26 results on '"Sun, Qi-Man"'
Search Results
2. The clinical implications and molecular features of intrahepatic cholangiocarcinoma with perineural invasion
- Author
-
Meng, Xian-Long, Lu, Jia-Cheng, Zeng, Hai-Ying, Chen, Zhen, Guo, Xiao-Jun, Gao, Chao, Pei, Yan-Zi, Hu, Shu-Yang, Ye, Mu, Sun, Qi-Man, Yang, Guo-Huang, Cai, Jia-Bin, Huang, Pei-Xin, Yv, Lei, Zhang, Lv, Shi, Ying-Hong, Ke, Ai-Wu, Zhou, Jian, Fan, Jia, Chen, Yi, Huang, Xiao-Yong, and Shi, Guo-Ming
- Published
- 2023
- Full Text
- View/download PDF
3. Macro CD5L+ deteriorates CD8+T cells exhaustion and impairs combination of Gemcitabine-Oxaliplatin-Lenvatinib-anti-PD1 therapy in intrahepatic cholangiocarcinoma
- Author
-
Lu, Jia-Cheng, Wu, Lei-Lei, Sun, Yi-Ning, Huang, Xiao-Yong, Gao, Chao, Guo, Xiao-Jun, Zeng, Hai-Ying, Qu, Xu-Dong, Chen, Yi, Wu, Dong, Pei, Yan-Zi, Meng, Xian-Long, Zheng, Yi-Min, Liang, Chen, Zhang, Peng-Fei, Cai, Jia-Bin, Ding, Zhen-Bin, Yang, Guo-Huan, Ren, Ning, Huang, Cheng, Wang, Xiao-Ying, Gao, Qiang, Sun, Qi-Man, Shi, Ying-Hong, Qiu, Shuang-Jian, Ke, Ai-Wu, Shi, Guo-Ming, Zhou, Jian, Sun, Yi-Di, and Fan, Jia
- Published
- 2024
- Full Text
- View/download PDF
4. Loss of 5-hydroxymethylcytosine induces chemotherapy resistance in hepatocellular carcinoma via the 5-hmC/PCAF/AKT axis
- Author
-
Guo, Xiao-Jun, Huang, Xiao-Yong, Yang, Xuan, Lu, Jia-Cheng, Wei, Chuan-Yuan, Gao, Chao, Pei, Yan-Zi, Chen, Yi, Sun, Qi-Man, Cai, Jia-Bin, Zhou, Jian, Fan, Jia, Ke, Ai-Wu, Shi, Yujiang G., Shen, Ying-Hao, Zhang, Peng-Fei, Shi, Guo-Ming, and Yang, Guo-Huan
- Published
- 2023
- Full Text
- View/download PDF
5. Amplification of spatially isolated adenosine pathway by tumor–macrophage interaction induces anti-PD1 resistance in hepatocellular carcinoma
- Author
-
Lu, Jia-Cheng, Zhang, Peng-Fei, Huang, Xiao-Yong, Guo, Xiao-Jun, Gao, Chao, Zeng, Hai-Ying, Zheng, Yi-Min, Wang, Si-Wei, Cai, Jia-Bin, Sun, Qi-Man, Shi, Ying-Hong, Zhou, Jian, Ke, Ai-Wu, Shi, Guo-Ming, and Fan, Jia
- Published
- 2021
- Full Text
- View/download PDF
6. A New Preoperative Prognostic System Combining CRP and CA199 For Patients with Intrahepatic Cholangiocarcinoma
- Author
-
Zheng, Bo-Hao, Yang, Liu-Xiao, Sun, Qi-Man, Fan, Hong-Kai, Duan, Men, Shi, Jie-Yi, Wang, Xiao-Ying, Zhou, Jian, Fan, Jia, Ma, Zheng-Yao, and Gao, Qiang
- Published
- 2017
- Full Text
- View/download PDF
7. High expression of IL-9R promotes the progression of human hepatocellular carcinoma and indicates a poor clinical outcome
- Author
-
LI, HONG-JUN, SUN, QI-MAN, LIU, LONG-ZI, ZHANG, JUN, HUANG, JUN, WANG, CHENG-HONG, DING, RUI, SONG, KANG, and TONG, ZHONG
- Published
- 2015
- Full Text
- View/download PDF
8. [Corrigendum] Macrophage-secreted IL-8 induces epithelial-mesenchymal transition in hepatocellular carcinoma cells by activating the JAK2/STAT3/Snail pathway.
- Author
-
Fu, Xiu-Tao, Dai, Zhi, Song, Kang, Zhang, Zhuo-Jun, Zhou, Zheng-Jun, Zhou, Shao-Lai, Zhao, Yi-Ming, Xiao, Yong-Sheng, Sun, Qi-Man, Ding, Zhen-Bin, and Fan, Jia
- Published
- 2024
- Full Text
- View/download PDF
9. Interferon-alpha 2a up-regulated thymidine phosphorylase and enhanced antitumor effect of capecitabine on hepatocellular carcinoma in nude mice
- Author
-
Xiao, Yong-Sheng, Tang, Zhao-You, Fan, Jia, Zhou, Jian, Wu, Zhi-Quan, Sun, Qi-Man, Xue, Qiong, Zhao, Yan, Liu, Yin-Kun, and Ye, Sheng-Long
