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| 1 | PGC-1α induces apoptosis in human epithelial ovarian cancer cells through a PPARy-dependent pathway显示文摘Peroxisome 激活 proliferator 的受体鲸鱼群妈(PPAR γ) coactivator-1 高山哈(PGC-1 α) coactivates 多重抄写因素并且调整几个代谢过程。Thecurrent 学习在人的上皮的卵巢的癌症房间在 apoptosis 的正式就职调查了 PGC-1 α的角色。在人的卵巢和人的卵巢的上皮的肿瘤之间的 PGC-1 α信使 rna 水平被量的 RT-PCR 检验。更少的 PGC-1 α表示与正常卵巢相比在恶意的肿瘤的表面上皮被发现。在人的上皮的卵巢的癌症房间线 Ho-8910 的 PGC-1 α的 Overexpression 通过 Bcl-2 和 Bax 表示的协调规定导致了房间 apoptosis。Microarray 分析证实 PGC-1 α戏剧性地在 Ho-8910 房间影响了 apoptosis 相关的基因。 Mitochondrial 功能的试金证明 apoptosis 的正式就职通过由细胞色素 c.Furthermore 的版本的终端阶段,导致的 apoptosis 部分是,然而并非完全,由 PPAR γa ntagonist ( GW9662 )堵住了的 PGC-1 α-,并且由 siRNA 的 PPAR γ 表示的抑制也在 Ho-8910 房间禁止了 PGC-1 α- inducedapoptosis 。这些数据建议 PGC-1 α通过 aPPAR γ - 依赖者小径施加了它的效果。我们的调查结果显示 PGC-1 α涉及 apoptotic signaltransduction 小径, PGC-1 α的 down 规定可以是在支持上皮的卵巢的癌症生长和前进的一个关键点。 | Yan Zhang Yi Ba Chang Liu Guoxun Sun Li Ding Songyuan Gao Jihui Hao Zhentao Yu Junfeng Zhang Ke Zen Zhongsheng Tong Yang Xiang Chen-Yu Zhang | 2007 | Cell Research2007，17，4： | 14 |
| 2 | PD-L1 is a direct target of cancer-FOXP3 in pancreatic ductal adenocarcinoma(PDAC),and combined immunotherapy with antibodies against PD-L1 and CCL5 is effective in the treatment of PDAC显示文摘High expression of PD-L1 marks the poor prognosis of pancreatic ductal adenocarcinomas(PDAC).However,the regulatory mechanism of PD-L1 remains elusive.We recently reported that cancer Forkhead box protein 3(Cancer-FOXP3 or C-FOXP3)promoted immune evasion of PDAC by recruiting Treg cells into PDAC via upregulation of CCL5.In this study,we confirmed that PD-L1 was overexpressed in PDAC samples from two independent cohorts of patients with radical resection.Moreover,C-FOXP3 was colocalized and correlated with the expression of PD-L1 in tumor cells at the mRNA and protein levels,and this finding was confirmed by the The Cancer Genome Atlas(TCGA)database.Chromatin immunoprecipitation(ChIP)revealed that C-FOXP3 directly bound to the promoter region of PD-L1 in pancreatic cancer cells.Furthermore,overexpression of C-FOXP3 activated the luciferase reporter gene under the control of the PD-L1 promoter.However,mutation of the binding motif-a completely reversed the luciferase activity.In addition,C-FOXP3-induced upregulation of PD-L1 effectively inhibited the activity of CD8+T cells.Based on our recent finding that the CCL-5 antibody achieved a better response to PDAC models with high C-FOXP3 levels,we further demonstrated that the PD-L1 antibody strengthened the antitumor effect of CCL-5 blockade in xenograft and orthotopic mouse models with high C-FOXP3 levels.In conclusion,C-FOXP3 directly activates PD-L1 and represents a core transcription factor that mediates the immune escape of PDAC.Combined blockade of PD-L1 and CCL-5 may provide an effective therapy for patients with PDAC that have high C-FOXP3 levels. | Xiuchao Wang Xin Li Xunbin Wei Haiping Jiang Chungen Lan Shengyu Yang Han Wang Yanhui Yang Caijuan Tian Zanmei Xu Jiangyan Zhang Jihui Hao He Ren | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 11 |
| 3 | A new combined criterion to better predict malignant lesions in patients with pancreatic cystic neoplasms显示文摘Objective:Cystic lesions of the pancreas have been increasingly recognized.Some lesions exhibit benign behavior,while others have unequivocal malignant potential.Thus,accurate identification of malignancy in patients diagnosed with pancreatic cystic neoplasms(PCNs)remains a major challenge.The aim of this study was to define a combined criterion to better predict malignant lesions in patients with PCNs.Methods:We retrospectively analyzed 165 patients who underwent resection of PCNs from October 2011 to May 2017.The relationship among malignancy and serum carbohydrate antigen 19-9(CA19-9),preoperative neutrophil-to-lymphocyte ratio(NLR),and the presence of enhanced solid component on imaging was analyzed.Results:NLR before surgery in patients with malignant PCNs(2.81±2.14)was significantly higher than