Fujian Key Laboratory of Translational Cancer Medicine

Fuzhou, China

Fujian Key Laboratory of Translational Cancer Medicine

Fuzhou, China
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Hao M.Z.,Fujian Provincial Cancer Hospital | Hao M.Z.,Fujian Key Laboratory of Translational Cancer Medicine | Lin H.L.,Fujian Provincial Cancer Hospital | Lin H.L.,Fujian Key Laboratory of Translational Cancer Medicine | And 6 more authors.
Journal of Digestive Diseases | Year: 2017

Objective: To investigate the safety and efficacy of transcatheter arterial chemoembolization (TACE) with embospheres for the treatment of unresectable hepatocellular carcinoma (HCC). Methods: Patients with unresectable HCC who were treated with TACE followed by embosphere treatment (Embo-TACE) or conventional TACE (cTACE) between May 2010 and March 2014 were retrospectively included in this study. The Embo-TACE group received lipiodol and chemotherapeutic agent emulsion, followed by embospheres. The cTACE group received lipiodol and chemotherapeutic agent emulsion, followed by gelatin sponge pellets. Time to progression (TTP), overall survival (OS), overall response rate (ORR), and safety were compared between the two groups. Univariate and multivariate regression analyses of the factors affecting survival were conducted. Results: The median TTP and OS in the Embo-TACE group were significantly longer than those in the cTACE group (TPP: 7.0 months vs 5.4 months, P = 0.035; OS: 15 months vs 12 months, P = 0.032). Seven days after the first TACE treatment, alanine aminotransferase level was higher in the cTACE group than in the Embo-TACE group (P = 0.015). The ORR did not significantly differ between the two groups (P = 0.827). Additional therapy and local responses one month after the first TACE treatment were associated with OS. Conclusions: Embo-TACE resulted in a significant improvement in TTP and OS for patients with unresectable HCC, compared with cTACE. Furthermore, Embo-TACE was better tolerated. Additional therapy and local responses one month after the first TACE were independent prognostic factors for OS. © 2016 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and John Wiley & Sons Australia, Ltd


Lin X.,Fujian Provincial Hospital | Lin M.,Fujian Medical University | Wei X.,Fujian Key Laboratory of Translational Cancer Medicine | Chen Q.,Fujian Provincial Hospital | Chen Q.,Fujian Medical University
Indian Journal of Cancer | Year: 2016

PURPOSES/OBJECTIVES: By observing and analyzing the clinical features of the colon cancer and the influence factors of liver metastasis, we try to find out independent risk factors with significant influence on colon cancer liver metastasis as well as to provide reference for clinical treatment. MATERIALS AND METHODS: A total of 306 cases of colon cancer patients' clinical data, including gender, age, primary focal size, primary focal intestinal segment, degree of differentiation, infiltration depth, level of serum carcinoembryonic antigen (CEA) before surgery, lymph node metastasis, liver basic diseases were collected and recorded. Single-factor Chi-square analysis and multifactor logistic regression analysis (SPSS 16.0 software) were used to retrospectively study the possible influence factors of colon liver metastases and to preliminary discuss the potential risk factors of liver metastasis in colon cancer patients. RESULTS: The Chi-square analysis showed that patients' primary focal segment, degree of differentiation, infiltration depth, level of serum CEA before surgery, and states of hepatitis B does 2 half-And-half had significant effect on the incidence of liver metastasis. However, in the further logistic regression analysis, it showed that only the infiltration depth and the states of hepatitis B does 2 half-And-half were the independent risk factors that influence the hepatic metastases. What was more, the both subgroups of positive hepatitis B with infection and vaccine showed significant statistical differences when comparing with hepatitis B all negative in the event of the probability of liver metastases (P = 0.011 and 0.004). CONCLUSIONS: The infiltration depth and the states of hepatitis B does 2 half-And-half were the independent risk factors on colon cancer patients' hepatic metastases. Those with the infiltration depth of T4 had a higher rate of hepatic metastases. Patients with does 2 half-And-half-positive hepatitis B (whether subgroup of hepatitis B virus infection or subgroup hepatitis B vaccine related) had a lower incidence rate of liver metastasis than those with hepatitis B all negative. © 2017 Indian Journal of Cancer.