- Published
- 2004
- Full Text
- View/download PDF
10. CTLA-4 Synergizes With PD1/PD-L1 in the Inhibitory Tumor Microenvironment of Intrahepatic Cholangiocarcinoma.
- Author
-
Guo, Xiao-Jun, Lu, Jia-Cheng, Zeng, Hai-Ying, Zhou, Rong, Sun, Qi-Man, Yang, Guo-Huan, Pei, Yan-Zi, Meng, Xian-Long, Shen, Ying-Hao, Zhang, Peng-Fei, Cai, Jia-Bin, Huang, Pei-Xin, Ke, Ai-Wu, Shi, Ying-Hong, Zhou, Jian, Fan, Jia, Chen, Yi, Yang, Liu-Xiao, Shi, Guo-Ming, and Huang, Xiao-Yong
- Subjects
CYTOTOXIC T lymphocyte-associated molecule-4 ,DISEASE risk factors ,TUMOR microenvironment ,FORKHEAD transcription factors ,PROPORTIONAL hazards models - Abstract
Intrahepatic cholangiocarcinoma (ICC) is highly invasive and carries high mortality due to limited therapeutic strategies. In other solid tumors, immune checkpoint inhibitors (ICIs) target cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) and programmed death 1 (PD1), and the PD1 ligand PD-L1 has revolutionized treatment and improved outcomes. However, the relationship and clinical significance of CTLA-4 and PD-L1 expression in ICC remains to be addressed. Deciphering CTLA-4 and PD-L1 interactions in ICC enable targeted therapy for this disease. In this study, immunohistochemistry (IHC) was used to detect and quantify CTLA-4, forkhead box protein P3 (FOXP3), and PD-L1 in samples from 290 patients with ICC. The prognostic capabilities of CTLA-4, FOXP3, and PD-L1 expression in ICC were investigated with the Kaplan–Meier method. Independent risk factors related to ICC survival and recurrence were assessed by the Cox proportional hazards models. Here, we identified that CTLA-4
+ lymphocyte density was elevated in ICC tumors compared with peritumoral hepatic tissues (P <.001), and patients with a high density of CTLA-4+ tumor-infiltrating lymphocytes (TILsCTLA-4 High ) showed a reduced overall survival (OS) rate and increased cumulative recurrence rate compared with patients with TILsCTLA-4 Low (P <.001 and P =.024, respectively). Similarly, patients with high FOXP3+ TILs (TILsFOXP3 High ) had poorer prognoses than patients with low FOXP3+ TILs (P =.021, P =.034, respectively), and the density of CTLA-4+ TILs was positively correlated with FOXP3+ TILs (Pearson r =.31, P <.001). Furthermore, patients with high PD-L1 expression in tumors (TumorPD-L1 High ) and/or TILsCTLA-4 High presented worse OS and a higher recurrence rate than patients with TILsCTLA-4 Low TumorPD-L1 Low . Moreover, multiple tumors, lymph node metastasis, and high TumorPD-L1 /TILsCTLA-4 were independent risk factors of cumulative recurrence and OS for patients after ICC tumor resection. Furthermore, among ICC patients, those with hepatolithiasis had a higher expression of CTLA-4 and worse OS compared with patients with HBV infection or undefined risk factors (P =.018). In conclusion, CTLA-4 is increased in TILs in ICC and has an expression profile distinct from PD1/PD-L1. TumorPD-L1 /TILsCTLA-4 is a predictive factor of OS and ICC recurrence, suggesting that combined therapy targeting PD1/PD-L1 and CTLA-4 may be useful in treating patients with ICC. [ABSTRACT FROM AUTHOR]- Published
- 2021
- Full Text
- View/download PDF
11. Graft Programmed Death Ligand 1 Expression as a Marker for Transplant Rejection Following Anti–Programmed Death 1 Immunotherapy for Recurrent Liver Tumors.
- Author
-
Shi, Guo‐Ming, Wang, Jiping, Huang, Xiao‐Wu, Huang, Xiao‐Yong, He, Yi‐Feng, Ji, Yuan, Chen, Yi, Wu, Dong, Lu, Jia‐Cheng, Sun, Qi‐Man, Liu, Wei‐Ren, Wang, Ting, Yang, Liu‐Xiao, Hou, Ying‐Yong, Shi, Ying‐Hong, Sun, Jian, Xiao, Yong‐Sheng, Wang, Zheng, Fan, Jia, and Bertagnolli, Monica M.