that in patients diagnosed with pancreatic neuroendocrine tumor(1.90±0.69,P=0.013)or healthy volunteers(1.40±0.48;P<0.001).Serum CA19-9≥39U/m L,NLR>1.976 and presence of enhanced solid component were independent predictors of PCN malignancy.A combined criterion meeting any two or more of the three elements including CA19-9≥39 U/m L,NLR>1.976,and presence of enhanced solid component on computed tomography imaging is an indicator with a high positive predictive value of 80.5%and a high negative predictive value of 87.9%,and thus,represents a highly accurate test(86.1%).Conclusions:The new combined criterion is an effective predictor of tumor malignancy in patients with PCNs. | Chungen Lan Xin Li Xiuchao Wang Jihui Hao He Ren | 2018 | Cancer Biology & Medicine2018，15，1： | 6 |
| 4 | Prognostic significance of combining high mobility group Box-1 and OV-6 expression in hepatocellular carcinoma显示文摘The inflammatory environment and existence of cancer stem cells are critical for progression and intrahepatic recurrence of hepatocellular carcinoma(HCC) after curative resections. Here, we investigated the prognostic significance of combining high mobility group box 1(HMGB1) expression and hepatic progenitor marker OV6 in hepatocellular carcinoma. Expression of HMGB1 and OV6 was evaluated using immunohistochemistry profiling in tissue microarrays containing samples from 208 HCC patients. Invasive clinical or pathological factors were found in patients with high expression of HMGB1 or OV6. Higher HMGB1 was associated with poorer clinical outcomes, and independently related to elevated 5-year recurrence incidence(85.5% vs. 62.4%, P<0.001). We also found that more OV6 positive staining was correlated with poor prognosis of HCC patients(P<0.001). Notably, expression of HMGB1 was positively correlated with OV6 in density(R2=0.032, P<0.001) and reversely related to HCC outcomes. Abnormal expression of HMGB1 in combination with positive staining of OV6 displayed poorer prognostic performance than single biomarker alone(area under curve(AUC) survival=0.696). Therefore, HMGB1 and OV6 positive staining are promising prognostic parameters for HCC, and we propose that HMGB1 and OV6 may cooperate with each other and predict poor prognosis of HCC. | Jihui Zhu Han Yu Shuzhen Chen Pinghua Yang Zihui Dong Yan Ling Hao Tang Shilei Bai Wen Yang Liang Tang Feng Shen Hongyang Wang Wen Wen | 2018 | Science China(Life Sciences)2018，61，8： | 4 |
| 5 | Quercetin promotes human epidermal stem cell proliferation through the estrogen receptor/β-catenin/c-Myc/cyclin A2 signaling pathway显示文摘Skin epidermal stem cells(EpSCs)play an important role in wound healing.Quercetin is a phytoestrogen reported to accelerate skin wound healing,but its effect on EpSCs is unknown.In this study,we investigated the effect of quercetin on human EpSC proliferation and explored the underlying mechanisms.We found that quercetin at 0.1~1μM significantly promoted EpSC proliferation and increased the number of cells in S phase.The pro-proliferative effect of quercetin on EpSCs was confirmed in cultured human skin tissue.Mechanistic studies showed that quercetin significantly upregulated the expressions ofβ-catenin,c-Myc,and cyclins A2 and E1.Inhibitor forβ-catenin or c-Myc significantly inhibited quercetin-induced EpSC proliferation.Theβ-catenin inhibitor XAV-939 suppressed quercetin-induced expressions ofβ-catenin,c-Myc,and cyclins A2 and E1.The c-Myc inhibitor 10058-F4 inhibited the upregulation of c-Myc and cyclin A2 by quercetin.Pretreatment of EpSCs with estrogen receptor(ER)antagonist ICI182780,but not the G protein-coupled ER1 antagonist G15,reversed quercetin-induced cell proliferation and upregulation ofβ-catenin,c-Myc,and cyclin A2.Collectively,these results indicate that quercetin promotes EpSC proliferation through ER-mediated activation ofβ-catenin/c-Myc/cyclinA2 signaling pathway and ER-independent upregulation of cyclin E1 and that quercetin may accelerate skin wound healing through promoting EpSC proliferation.As EpSCs are used not only in clinic to treat skin wounds but also as seed cells in skin tissue engineering,quercetin is a useful reagent to expand EpSCs for basic research,skin wound treatment,and skin tissue engineering. | Zhaodong Wang Guangliang Zhang Yingying Le Jihui Ju Ping Zhang Dapeng Wan Qiang Zhao Guangzhe Jin Hao Su Jinwei Liu Jiaxuan Feng Yi Fu Ruixing Hou | 2020 | Acta Biochimica et Biophysica Sinica2020，52，10： | 3 |
