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| 1 | 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://gffzz301f03ad8b874f7es5n6npwvc955p6qw6.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 |
| 2 | 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 |
| 3 | 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 |
| 4 | 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 |
| 5 | 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 |
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