- Published
- 2021
- Full Text
- View/download PDF
12. Identification of FOS as a Candidate Risk Gene for Liver Cancer by Integrated Bioinformatic Analysis.
- Author
-
Hu, Jin-Wu, Ding, Guang-Yu, Fu, Pei-Yao, Tang, Wei-Guo, Sun, Qi-Man, Zhu, Xiao-Dong, Shen, Ying-Hao, Zhou, Jian, Fan, Jia, Sun, Hui-Chuan, and Huang, Cheng
- Subjects
CANCER patients ,CELL receptors ,CELLULAR signal transduction ,GENE expression ,GENETIC techniques ,HEPATOCELLULAR carcinoma ,LIVER tumors ,MESSENGER RNA ,ONCOGENES ,PROTEIN kinases ,BIOINFORMATICS ,GENOMICS ,DISEASE progression ,GENE expression profiling ,MICRORNA - Abstract
Liver cancer is a lethal disease that is associated with poor prognosis. In order to identify the functionally important genes associated with liver cancer that may reveal novel therapeutic avenues, we performed integrated analysis to profile miRNA and mRNA expression levels for liver tumors compared to normal samples in The Cancer Genome Atlas (TCGA) database. We identified 405 differentially expressed genes and 233 differentially expressed miRNAs in tumor samples compared with controls. In addition, we also performed the pathway analysis and found that mitogen-activated protein kinases (MAPKs) and G-protein coupled receptor (GPCR) pathway were two of the top significant pathway nodes dysregulated in liver cancer. Furthermore, by examining these signaling networks, we discovered that FOS (Fos proto-oncogene, AP-1 transcription factor subunit), LAMC2 (laminin subunit gamma 2), and CALML3 (calmodulin like 3) were the most significant gene nodes with high degrees involved in liver cancer. The expression and disease prediction accuracy of FOS, LAMC2, CALML3, and their interacting miRNAs were further performed using a HCC cohort. Finally, we investigated the prognostic significance of FOS in another HCC cohort. Patients with higher FOS expression displayed significantly shorter time to recurrence (TTR) and overall survival (OS) compared with patients with lower expression. Collectively, our study demonstrates that FOS is a potential prognostic marker for liver cancer that may reveal a novel therapeutic avenue in this lethal disease. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
13. Long non-coding RNA 00607 as a tumor suppressor by modulating NF-κB p65/p53 signaling axis in hepatocellular carcinoma.
- Author
-
Sun, Qi-Man, Hu, Bo, Fu, Pei-Yao, Tang, Wei-Guo, Zhang, Xin, Zhan, Hao, Sun, Chao, He, Yi-Feng, Song, Kang, Xiao, Yong-Sheng, Sun, Jian, Xu, Yang, Zhou, Jian, and Fan, Jia
- Subjects
- *
NON-coding RNA , *LIVER cancer , *XENOGRAFTS , *TUMORS , *CANCER chemotherapy - Abstract
Accumulating evidence suggests that long non-coding RNA (lncRNA) plays important roles in some malignant tumors. However, the mechanism underlying how lncRNA regulates hepatocellular carcinoma (HCC) process remains largely unknown. In this study, we explored the potential role of lncRNA 00607 as a novel tumor suppressor in HCC. In this study, we examined the regulation of lncRNA 00607 by the important inflammatory cytokine tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). We also determined the expression of LINC000607 in 159 HCC tumors and paired adjacent tissues. Effects of LINC000607 in HCC proliferation and apoptosis were examined in vitro in HCC cell lines and in vivo tumor xenografts. Furthermore, we also examine underlying mechanism by which lncRNA 00607 regulates NF-κB p65 and how LIN00607 exerts its tumor suppressor role in HCC. We found that lncRNA 00607 expression level is lower in HCC tumors compared with matched normal liver tissue, and its low expression predicts worse prognosis in HCC. Functionally, lncRNA 00607 overexpression leads to decreased HCC cell proliferation in vitro and in vivo, enhanced apoptosis and chemotherapeutic drug sensitivity. Mechanistically, lncRNA 00607 inhibits the p65 transcription by binding to the p65 promoter region, therefore contributing to increased p53 levels in HCC. Taken together, the findings of this study show that the TNF-α/IL-6-lncRNA 00607-NF-κB p65/p53 signaling axis represents a novel therapeutic avenue in cancer chemotherapy. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
- View/download PDF
14. Naive Treg-like CCR7 mononuclear cells indicate unfavorable prognosis in hepatocellular carcinoma.
- Author
-
Shi, Jie-Yi, Duan, Meng, Sun, Qi-Man, Yang, Liuxiao, Wang, Zhi-Chao, Mynbaev, Ospan, He, Yi-Feng, Wang, Ling-Yan, Zhou, Jian, Tang, Qi-Qun, Cao, Ya, Fan, Jia, Wang, Xiao-Ying, and Gao, Qiang
- Abstract
Chemokine receptor-like 1 (CCRL1) has the potential in creating a low level of CCL19 and CCL21 to hinder CCR7 cell tracking to tumor tissue. Previously, we found a tumor suppressive role of CCRL1 by impairing CCR7-related chemotaxis of tumor cells in human hepatocellular carcinoma (HCC). Here, we reported a contribution of CCR7 mononuclear cells in the tumor microenvironment to the progression of disease. Immunohistochemistry was used to investigate the distribution and clinical significance of CCR7 cells in a cohort of 240 HCC patients. Furthermore, the phenotype, composition, and functional status of CCR7 cells were determined by flow cytometry, immunofluorescence, and in vitro co-culture assays. We found that CCR7 mononuclear cells were dispersed around tumor tissue and negatively related to tumoral expression of CCRL1 ( P < 0.001, r = 0.391). High density of CCR7 mononuclear cells positively correlated with the absence of tumor capsule, vascular invasion, and poor differentiation ( P < 0.05). Survival analyses revealed that increased number of CCR7 mononuclear cells was significantly associated with worse survival and increased recurrence. We found that CCR7 mononuclear cells featured a naive Treg-like phenotype (CD45RACD25FOXP3) and possessed tumor-promoting potential by producing TGF-β1. Moreover, CCR7 cells were also composed of several immunocytes, a third of which were CD8 T cells. CCR7 Treg-like cells facilitate tumor growth and indicate unfavorable prognosis in HCC patients, but fortunately, their tracking to tumor tissue is under the control of CCRL1. [ABSTRACT FROM AUTHOR]
- Published
- 2016
- Full Text
- View/download PDF
15. Tie2-Expressing Monocytes Are Associated with Identification and Prognoses of Hepatitis B Virus Related Hepatocellular Carcinoma after Resection.