| 6 | Hypoxic microenvironment induced spatial transcriptome changes in pancreatic cancer显示文摘Objective: Hypoxia is a significant feature of solid tumors, including pancreatic ductal adenocarcinoma(PDAC). It is associated with tumor invasion, metastasis, and drug resistance. However, the spatial distribution of hypoxia-related heterogeneity in PDAC remains unclear.Methods: Spatial transcriptomics(STs), a new technique, was used to investigate the ST features of engrafted human PDAC in the ischemic hind limbs of nude mice. Transcriptomes from ST spots in the hypoxic tumor and the control were clustered using differentially-expressed genes. These data were compared to determine the spatial organization of hypoxia-induced heterogeneity in PDAC. Clinical relevance was validated using the Tumor Cancer Genome Atlas and KM-plotter databases. The CMAP website was used to identify molecules that may serve as therapeutic targets for PDAC.Results: ST showed that the tumor cell subgroups decreased to 7 subgroups in the hypoxia group, compared to 9 subgroups in the control group. Different subgroups showed positional characteristics and different gene signatures. Subgroup 6 located at the invasive front showed a higher proliferative ability under hypoxia. Subgroup 6 had active functions including cell proliferation, invasion, and response to stress. Expressions of hypoxia-related genes, LDHA, TPI1, and ENO1, induced changes. CMAP analysis indicated that ADZ-6482, a PI3 K inhibitor, was targeted by the invasive subgroup in hypoxic tumors.Conclusions: This study is the first to describe hypoxic microenvironment-induced spatial transcriptome changes in PDAC, and to identify potential treatment targets for PDAC. These data will provide the basis for further investigations of the prognoses and treatments of hypoxic tumors. | Huizhi Sun Danfang Zhang Chongbiao Huang Yuhong Guo Zhao Yang Nan Yao Xueyi Dong Runfen Cheng Nan Zhao Jie Meng Baocun Sun Jihui Hao | 2021 | Cancer Biology & Medicine2021，18，2： | 2 |
| 7 | Preoperative ultrasound combined with routine blood tests in predicting the malignant risk of pancreatic cystic neoplasms显示文摘Objective:Accurate preoperative identification of benign or malignant pancreatic cystic neoplasms(PCN)may help clinicians make better intervention choices and will be essential for individualized treatment.Methods:Preoperative ultrasound and laboratory examination findings,and demographic characteristics were collected from patients.Multiple logistic regression was used to identify independent risk factors associated with malignant PCN,which were then included in the nomogram and validated with an external cohort.The Net Reclassification Index(NRI)and Integrated Discrimination Improvement(IDI)were calculated to evaluate the improvement in the predictive power of the new model with respect to that of a combined imaging and tumor marker prediction model.Results:Malignant PCN were found in 83(40.7%)and 33(38.7%)of the model and validation cohorts,respectively.Multivariate analysis identified age,tumor location,imaging of tumor boundary,blood type,mean hemoglobin concentration,neutrophil-tolymphocyte ratio,carbohydrate antigen 19-9,and carcinoembryonic antigen as independent risk factors for malignant PCN.The calibration curve indicated that the predictions based on the nomogram were in excellent agreement with the actual observations.A nomogram score cutoff of 192.5 classified patients as having low vs.high risk of malignant PCN.The model achieved good C-statistics of 0.929(95%CI 0.890–0.968,P<0.05)and 0.951(95%CI 