Hou P.,Beckman Research Institute | Hou P.,Fujian Medical University | Hou P.,Fujian Key Laboratory of Translational Cancer Medicine | Kuo C.-Y.,Beckman Research Institute | And 5 more authors.
PLoS ONE | Year: 2014

Hypoxia-inducible factor 1 a (HIF-1α), a major mediator of tumor physiology, is activated during tumor progression, and its abundance is correlated with therapeutic resistance in a broad range of solid tumors. The accumulation of HIF-1α is mainly caused by hypoxia or through the mutated succinate dehydrogenase A (SDHA) or fumarate hydratase (FH) expression to inhibit its degradation. However, its activation under normoxic conditions, termed pseudohypoxia, in cells without mutated SDHA or FH is not well documented. Here, we show that dimethyl-2-ketoglutarate (DKG), a cell membrane-permeable precursor of a key metabolic intermediate, α-ketoglutarate (α-KG), known for its ability to rescue glutamine deficiency, transiently stabilized HIF-1α by inhibiting activity of the HIF prolyl hydroxylase domain-containing protein, PHD2. Consequently, prolonged DKGtreatment under normoxia elevated HIF-1α abundance and up-regulated the expression of its downstream target genes, thereby inducing a pseudohypoxic condition. This HIF-1α stabilization phenotype is similar to that from treatment of cells with desferrioxamine (DFO), an iron chelator, or dimethyloxalyglycine (DMOG), an established PHD inhibitor, but was not recapitulated with other α-KG analogues, such as Octyl-2KG, MPTOM001 and MPTOM002. Our study is the first example of an α-KG precursor to increase HIF-1a abundance and activity. We propose that DKG acts as a potent HIF-1α activator, highlighting the potential use of DKG to investigate the contribution of PHD2-HIF-1α pathway to tumor biology. © 2014 Hou et al.


Chen Y.,Fujian Medical University | Chen Y.,Fujian Key Laboratory of Translational Cancer Medicine | Lin G.,Fujian Medical University | Lin G.,Fujian Key Laboratory of Translational Cancer Medicine | And 9 more authors.
PLoS ONE | Year: 2013

Objective:To investigate the clinical significance of the expression of MHC class I chain-related gene A (MICA) in patients with advanced non-small cell lung cancer and explore the relationship between MICA expression and the efficacy of cytokine-induced killer cell (CIK) therapy for treating advanced non-small cell lung cancer.Methods:We obtained data on 222 patients with advanced non-small cell lung cancer, including data on MICA expression, age, gender, ECOG score, pathological type, stage, treatment history (including 38 patients who were given autologous CIK cell infusion), and overall survival (OS). MICA expression in lung cancer tissue was evaluated by immunohistochemical staining. Analyses of MICA expression, and CIK therapy association with survival outcomes were performed using Cox proportional models, Kaplan-Meier methods, and the log-rank test.Result:s MICA was expressed in both membrane and cytoplasm. MICA expression correlated with the stage of lung cancer, ECOG score, gender and age. Multivariate COX regression analysis showed that the expression of MICA was an independent prognostic factor of advanced non-small cell lung cancer (p = 0.002). In subgroup analysis, we divided the 222 patients into CIK and control groups. In the CIK group, the medium OS (mOS) of patients with a high expression of MICA was longer than in those with low expression of MICA (27 months vs. 13 months). In the control group, the mOS in patients with a high expression of MICA was shorter than in patients with low MICA expression (9 months vs. 18 months). COX regression analysis showed that the MICA expression affects the effect of CIK therapy (p<0.0001).Conclusion:1) The high expression of MICA is one of the indicators of a poor prognosis for advanced non-small cell lung cancer patients. 2) The high expression of MICA might be one of the predictive factors for successful CIK therapy. © 2013 Chen et al.


Zhong D.T.,Fujian Medical University | Zhong D.T.,Fujian Key Laboratory of Translational Cancer Medicine | Shi C.M.,Fujian Medical University | Shi C.M.,Fujian Key Laboratory of Translational Cancer Medicine | And 4 more authors.
Annals of Hematology | Year: 2012