- Author
-
He, Yi-Feng, Wang, Chao-Qun, Yu, Yao, Qian, Jing, Song, Kang, Sun, Qi-Man, and Zhou, Jian
- Subjects
HEPATITIS B ,MONOCYTES ,LIVER cancer ,SURGICAL excision ,FLOW cytometry ,HEPATECTOMY ,PROGNOSIS - Abstract
Background: Tie2-expressing monocytes (TEMs) are found in various tumors, involved in forming tumor blood vessels and expressing several important proangiogenic factors. The goals of this study were to evaluate the value of TEMs in diagnosing and predicting the prognosis of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). Methods: Flow cytometry was performed to identify and count TEMs in peripheral blood monocytes from HCC patients (n = 84) receiving hepatectomy, HBV cirrhotic patients (n = 21), benign tumors patients (n = 15) and healthy volunteers (n = 23). Angiopoietin-2 (Ang-2) levels in the plasma were determined by enzyme linked immunosorbent assay. The distribution of TEMs in tumor tissue was observed by immunofluorescence staining. Then we determined the vascular area as a percentage of tumor area (vascular area/tumor area) by immunohistochemical staining. Finally the prognostic significance of TEMs and other clinicopathologic factors was evaluated. Results: Percentage of TEMs in peripheral blood monocytes significantly increased in HCC patients compared with HBV cirrhotic patients and healthy donors (both P< 0.001). However there was no significance in benign liver tumor (P = 0.482). In addition, the percentage of circulating TEMs was positively correlated with plasma Ang-2 concentration (P<0.001, r
2 = 0.294) and vascular area/tumor area (P<0.001, r2 = 0.126). Furthermore the percentage of intratumoral TEMs was significantly higher than that of paratumoral TEMs (P<0.001). Increased circulating TEMs was associated with poor overall survival (P = 0.043) and a shorter time to recurrence (P = 0.041). Multivariate Cox analysis also revealed that the percentage of TEMs in peripheral blood was an independent factor for HCC patients’ prognosis. Conclusions: TEMs may promote angiogenesis in HCC regarding the angiopoietin/Tie2 signal pathway. Percentage of TEMs in peripheral blood monocytes may be applied as a biomarker for identifying HBV-related HCC and predicting the prognosis of these patients after resection. [ABSTRACT FROM AUTHOR]- Published
- 2015
- Full Text
- View/download PDF
16. Plasma MicroRNA, a Potential Biomarker for Acute Rejection After Liver Transplantation.
- Author
-
Hu, Jie, Wang, Zheng, Tan, Chang-Jun, Liao, Bo-Yi, Zhang, Xin, Xu, Min, Dai, Zhi, Qiu, Shuang-Jian, Huang, Xiao-Wu, Sun, Jian, Sun, Qi-Man, He, Yi-Feng, Song, Kang, Pan, Qi, Wu, Ying, Fan, Jia, and Zhou, Jian
- Published
- 2013
- Full Text
- View/download PDF
17. Circumventing intratumoral heterogeneity to identify potential therapeutic targets in hepatocellular carcinoma.
- Author
-
Huang, Ao, Zhao, Xin, Yang, Xin-Rong, Li, Fu-Qiang, Zhou, Xin-Lan, Wu, Kui, Zhang, Xin, Sun, Qi-Man, Cao, Ya, Zhu, Hong-Mei, Wang, Xiang-Dong, Yang, Huan-Ming, Wang, Jian, Tang, Zhao-You, Hou, Yong, Fan, Jia, and Zhou, Jian
- Subjects
- *
LIVER cancer , *GENETIC mutation , *EXOMES , *GENOMES , *DNA - Abstract
Background & Aims Identifying target genetic mutations in hepatocellular carcinoma (HCC) for therapy is made challenging by intratumoral heterogeneity. Circulating cell-free DNAs (cfDNA) may contain a more complete mutational spectrum compared to a single tumor sample. This study aimed to identify the most efficient strategy to identify all the mutations within heterogeneous HCCs. Methods Whole exome sequencing (WES) and targeted deep sequencing (TDS) were carried out in 32 multi-regional tumor samples from five patients. Matched preoperative cfDNAs were sequenced accordingly. Intratumoral heterogeneity was measured using the average percentage of non-ubiquitous mutations (present in parts of tumor regions). Profiling efficiencies of single tumor specimen and cfDNA were compared. The strategy with the highest performance was used to screen for actionable mutations. Results Variable levels of heterogeneity with branched and parallel evolution patterns were observed. The heterogeneity decreased at higher sequencing depth of TDS compared to measurements by WES (28.1% vs. 34.9%, p <0.01) but remained unchanged when additional samples were analyzed. TDS of single tumor specimen identified an average of 70% of the total mutations from multi-regional tissues. Although genome profiling efficiency of cfDNA increased with sequencing depth, an average of 47.2% total mutations were identified using TDS, suggesting that tissue samples outperformed it. TDS of single tumor specimen in 66 patients and cfDNAs in four unresectable HCCs showed that 38.6% (26/66 and 1/4) of patients carried mutations that were potential therapeutic targets. Conclusions TDS of single tumor specimen could identify actionable mutations targets for therapy in HCC. cfDNA may serve as secondary alternative in profiling HCC genome. Lay summary Targeted deep sequencing of single tumor specimen is a more efficient method to identify mutations in hepatocellular carcinoma made from mixed subtypes compared to circulating cell-free DNA in blood. cfDNA may serve as secondary alternative in profiling HCC genome. Identifying mutations may help clinicians choose targeted therapy for better individual treatments. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
18. Corrigendum to “Circumventing intratumoral heterogeneity to identify potential therapeutic targets in hepatocellular carcinoma” [J Hepatol 67 (2017) 293–301].