0.903–0.998,P<0.05)in predicting malignancy in the development and validation cohorts,respectively.NRI=0.268;IDI=0.271(P<0.001 for improvement).The DCA curve indicated that our model yielded greater clinical benefits than the comparator model.Conclusions:The nomogram showed excellent performance in predicting malignant PCN and may help surgeons select patients for detailed examination and surgery.The nomogram is freely available at http://gffzz301f03ad8b874f7esknkfo66b5q5b6qkn.ffgz.tsg.suse.edu.cn/DynNomapp/. | Xiuchao Wang Junjin Wang Xi Wei Lihui Zhao Bo Ni Zekun Li Chuntao Gao Song Gao Tiansuo Zhao Jian Wang Weidong Ma Xiao Hu Jihui Hao | 2022 | Cancer Biology & Medicine2022，19，10： | 1 |
| 8 | Hypoxia inducible factor (HIF)-1α directly activates leptin receptor (Ob-R) in pancreatic cancer cells显示文摘 | He Ren Lingling Jia Tiansuo Zhao Huan Zhang Jing Chen Shaoguang Yang Jingcheng Liu Ming Yu Jihui Hao | 2014 | Cancer Letters2014，，1： | 1 |
| 9 | Leptin upregulates telomerase activity and transcription of human telomerase reverse transcriptase in MCF-7 breast cancer cells显示文摘 | He Ren Tiansuo Zhao Xiuchao Wang Chuntao Gao Jian Wang Ming Yu Jihui Hao | 2010 | Biochemical and Biophysical Research Communications2010，，1： | 1 |
| 10 | Guidelines for the diagnosis and treatment of acute pancreatitis in China (2021)显示文摘Acute pancreatitis(AP)is a common acute abdominal condition of the digestive system.In recent years,treatment concepts,methods,and strategies for the diagnosis of AP have advanced,and this has played an important role in promoting the standardization of AP diagnosis and treatment and improving the treatment quality of AP patients.On the basis of previous guidelines and expert consensus,this guideline adopts an evidence-based,problem-based expression;synthesizes important clinical research data at home and abroad in the most recent 5 years;and forms 29 recommendations through multidisciplinary expert discussion,including diagnosis,treatment,and follow-up.It is expected to provide evidence support for the treatment of AP in the clinical setting in China. | Fei Li Shouwang Cai Feng Cao Rufu Chen Deliang Fu Chunlin Ge Chunyi Hao Jihui Hao Heguang Huang Zhixiang Jian Gang Jin Ang Li Haimin Li Shengping Li Weiqin Li Yixiong Li Tingbo Liang Xubao Liu Wenhui Lou Yi Miao Yiping Mou Chenghong Peng Renyi Qin Chenghao Shao Bei Sun Guang Tan Xiaodong Tian Huaizhi Wang Lei Wang Wei Wang Weilin Wang Junmin Wei Heshui Wu Wenming Wu Zheng Wu Changqing Yan Yinmo Yang Xiaoyu Yin Xianjun Yu Chunhui Yuan Taiping Zhang Yupei Zhao on behalf of the Chinese Pancreatic Surgery Association | 2021 | Journal of Pancreatology2021，4，2： | 1 |
| 11 | BICC1 drives pancreatic cancer progression by inducing VEGF-independent angiogenesis显示文摘VEGF inhibitors are one of the most successful antiangiogenic drugs in the treatment of many solid tumors.Nevertheless,pancreatic adenocarcinoma(PAAD)cells can reinstate tumor angiogenesis via activation of VEGF-independent pathways,thereby conferring resistance to VEGF inhibitors.Bioinformatic analysis showed that BICC1 was one of the top genes involved in the specific angiogenesis process of PAAD.The analysis of our own cohort confirmed that BICC1 was overexpressed in human PAAD tissues and was correlated to increased microvessel density and tumor growth,and worse prognosis.In cells and mice with xenograft tumors,BICC1 facilitated angiogenesis in pancreatic cancer in a VEGF-independent manner.Mechanistically,as an RNA binding protein,BICC1 bounds to the 3’UTR of Lipocalin-2(LCN2)mRNA and post-transcriptionally up-regulated LCN2 expression in PAAD cells.When its level is elevated,LCN2 binds to its receptor 24p3R,which directly phosphorylates JAK2 and activates JAK2/STAT3 signal,leading to increased production of an angiogenic factor CXCL1.Blocking of the BICC1/LCN2 signalling reduced the microvessel density and tumor volume of PAAD cell grafts in mice,and increased the tumor suppressive effect of gemcitabine.In conclusion,BICC1 plays a pivotal role in the process of VEGF-independent angiogenesis in pancreatic cancer,leading to resistance to VEGF inhibitors.BICC1/LCN2 signaling may serve as a promising anti-angiogenic therapeutic target for pancreatic cancer patients. | Chongbiao Huang Hui Li Yang Xu Chao Xu Huizhi Sun Zengxun Li Yi Ge Hongwei Wang Tiansuo Zhao Song Gao Xiuchao Wang Shengyu Yang Peiqing Sun Zhe Liu Jing Liu Antao Chang Jihui Hao | 2023 | Signal Transduction and Targeted Therapy2023，8，8： | 1 |