Non-Hodgkin's lymphoma (NHL) remains the second most common malignant complication in patients with human immunodeficiency virus (HIV) infection. Even though NHL is commonly chemosensitive to primary treatment, failure or relapse still occurs in a large number of patients. We conducted this retrospective study to evaluate the efficacy and safety of gemcitabine, dexamethasone, and cisplatin (GDP) for relapsed or refractory AIDS-related NHL (AIDS-NHL). Forty-eight patients with relapsed or refractory AIDS-NHL were treated with intravenous combination chemotherapy with GDP. The overall objective response rate was 54.1 % (95 % confidence interval, CI, 40.1-68.3 %), with 10 complete responses and 16 partial responses. The 2-year overall survival rate (OS) was 70.8 % (95 % CI 58.0-83.7 %), and the 5-year OS was 41.7 % (95 % CI 27.7-55.6 %). The 2-year progression-free survival rate (PFS) was 37.5 % (95 % CI 23.8-51.2 %), and the 5-year PFS was 25.0 % (95 % CI 12.8-37.3 %). The median progression-free survival was 8.8 months (95 % CI 0-20.3 months), and the median overall survival was 40.6 months (95 % CI 22.6-58.6 months). Patients with B cell tumors who relapsed but had no B symptoms were clinical stage I/II, had infiltration fewer than two extranodal sites, had CD4+ counts >200 cells/μL, and had lactate dehydrogenase (LDH) less than the upper limit of normal benefited from GDP. The level of LDH had a significant impact on the response rate to chemotherapy with GDP (P=0.015). Myelosuppression was the main side effect; the incidence of grade 3-4 anemia was 8.3 %; leukopenia, 37.5 %; and thrombocytopenia, 48.3 %. Univariate and multivariate analyses were performed to determine variables for OS and PFS. This study confirms that GDP is an effective and safe salvage regimen in relapsed or refractory AIDSNHL, was associated with modest declines in CD4+ lymphocyte counts, and did not promote HIV-1 viral replication. © Springer-Verlag 2012.


Lin G.,Fujian Medical University | Lin G.,Fujian Provincial Cancer Hospital | Zheng X.-W.,Fujian Medical University | Li C.,Fujian Medical University | And 4 more authors.
Digestive Diseases and Sciences | Year: 2012

Background: Evidence shows a strong relationship between KRAS mutations and the NF-κB signaling pathway. In colorectal cancer, however, the study of this subject has been very limited and results are inconsistent. Aims: To examine the relationship between KRAS mutations and NF-κB activation and their effect on chemotherapy response and survival of colorectal cancer patients. Materials and Methods: NF-κB activation was analyzed by immunohistochemistry in 167 primary colorectal cancer specimens in which the KRAS mutation status was confirmed. Clinical and pathologic data were extracted from the medical records and reviewed. Results: Of 167 tumors screened, 63 (37.7 %) had NF-κB activation, 59 (35.3 %) had KRAS mutations, and 30 (18.0 %) had both NF-κB activation and KRAS mutations. The frequency of NF-κB activation in tumors with KRAS mutations was significantly higher than in tumors with wild type KRAS; 50.8 versus 30.6 %, P = 0.012. Patients with both KRAS mutations and NF-κB activation had a lower objective response to first-line chemotherapy than patients with other tumors, 23.8 versus 49.4 % (P = 0.035). Compared to patients with both KRAS mutations and NF-κB activation, overall survival of patients in other groups was significantly higher; median overall survival was 28.4 months (95 % CI 21.0-35.8) versus 46.3 months (95 % CI 39.4-53.2), hazard ratio 0.259 (95 % CI 0.125-0.538), P = 0.005. Conclusions: NF-κB activation was associated with KRAS mutation, and both KRAS mutation and NF-κB activation were indicative of high tolerance of chemotherapy and poor prognosis for colorectal cancer patients. Tumors with KRAS mutations and NF-κB activation may be a unique subtype of colorectal cancer. © 2012 Springer Science+Business Media, LLC.


Lai X.,Fujian Medical University | Liao J.,Fujian Medical University | Lin W.,Fujian Medical University | Lin W.,Fujian Key Laboratory of Translational Cancer Medicine | And 9 more authors.
Oncology Reports | Year: 2014

Inhibitor of DNA-binding protein 1 (ID1) is commonly abnormally overexpressed in colorectal cancer (CRC); yet, the functional significance of ID1 in the growth and invasive properties of CRC cells remains largely unclear. The present study investigated the effects of ID1 downregulation on the cell growth and metastatic features of CRC. Using lentiviral shRNA infection, stable ID1-knockdown (KD) HCT116 and SW620 cells, human metastatic CRC cell lines, were created. In vitro, the migration/invasion capacity of the ID1-KD CRC cells was assessed by a wound healing assay. The activities of MMP2 and MMP-9 were measured by gelatin zymography. The expression of CXC chemokine receptor 4 (CXCR4), PCNA and survivin were determined by immunoblot analysis and qRT-PCR. The effects of ID1 knockdown on tumor growth and hepatic metastasis were demonstrated by a xenograft study in mice. The results showed evident decreases in proliferation, migration and invasion and an increased apoptosis rate in the ID1-KD CRC cells. Similarly, ID1 knockdown significantly decreased mRNA and protein levels of PCNA, survivin, CXCR4, MMP2 and MMP9. Overexpression of CXCR4 antagonized the negative effect on the migration and invasion abilities of the ID1-KD cells. As compared with the control, ID1 knockdown prevented tumor growth and profoundly suppressed hepatic metastasis in vivo. The present study demonstrated the significance of ID1 in colon cancer progression, and its effect on tumor invasiveness and metastatic properties may be partly dependent on CXCR4.