- Author
-
Huang, Ao, Zhao, Xin, Yang, Xin-Rong, Li, Fu-Qiang, Zhou, Xin-Lan, Wu, Kui, Zhang, Xin, Sun, Qi-Man, Cao, Ya, Zhu, Hong-Mei, Wang, Xiang-Dong, Yang, Huan-Ming, Wang, Jian, Tang, Zhao-You, Hou, Yong, Fan, Jia, and Zhou, Jian
- Subjects
- *
LIVER cancer , *HETEROGENEITY - Abstract
A correction to the article "Circumventing Intratumoral Heterogeneity to Identify Potential Therapeutic Targets in Hepatocellular Carcinoma," published in a previous issue of the journal is presented.
- Published
- 2017
- Full Text
- View/download PDF
19. [Corrigendum] Macrophage‑secreted IL‑8 induces epithelial‑mesen-chymal transition in hepatocellular carcinoma cells by activating the JAK2/STAT3/Snail pathway.
- Author
-
Fu XT, Dai Z, Song K, Zhang ZJ, Zhou ZJ, Zhou SL, Zhao YM, Xiao YS, Sun QM, Ding ZB, and Fan J
- Abstract
Subsequently to the publication of the above article, an interested reader drew to the authors' attention that a possible error had been identified in the selection of images in Figs. 1 and/or 7. After having consulted their original data, the authors realized that an erroneous image appeared on p. 593, in Fig. 7F [the 'Hep‑G2 / IL‑8 (5 ng/ml)' data panel], where part of this figure panel was overlapping with an image on p. 589 in Fig. 1C (the 'Hep‑G2 Co‑cultured' data panel). After a thorough review and verification of the data by all the authors, they have confirmed that the original data presented in the paper were accurate, and the error was solely due to the selection of an incorrect image during figure arrangement. The authors confirm that this mistake in image selection did not affect the overall conclusions reported in the article. A corrected version of Fig. 7, including the correct data for the 'Hep‑G2 / IL‑8 (5 ng/ml)' panel in Fig. 7F, is shown on the next page. The authors are grateful to the Editor of International Journal of Oncology for granting them the opportunity to publish this Corrigendum. All the authors agree to the publication of this Corrigendum, and apologize to the readership for any inconvenience caused. [International Journal of Oncology 46: 587‑596, 2015; DOI: 10.3892/ijo.2014.2761].
- Published
- 2024
- Full Text
- View/download PDF
20. Plasma MicroRNA Panel Predicts Early Tumor Recurrence in Patients with Hepatocellular Carcinoma after Liver Transplantation.
- Author
-
Huang A, Guo DZ, Wang YP, Yang GH, Sun QM, Zhang X, He YF, Song K, Huang XW, Yang XR, Fan J, Zhou J, and Hu J
- Abstract
Background: This study aimed to evaluate the role of plasma microRNA panel (miR-122, miR-192, miR-21, miR-223, miR-26a, miR-27a and miR-801) for prediction and surveillance of early tumor recurrence in hepatocellular carcinoma (HCC) patients who had undergone liver transplantation (LT). Methods: The expression of plasma microRNA panel was assayed in 193 HCC patients (training cohort, n =151; validation cohort, n = 42). Sensitivity and specificity for detecting post-transplant HCC recurrence, and the relationship of microRNA panel expression with clinical characteristics were analyzed accordingly. The prognostic value of microRNA panel was compared with that of AFP (alpha-fetoprotein) and DCP (Des-gamma-carboxyprothrombin). Cox regression analyses were used to evaluate independent prognostic factors. Results: In the training cohort, the rate of positive plasma microRNA panel status at 7-14 days after LT (late phase; 44.2%) decreased than that before (76.2%, P < 0.001) and 1-6 days after LT (early phase; 78.5%, P < 0.001). At late phase, positive microRNA panel status correlated with higher early tumor recurrence rate (one year after LT) than negative status (45.9% vs 10.7%; P < 0.001). Patients with persistent positive microRNA panel status both before and after LT had the highest early tumor recurrence rate in this cohort (54.9%, P < 0.001). The results were consistent in the validation cohort. Cox regression analysis found that positive plasma microRNA panel status at late phase was the only independent risk factor for early recurrence (HR: 4.903, 95% CI = 2.195 - 10.951; P < 0.001). Dynamic monitoring demonstrated plasma microRNA panel status changed from negative to positive earlier than AFP and DCP upon recurrence, and the median time between positivity of plasma microRNA and imaging evidence of recurrence was 2.4 (0.5-10.0) months. Conclusions: Plasma microRNA panel could be a noninvasive biomarker for prediction and surveillance of early tumor recurrence in HCC patients who have undergone LT., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)
- Published
- 2021
- Full Text
- View/download PDF
21. Distinct PD-L1/PD1 Profiles and Clinical Implications in Intrahepatic Cholangiocarcinoma Patients with Different Risk Factors.