| 12 | The Hippo/YAP signaling pathway:the driver of cancer metastasis显示文摘Despite major improvements in cancer survival,metastasis is responsible for almost 90%of cancer-related mortality^(1,2).Nonetheless,the pathogenesis and molecular mechanisms of cancer metastasis remain poorly understood. | Tianxing Zhou Xueyang Li Jing Liu Jihui Hao | 2023 | Cancer Biology & Medicine2023，20，7： | 0 |
| 13 | High frequency of alternative splicing variants of the oncogene Focal Adhesion Kinase in neuroendocrine tumors of the pancreas and breast显示文摘The characteristic genetic abnormality of neuroendocrine neoplasms(NENs),a heterogeneous group of tumors found in various organs,remains to be identified.Here,based on the analysis of the splicing variants of an oncogene Focal Adhesion Kinase(FAK)in The Cancer Genome Atlas datasets that contain 9193 patients of 33 cancer subtypes,we found that Box 6/Box 7-containing FAK variants(FAK^(6/7))were observed in 7(87.5%)of 8 pancreatic neuroendocrine carcinomas and 20(11.76%)of 170 pancreatic ductal adenocarcinomas(PDACs).We tested FAK variants in 157 tumor samples collected from Chinese patients with pancreatic tumors,and found that FAK^(6/7)was positive in 34(75.6%)of 45 pancreatic NENs,19(47.5%)of 40 pancreatic solid pseudopapillary neoplasms,and 2(2.9%)of 69 PDACs.We further tested FAK splicing variants in breast neuroendocrine carcinoma(BrNECs),and found that FAK^(6/7)was positive in 14(93.3%)of 15 BrNECs but 0 in 23 non-NEC breast cancers.We explored the underlying mechanisms and found that a splicing factor serine/arginine repetitive matrix protein 4(SRRM4)was overexpressed in FAK^(6/7)-positive pancreatic tumors and breast tumors,which promoted the formation of FAK^(6/7)in cells.These results suggested that FAK^(6/7)could be a biomarker of NENs and represent a potential therapeutic target for these orphan diseases. | Dawei Xie Zheng Wang Beibei Sun Liwei Qu Musheng Zeng Lin Feng Mingzhou Guo Guizhen Wang Jihui Hao Guangbiao Zhou | 2023 | Frontiers of Medicine2023，17，5： | 0 |
| 14 | ENO1 expression and Erk phosphorylation in PDAC and their effects on tumor cell apoptosis in a hypoxic microenvironment显示文摘Objective: Hypoxia is an important feature of pancreatic ductal adenocarcinoma(PDAC). Previously, we found that hypoxia promotes ENO1 expression and PDAC invasion. However, the underlying molecular mechanism was remains unclear.Methods: The relationship between ENO1 expression and clinicopathological characteristics was analyzed in 84 patients with PADC. The effects of CoCl2-induced hypoxia and ENO1 downregulation on the apoptosis, invasion, and proliferation of PDAC cells were evaluated in vitro and in vivo. Hypoxia-and ENO1-induced gene expression was analyzed by transcriptomic sequencing.Results: The prognosis of PDAC with high ENO1 expression was poor(P < 0.05). High ENO1 expression was closely associated with histological differentiation and tumor invasion in 84 PDAC cases(P < 0.05). Hypoxia increased ENO1 expression in PDAC and promoted its migration and invasion. Apoptotic cells and the apoptosis marker caspase-3 in the CoCl_(2)-treated ENO1-sh group were significantly elevated(P < 0.05). Transcriptomic sequencing indicated that CoCl_(2)-induced PDAC cells initiated MAPK signaling. Under hypoxic conditions, PDAC cells upregulated ENO1 expression, thereby accelerating ERK phosphorylation and inhibiting apoptosis(P < 0.05). Consistent results were also observed in a PDAC-bearing mouse hindlimb ischemia model.Conclusions: Hypoxia-induced ENO1 expression promotes ERK phosphorylation and inhibits apoptosis, thus leading to PDAC survival and invasion. These results suggest that ENO1 is a potential therapeutic target for PDAC. | Huizhi Sun Jing Mo Runfen Cheng Fan Li Yue Li Yuhong Guo Yanlei Li Yanhui Zhang Xiaoyu Bai Yalei Wang Xueyi Dong Danfang Zhang Jihui Hao | 2022 | Cancer Biology & Medicine2022，19，11： | 0 |