Zhong D.T.,Fujian Medical University | Zhong D.T.,Fujian Key Laboratory of Translational Cancer Medicine | Shi C.M.,Fujian Medical University | Shi C.M.,Fujian Key Laboratory of Translational Cancer Medicine | And 5 more authors.
Journal of Cancer Research and Clinical Oncology | Year: 2012

Objective To evaluate through retrospective analysis the efficacy and toxicity of combination chemotherapy with etoposide, vincristine, doxorubin and dexamethasone (EVAD) as second-line therapy in patients with advanced AIDS-related Kaposi's sarcoma (AIDS-KS) after failure of first-line chemotherapy. Methods Eighty-eight patients with poor-risk AIDS-KS were treated intravenously with combination chemotherapy with EVAD; etoposide at a dose of 100 mg/m 2 on three consecutive days, vincristine 1.4 mg/m 2 with a maximum single dosage of 2.0 mg on day one, doxorubicin 30 mg/m 2 on day one and dexamethasone 40 mg on three consecutive days, with a three week cycle. All eligible patients had relapsed or progressed after prior two to six cycles of combination chemotherapy with doxorubicin, bleomycin and vincristine (ABV) or bleomycin and vincristine (BV). Results Assessment of the response of all the patients was made. The overall objective response rate was 59.1% (95% CI 48.83-69.37%), with five complete responses and 47 partial responses. Twenty-six cases of stable disease and 10 of progressive disease were observed in the remaining patients. The median follow-up period was 27 months (range 8-52 months). The median time to progression was 6.80 months (95% CI 2.04-11.56 months), and the median overall survival was 14.24 months (95% CI 10.26- 18.22 months). Leucopenia was seen in 92.0% of patients, of which 20 patients had grade 3 and 12 had grade 4. Conclusions Combination chemotherapy with EVAD oVers a new, active and safe therapeutic approach for the treatment of advanced AIDS-related KS. © Springer-Verlag 2011.


Feng R.,Fujian Medical University | Yang S.,Fujian Medical University | Yang S.,Fujian Key Laboratory of Translational Cancer Medicine
Journal of International Medical Research | Year: 2016

Objective: To investigate the synergistic effects of combining erlotinib and RNA-interference downregulation of focal adhesion kinase (FAK) expression on the proliferation, apoptosis, invasion and migration of the human gastric adenocarcinoma cell line AGS. Methods: Cells were divided into five experimental groups: Group A, nontransfected control; Group B, transfected with empty vector; Group C, transfected with FAK-shRNA; Group D, erlotinib treatment; Group E, combination erlotinib treatment and transfected with FAK-shRNA. FAK protein levels were confirmed via Western blotting. Cell proliferation (CCK-8 assay, apoptosis (flow cytometry), cell invasion (transwell assay) and migration (scratch assay) were evaluated. Results: RNA interference significantly decreased FAK protein levels. Cell proliferation, invasion and migration were significantly lower in Groups C, D and E compared with Group A, and significantly lower in Group E than in Groups C and D. Conclusions: RNA interference effectively silences FAK expression and inhibits malignant cell proliferation and invasion in gastric cancer cells. The effect of FAK inhibition is increased by co-treatment with erlotinib. © 2016, © The Author(s) 2016.


Ye Y.B.,Fujian Key Laboratory of Translational Cancer Medicine
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2011

To reveal the classification of lymphocytes and expression of cytokines infiltrating in HCC, and investigate the significance of changes of immune microenvironment in HCC. 76 tumor and non-tumor tissues of HCC were collected to detect the amount of immune cells in the tissues by FCM and immunohistochemistry (IHC). Th1/Th2 cytokines in tissues were detected by Cytometric bead array (CBA), and TGF-1, VEGF detected by ELISA. There were more CD3(+); T cells, CD4(+); Th cells, Treg cells, and CD45RO(+); memory T cells in tumors than in non-tumor tissues. On the contrary there were less CD8(+); CTLs in tumors. There was negative correlation between Treg and Th or CTL cells. CD69, which is the early activating factor, expressed less on CD3(+); T cells and NK cells in tumors than non-tumor tissues. Whereas HLA-DR, which is the late activating factor, expressed more on CD3(+); T cells in tumors than non-tumor tissues. More IL-10, TGF-1 and VEGF were secreted in tumors than non-tumor tissues. Along with the decrease of effective immune cells and increase of suppressor immune cells and cytokines, the lymphocytes infiltrating in the tumor were immune incompitence, which contributed to the tumorigenesis.

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