- Author
-
Lu JC, Zeng HY, Sun QM, Meng QN, Huang XY, Zhang PF, Yang X, Peng R, Gao C, Wei CY, Shen YH, Cai JB, Dong RZ, Shi YH, Sun HC, Shi YG, Zhou J, Fan J, Ke AW, Yang LX, and Shi GM
- Subjects
- Adult, Aged, Cholangiocarcinoma metabolism, Cholangiocarcinoma virology, Female, Hepatitis B virus physiology, Humans, Liver Neoplasms metabolism, Liver Neoplasms virology, Male, Middle Aged, Programmed Cell Death 1 Receptor metabolism, Retrospective Studies, Risk Factors, Cholangiocarcinoma genetics, Liver Neoplasms genetics, Programmed Cell Death 1 Receptor genetics
- Abstract
Rationale : PD1/PD-L1 immune checkpoint inhibitors have shown promising results for several malignancies. However, PD1/PD-L1 signaling and its therapeutic significance remains largely unknown in intrahepatic cholangiocarcinoma (ICC) cases with complex etiology. Methods : We investigated the expression and clinical significance of CD3 and PD1/PD-L1 in 320 ICC patients with different risk factors. In addition, we retrospectively analyzed 7 advanced ICC patients who were treated with PD1 inhibitor. Results : The cohort comprised 233 patients with HBV infection, 18 patients with hepatolithiasis, and 76 patients with undetermined risk factors. PD-L1 was mainly expressed in tumor cells, while CD3 and PD1 were expressed in infiltrating lymphocytes of tumor tissues. PD1/PD-L1 signals were activated in tumor tissues, and expression was positively correlated with HBV infection and lymph node invasion. More PD1
+ T cells and higher PD-L1 expression were observed in tumor tissues of ICC patients with HBV infection compared to patients with hepatolithiasis or undetermined risk factors. More PD1+ T cells and/or high PD-L1 expression negatively impacted the prognosis of patients with HBV infection but not those with hepatolithiasis. Multivariate analysis showed PD1/PD-L1 expression was an independent indicator of ICC patient prognosis. Advanced ICC patients with HBV infection and less PD1+ T cells tended to have good response to anti-PD1 therapy. Conclusion : Hyperactivated PD1/PD-L1 signals in tumor tissues are a negative prognostic marker for ICCs after resection. HBV infection- and hepatolithiasis-related ICCs have distinct PD1/PD-L1 profiles. Further, PD1+ T cells could be used as a biomarker to predict prognosis and assay the efficiency of anti-PD1 immunotherapy in ICC patients with HBV infection., Competing Interests: Competing Interests: The authors have declared that no competing interest exists.- Published
- 2019
- Full Text
- View/download PDF
22. Long non-coding RNA00364 represses hepatocellular carcinoma cell proliferation via modulating p-STAT3-IFIT2 signaling axis.
- Author
-
Tang WG, Hu B, Sun HX, Sun QM, Sun C, Fu PY, Yang ZF, Zhang X, Zhou CH, Fan J, Ren N, and Xu Y
- Abstract
The effects of long non-coding RNAs (lncRNAs) on hepatocellular carcinoma (HCC) remain largely unclear. In this study, we identified an interferon (IFN)-γ-induced LncRNA, LncRNA00364, in HCC by microarray. LncRNA00364 displays lower expression in HCC tumor samples compared to paired normal controls. Overexpression of LncRNA00364 inhibits cell proliferation, G1/S cell cycle progression and promotes apoptosis in HCC cell lines. Consistently, LncRNA00364 overexpression leads to decreased HCC tumor formation in vivo . Mechanistically, LncRNA00364 specifically binds with STAT3, resulting in inhibition of STAT3 phosphorylation and therefore leads to upregulation of IFIT2. In a clinical setting, LncRNA00364 shows an independent prognostic indicator for overall survival and cumulative recurrence in HCC patients, and correlates with IFIT2. Therefore, our study provides new insights into a novel therapeutic avenue targeting the LncRNA00364 signaling axis in HCC., Competing Interests: CONFLICTS OF INTEREST The authors declare no conflicts of interest.
