular mechanisms. The regulation of CD147 and MCTs may prove to be with a therapeutic potential for tumors through the metabolic modification of the tumor microenvironment. Source
Qi L.,Tianjin Medical University |
Qi L.,The Key Laboratory of Tianjin Cancer Prevention and Treatment |
Qi L.,National Clinical Research Center for Cancer |
Song W.,Tianjin Medical University |
And 12 more authors.
International Journal of Molecular Sciences
Our previous study provided evidence that non-canonical Wnt signaling is involved in regulating vasculogenic mimicry (VM) formation. However, the functions of canonical Wnt signaling in VM formation have not yet been explored. In this study, we found the presence of VM was related to colon cancer histological differentiation (p < 0.001), the clinical stage (p < 0.001), and presence of metastasis and recurrence (p < 0.001). VM-positive colon cancer samples showed increased Wnt3a expression (p < 0.001) and P-catenin nuclear expression (p < 0.001) compared with the VM-negative samples. In vitro, over-regulated Wnt3a expression in HT29 colon cancer cells promoted the capacity to form tube-like structures in the three-dimensional (3-D) culture together with increased expression of endothelial phenotype-associated proteins such as VEGFR2 and VE-cadherin. The mouse xenograft model showed that Wnt3a-overexpressing cells grew into larger tumor masses and formed more VM than the control cells. In addition, the Wnt/P-catenin signaling antagonist Dickkopf-1(Dkk1) can reverse the capacity to form tube-like structures and can decrease the expressions of VEGFR2 and VE-cadherin in Wnt3a-overexpressing cells. Taken together, our results suggest that Wnt/β-catenin signaling is involved in VM formation in colon cancer and might contribute to the development of more accurate treatment modalities aimed at VM. © 2015 by the authors; licensee MDPI, Basel, Switzerland. Source