| 15 | Nuclear PLD1 combined with NPM1 induces gemcitabine resistance through tumorigenic IL7R in pancreatic adenocarcinoma显示文摘Objective:Pancreatic ductal adenocarcinoma(PDAC)is a highly malignant gastrointestinal cancer with a 5-year survival rate of only 9%.Of PDAC patients,15%-20%are eligible for radical surgery.Gemcitabine is an important chemotherapeutic agent for patients with PDAC;however,the efficacy of gemcitabine is limited due to resistance.Therefore,reducing gemcitabine resistance is essential for improving survival of patients with PDAC.Identifying the key target that determines gemcitabine resistance in PDAC and reversing gemcitabine resistance using target inhibitors in combination with gemcitabine are crucial steps in the quest to improve survival prognosis in patients with PDAC.Methods:We constructed a human genome-wide CRISPRa/dCas 9 overexpression library in PDAC cell lines to screen key targets of drug resistance based on sgRNA abundance and enrichment.Then,co-IP,ChIP,ChIP-seq,transcriptome sequencing,and qPCR were used to determine the specific mechanism by which phospholipase D1(PLD1)confers resistance to gemcitabine.Results:PLD1 combines with nucleophosmin 1(NPM1)and triggers NPM1 nuclear translocation,where NPM1 acts as a transcription factor to upregulate interleukin 7 receptor(IL7R)expression.Upon interleukin 7(IL-7)binding,IL7R activates the JAK1/STAT5 signaling pathway to increase the expression of the anti-apoptotic protein,BCL-2,and induce gemcitabine resistance.The PLD1 inhibitor,Vu0155069,targets PLD1 to induce apoptosis in gemcitabine-resistant PDAC cells.Conclusions:PLD1 is an enzyme that has a critical role in PDAC-associated gemcitabine resistance through a non-enzymatic interaction with NPM1,further promoting the downstream JAK1/STAT5/Bcl-2 pathway.Inhibiting any of the participants of this pathway can increase gemcitabine sensitivity. | Danqi Fu Jingrui Yan Zhaoyu Zhang Yang Liu Xiaoqing Ma Jinsheng Ding Shengyu Yang Ran Zhao Antao Chang Chuntao Gao Jing Liu Tiansuo Zhao Xiuchao Wang Chongbiao Huang Song Gao Ying Ma Bo Tang Yukuan Feng Hongwei Wang Jihui Hao | 2023 | Cancer Biology & Medicine2023，20，8： | 0 |
| 16 | The role of biomarker in pancreatic neuroendocrine tumor:a narrative review显示文摘Pancreatic neuroendocrine tumors(pNET)are heterogenous tumors originated from the diffuse neuroendocrine cells of pancreas,which show the function of synthesis,storage and secretion of peptide hormones and biomimetic amines.Biomarkers play a crucial role in the diagnosing,evaluating prognosis and predicting treatment response for pNET patients.Traditional NET markers such as chromogranin A and Neuron Specific Enolase,as a diagnostic biomarker,have relatively low sensitivity and specificity in pNET patients.The emergence of new types of biomarkers provides more reliable indicators for diagnosis and prognosis evaluation.Among them,NETest score is a promising biomarker with the highest diagnostic sensitivity(80%)and specificity(94%).In addition,this molecule can be also used as a prognostic biomarker,which can predict disease progression and shorter overall survival.Biomarkers related to therapeutic targets,such as vascular endothelial growth factor,vascular endothelial growth factor receptor,and key molecules of mTOR signaling pathway,have capability to predict response of treatment.With the development of nextgeneration sequencing,chip array,and digital droplet PCR,novel biomarkers such as circulating tumor cells,tumor-derived exosomes,and circulating tumor DNA and mRNA are expected to provide more accurate diagnosis,prognostic information,and prospective therapeutic targets.In this paper,biomarkers of pancreatic neuroendocrine tumor and their role in diagnosis,prognosis,diagnosis,treatment and monitoring are systematically introduced.Our conclusions can provide new basis for clinicians in the diagnosis and treatment process. | Xiaofan Guo Song Gao Zekun Li Jihui Hao | 2021 | Journal of Pancreatology2021，4，3： | 0 |