- Published
- 2017
- Full Text
- View/download PDF
23. Naive Treg-like CCR7(+) mononuclear cells indicate unfavorable prognosis in hepatocellular carcinoma.
- Author
-
Shi JY, Duan M, Sun QM, Yang L, Wang ZC, Mynbaev OA, He YF, Wang LY, Zhou J, Tang QQ, Cao Y, Fan J, Wang XY, and Gao Q
- Subjects
- Apoptosis, Blotting, Western, CD8-Positive T-Lymphocytes immunology, Carcinoma, Hepatocellular metabolism, Carcinoma, Hepatocellular pathology, Cell Proliferation, Chemokine CCL19 metabolism, Chemokine CCL21 metabolism, Cohort Studies, Flow Cytometry, Fluorescent Antibody Technique, Follow-Up Studies, Humans, Immunoenzyme Techniques, Liver Neoplasms metabolism, Liver Neoplasms pathology, Neoplasm Recurrence, Local metabolism, Neoplasm Recurrence, Local pathology, Neoplasm Staging, Prognosis, Transforming Growth Factor beta1 metabolism, Tumor Cells, Cultured, Tumor Microenvironment, Xenograft Model Antitumor Assays, Biomarkers, Tumor metabolism, Carcinoma, Hepatocellular immunology, Liver Neoplasms immunology, Neoplasm Recurrence, Local immunology, Receptors, CCR metabolism, Receptors, CCR7 metabolism, T-Lymphocytes, Regulatory immunology
- Abstract
Chemokine receptor-like 1 (CCRL1) has the potential in creating a low level of CCL19 and CCL21 to hinder CCR7(+) cell tracking to tumor tissue. Previously, we found a tumor suppressive role of CCRL1 by impairing CCR7-related chemotaxis of tumor cells in human hepatocellular carcinoma (HCC). Here, we reported a contribution of CCR7(+) mononuclear cells in the tumor microenvironment to the progression of disease. Immunohistochemistry was used to investigate the distribution and clinical significance of CCR7(+) cells in a cohort of 240 HCC patients. Furthermore, the phenotype, composition, and functional status of CCR7(+) cells were determined by flow cytometry, immunofluorescence, and in vitro co-culture assays. We found that CCR7(+) mononuclear cells were dispersed around tumor tissue and negatively related to tumoral expression of CCRL1 (P < 0.001, r = 0.391). High density of CCR7(+) mononuclear cells positively correlated with the absence of tumor capsule, vascular invasion, and poor differentiation (P < 0.05). Survival analyses revealed that increased number of CCR7(+) mononuclear cells was significantly associated with worse survival and increased recurrence. We found that CCR7(+) mononuclear cells featured a naive Treg-like phenotype (CD45RA(+)CD25(+)FOXP3(+)) and possessed tumor-promoting potential by producing TGF-β1. Moreover, CCR7(+) cells were also composed of several immunocytes, a third of which were CD8(+) T cells. CCR7(+) Treg-like cells facilitate tumor growth and indicate unfavorable prognosis in HCC patients, but fortunately, their tracking to tumor tissue is under the control of CCRL1.
- Published
- 2016
- Full Text
- View/download PDF
24. Macrophage-secreted IL-8 induces epithelial-mesenchymal transition in hepatocellular carcinoma cells by activating the JAK2/STAT3/Snail pathway.
- Author
-
Fu XT, Dai Z, Song K, Zhang ZJ, Zhou ZJ, Zhou SL, Zhao YM, Xiao YS, Sun QM, Ding ZB, and Fan J
- Subjects
- Carcinoma, Hepatocellular pathology, Epithelial-Mesenchymal Transition genetics, Gene Expression Regulation, Neoplastic, Hep G2 Cells, Humans, Interleukin-8 genetics, Janus Kinase 2 genetics, Liver Neoplasms pathology, Macrophages metabolism, STAT3 Transcription Factor genetics, Signal Transduction genetics, Snail Family Transcription Factors, Transcription Factors genetics, Carcinoma, Hepatocellular genetics, Interleukin-8 metabolism, Janus Kinase 2 biosynthesis, Liver Neoplasms genetics, STAT3 Transcription Factor biosynthesis, Transcription Factors biosynthesis
- Abstract
Macrophages are a major component of the leukocyte infiltrate of tumors and play a pivotal role in the progression of hepatocellular carcinoma (HCC). However, the molecular mechanisms by which macrophages promote HCC invasion are poorly understood. The present study was undertaken to investigate the relationship between macrophages and epithelial-mesenchymal transition (EMT) of HCC. Double-staining immunohistochemistry was used to observe the association between macrophages and EMT markers in clinical HCC samples and it showed that EMT primarily occurred at the edge of the tumor nest, in which infiltrating macrophages were always observed. This indicated that CD68 which is a marker of macrophages, was correlated with EMT marker levels. In addition, after being cultured with macrophages for 24 h, the ability of HCC cells to migrate and invade increased, Snail and N-Cadherin expression was upregulated, and E-Cadherin was downregulated. An antibody array assay was applied to analyze the supernatant of these cultures and it demonstrated IL-8 increased significantly in the macrophage co-culture system. Finally, the role of macrophage-derived IL-8 in the invasion of HCC cells was assayed, and downstream signaling pathways were also investigated. We found that IL-8: i) may induce EMT and promote HCC cell migration and invasion and ii) is associated with the JAK2/STAT3/Snail signaling pathway. Taking together, these findings revealed that macrophages that have infiltrated tumors may induce epithelial-mesenchymal transition of HCC cells via the IL-8 activated JAK2/STAT3/Snail pathway. Thus, this may offer a potential target for developing new HCC therapies.
- Published
- 2015
- Full Text
- View/download PDF
25. Genetic variations in plasma circulating DNA of HBV-related hepatocellular carcinoma patients predict recurrence after liver transplantation.