| 17 | Consensus of clinical diagnosis and treatment for non-functional pancreatic neuroendocrine neoplasms with diameter<2 cm显示文摘In clinical practice,pancreatic neuroendocrine neoplasms(pNENs)with a diameter smaller than 2 cm are commonly referred to as small pNENs.Due to their generally favorable biological characteristics,the diagnosis and treatment of small pNENs differ from other pNENs and are somewhat controversial.In response to this,the Chinese Pancreatic Surgery Association,Chinese Society of Surgery,Chinese Medical Association have developed a consensus on the diagnosis and treatment of small pNENs,which is based on evidence-based medicine and expert opinions.This consensus covers various topics,including concepts,disease assessment,treatment selection,follow-up,and other relevant aspects. | Wu Wenming Cai Shouwang Chen Rufu Fu Deliang Ge Chunlin Hao Chunyi Hao Jihui Huang Heguang Jian Zhixiang Jin Gang Li Fei Li Haimin Li Shengping Li Weiqin LiYixiong Liang Tingbo Liu Xubao Lou Wenhui Miao Yi Mou Yiping Peng Chenghong Qin Renyi Shao Chenghao Sun Bei Tan Guang Wang Huaizhi Wang Lei Wang Wei Wang Weilin Wei Junmin Wu Heshui Wu Zheng Yan Changqing Yang Yinmo Yin Xiaoyu Yu Xianjun Yuan Chunhui Zhao Yupei | 2023 | Journal of Pancreatology2023，6，3： | 0 |
| 18 | Proteasome Inhibitors Sensitize Hepatocellular Carcinoma Cells to TRAIL显示文摘OBJECTIVE To investigate the effect of proteasome inhibition on the sensitivity of carcinoma cells to TRAIL-inducing apoptosis, and to study the mechanism of the response. METHODS Human hepatocellular carcinoma cells, pretreated with the proteasome inhibitor, MG132, were cotreated with TRAIL. Western blot assays, immunoprecipitation and RT-PCR were performed to test the expression of the Bcl-2 family proteins and Bax mRNA. RESULTS We found that (i) proteasome inhibition sensitized the human hepatocellular carcinoma cells to TRAIL; and (ii) resulted in Bax accumulation before release of cytochrome C and induction of apoptosis. These results were associated with the ability of proteasome inhibitors to overcome Bcl-2-mediated antiapoptotic function; (iii) Bax is regulated by an ubiquitin/proteasome-dependent degradation pathway. CONCLUSION Proteasome inhibition sensitized hepatocellular carcinoma cells to TRAIL by the inhibition of the ubiquitin/proteasome-mediated Bax degradation pathway. | Qingfeng Sheng Yurong Shi Qiang Li Jihui Hao Ruifang Niu Xiyin Wei Yi Yang Lin Zhang | 2006 | Chinese Journal of Clinical Oncology2006，3，6： | 0 |
| 19 | Study on T700/Cyanate/PS/Epoxy Composites with ex-situ Toughening Technique显示文摘Composites were prepared with polysulfone through ex-situ toughening technique. The dynamic parameters of cyanate/epoxy resin were studied by differential scanning calorimetric(DSC) analysis and dynamic mechanical analysis(DMA). Microstructual toughening mechanism was studied through scanning electron microscopy(SEM). The particle microstructure in interlaminar region of composites toughened through ex-situ toughening technique revealed that a reaction induced phase decomposition and phase inversion happened in the interlaminar region. The thermosetting particles were surrounded by the PS phase, which could signifi cantly improve the delamination resistance of composites. The compression after impact(CAI) can be signifi cantly improved from 180 MPa to 260 MPa by using ex-situ toughening while the mechanical properties are not affected. | 郑亚萍 WANG Hao ZHANG Jiaoxia XU Yahong DAI Feng WANG Jihui | 2014 | Journal of Wuhan University of Technology(Materials Science)2014，29，4： | 0 |
| 20 | Occurrence and influential factors of depression in patients with Alzheimer disease显示文摘BACKGROUND: The differential diagnosis between depressive pseudodementia and Alzheimer disease (AD) is a clinical problem, and it is more difficult to diagnose depression in AD. OBJECTIVE: To analyze the incidence and characters of depression in AD patients, and investigate the correlative factors. DESIGN: A randomized controlled study. SETTING: Beijing Geriatrics Hospital. PARTICIPANTS: From October 2005 to July 2006, 34 patients with probable AD were selected from the Department of Dementia, Beijing Geriatrics Hospital according to National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer Disease and Related Disorders Association (NINCDS-ADRDA) criteria for AD. There were 16 males and 18 females, aged 63-85 years. Meanwhile, 30 patients with other chronic neurological disorders (CND) were selected from our hospital as the CND control group, there were 16 males and 14 females, aged 55-85 years, including 18 cases of cerebrovascular sequela, 9 of Parkinson disease and 3 of migraineurs. Another 30 patients with chronic physical diseases (CPD) were enrolled as the CPD control group, there were 15 males and 15 females, aged 57-83 years, including 15 cases of chronic bronchitis, 8 of hypertension and 7 of diabetes mellitus. Besides, 30 physical examinees were enrolled as the healthy control group, including 15 males and 15 females, aged 55-80 years. All the subjects were informed and agreed with the detection. METHODS: ① All the subjects underwent the Hamilton rating scale for depression (HAMD) (24 items) assessment, and the total score < 8 points was regarded as no depression, 8-20 as mild depression, 20-35 as moderate depression, ≥ 35 as severe depression. ② All the AD patients were assessed with Cornell scale for depression in dementia (CSDD) (19 items), and the total score < 8 points was regarded as no depression, and ≥ 8 as depression. CSDD consisted of five subscales, including mood-related signs, behavioral disturbance, cyclic functions, ideational disturbance and physical signs, which were scored as 0-2 points respectively, and the abnormal rate of each factor was observed, the abnormal rate was the percentage of number of patients suffering from the symptoms in the subscales to the total number of patients. ③ The cognitive function of the AD patients was assessed with Mini-mental status examination (MMSE) (the total score ranged 0-30 points; ≤17 in illiterate, ≤ 20 in primary school and ≤ 24 in middle school and higher was regarded as cognitive deficit) and the daily living ability of the AD patients was assessed with ADL. MAIN OUTCOME MEASURES: ① HAMD scores in all the groups; ② CDSS scores and abnormal rate of factors in AD patients; ③ MMSE score and activity of daily life (ADL) score in AD patients; ④ Correlation between depression and correlative factors in AD patients. RESULTS: All the 124 subjects were involved in the analysis of results. ① The HAMD average score of the AD group was significantly higher than those of the CND, CPD and healthy control groups [(12.7±3.2), (5.5±2.5), (3.4±1.3), (2.6±1.7) points, P < 0.01]. ② In the AD group, the CDSS average score was (5.8±4.3) points, 41.2% (14/34) met the criteria for depression. The abnormal rates in order were 44% (15/34) for mood-related signs, 32% (11/34) for behavioral disturbance, 24% (8/34) for cyclic function, 12% (4/34) for ideational disturbance and 12% (4/34) for physical signs. ③ The factors of age, course, MMSE score and ADL score were finally excluded after a multiple regression (P > 0.05). There was a negative correlation between CSDD score and onset age (P < 0.05), sex was also obviously correlated with CSDD score (P < 0.05). CONCLUSION: The incidence of depression in AD is much higher with various manifestations. Female patients are the susc and earlier onset age is the risk factor for the presence of depression in AD. | Jihui Lü Junpeng Xing Weishan Wang Zhihui Hao Li Zhao Li Zhang Wenjie Li Yu Xue | 2006 | Neural Regeneration Research2006，1，8： | 0 |
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