- Author
-
Hu J, Wang Z, Fan J, Dai Z, He YF, Qiu SJ, Huang XW, Sun J, Xiao YS, Song K, Shi YH, Sun QM, Yang XR, Shi GM, Yu L, Yang GH, Ding ZB, Gao Q, Tang ZY, and Zhou J
- Subjects
- Carcinoma, Hepatocellular genetics, Carcinoma, Hepatocellular pathology, Carcinoma, Hepatocellular virology, Female, Genotyping Techniques, Humans, Liver Neoplasms genetics, Liver Neoplasms pathology, Liver Neoplasms virology, Male, Middle Aged, Neoplasm Metastasis, Oligonucleotide Array Sequence Analysis, Prognosis, ROC Curve, Recurrence, Reproducibility of Results, Carcinoma, Hepatocellular diagnosis, DNA blood, DNA genetics, Genetic Variation genetics, Hepatitis B virus physiology, Liver Neoplasms diagnosis, Liver Transplantation
- Abstract
Background: Recurrence prediction of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) patients undergoing liver transplantation (LT) present a great challenge because of a lack of biomarkers. Genetic variations play an important role in tumor development and metastasis., Methods: Oligonucleotide microarrays were used to evaluate the genetic characteristics of tumor DNA in 30 HBV-related HCC patients who were underwent LT. Recurrence-related single-nucleotide polymorphism were selected, and their prognostic value was assessed and validated in two independent cohorts of HCC patients (N = 102 and N = 77), using pretransplant plasma circulating DNA. Prognostic significance was assessed by Kaplan-Meier survival estimates and log-rank tests. Multivariate analyses were performed to evaluate prognosis-related factors., Results: rs894151 and rs12438080 were significantly associated with recurrence (P = .003 and P = .004, respectively). Multivariate analyses demonstrated that the co-index of the 2 SNPs was an independent prognostic factor for recurrence (P = .040). Similar results were obtained in the third cohort (N = 77). Furthermore, for HCC patients (all the 3 cohorts) exceeding Milan criteria, the co-index was a prognostic factor for recurrence and survival (P<.001 and P = .002, respectively)., Conclusions: Our study demonstrated first that genetic variations of rs894151 and rs12438080 in pretransplant plasma circulating DNA are promising prognostic markers for tumor recurrence in HCC patients undergoing LT and identify a subgroup of patients who, despite having HCC exceeding Milan criteria, have a low risk of post-transplant recurrence.
- Published
- 2011
- Full Text
- View/download PDF
26. Capecitabine inhibits postoperative recurrence and metastasis after liver cancer resection in nude mice with relation to the expression of platelet-derived endothelial cell growth factor.
- Author
-
Zhou J, Tang ZY, Fan J, Wu ZQ, Ji Y, Xiao YS, Shi YH, Li XM, Sun QM, Liu YK, and Ye SL
- Subjects
- Animals, Capecitabine, Carcinoma, Hepatocellular metabolism, Carcinoma, Hepatocellular prevention & control, Fluorouracil analogs & derivatives, Humans, Liver Neoplasms, Experimental metabolism, Liver Neoplasms, Experimental prevention & control, Male, Mice, Mice, Inbred BALB C, Mice, Nude, Neoplasm Metastasis drug therapy, Postoperative Care, Transplantation, Heterologous, Antimetabolites, Antineoplastic therapeutic use, Carcinoma, Hepatocellular surgery, Deoxycytidine analogs & derivatives, Deoxycytidine therapeutic use, Liver Neoplasms, Experimental surgery, Neoplasm Recurrence, Local drug therapy, Thymidine Phosphorylase metabolism
- Abstract
Purpose: This study was to investigate the effect of capecitabine on recurrent tumor and metastasis after curative resection of liver cancer, xenograft of a highly metastatic human hepatocellular carcinoma (HCC) tumor (LCI-D20), with special reference to the expression of platelet-derived endothelial cell growth factor (PD-ECGF)., Experimental Design: LCI-D20 and LCI-D35 (a low metastatic human HCC model) liver tumors were orthotopically implanted in 96 nude mice and divided into a treatment group (24 LCI-D20 mice and 24 LCI-D35 mice) and a prevention group (48 LCI-D20 mice). In the prevention group, curative resection of liver tumors was done 10 days after the orthotopic implantation of LCI-D20 tumor. Arabic gum (control), 5-fluorouracil (5-FU), and capecitabine were administrated respectively to all of the 96 mice., Results: In the treatment group, tumor volume was 468 +/- 138, 442 +/- 81, and 240 +/- 119 mm3 (P<0.01) in the control, 5-FU, and capecitabine subgroups, respectively, in LCI-D20 mice, whereas it was 168 +/- 35, 164 +/- 23, and 144 +/- 21 mm3 (P>0.05), respectively, in LCI-D35 mice. In the prevention group, incidence of liver recurrence in the control, 5-FU, and capecitabine subgroups was 100, 100, and 50%; lung metastasis being 100, 100, and 17%; and life span being 31 +/- 5, 37 +/- 5, and 77 +/- 19 days, respectively. PD-ECGF was highly expressed in HCC and its metastatic tissues in LCI-D20 mice and hardly expressed in HCC tissues in LCI-D35 mice., Conclusions: Capecitabine inhibits tumor growth and metastatic recurrence after resection of HCC in highly metastatic nude mice model. The effect of capecitabine may be attributed to the high expression of PD-ECGF in tumors.
- Published
- 2003
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.