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您的检索式：作者名="Eric Y.Cheng"
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| 1 | Incidence and risk of herpes zoster in patients with ulcerative colitis and Crohn’s disease in the USA显示文摘Background:Patients with inflammatory bowel disease(IBD)are at increased risk of herpes zoster(HZ).We evaluated the incidence of HZ in ulcerative colitis(UC)and Crohn’s disease(CD)patients and compared this with HZ incidence in a non-IBD population.Methods:We conducted a retrospective cohort study(GSK study identifier:VEO-000043)of adults aged18 years with UC and CD and without IBD who were identified from claims recorded in a US healthcare database between October 2015 and February 2020.Crude HZ incidence rates/1,000 person-years(PY)were calculated,and comparisons of HZ incidence rates between UC or CD and non-IBD cohorts were made using adjusted generalized linear models.Results:The study population comprised a total of 29,928 UC,25,959 CD,and 11,839,329 non-IBD patients.Crude overall HZ incidence rates were 13.64/1,000 PY(UC),15.94/1,000 PY(CD),and 7.95/1,000 PY(non-IBD).UC and CD patients had increased HZ incidence rates,with adjusted incidence rate ratios of 1.35(95%confidence interval[CI],1.26–1.44)and 1.66(95%CI,1.56–1.77),respectively,compared with non-IBD patients.Stratified analysis indicated increased relative rates of HZ in progressively younger age strata in the UC and CD patients compared with non-IBD patients.HZ incidence rates were higher in UC and CD patients who had previously received thiopurines or methotrexate,TNF-inhibitors,or corticosteroids than in UC and CD patients who did not take those medicines.Conclusion:UC and CD patients had increased HZ incidence rates compared with patients without IBD,demonstrating the importance of HZ prevention in IBD patients. | David Singer Philippe Thompson-Leduc Deepshekhar Gupta Wendy Y.Cheng Sara Poston Siyu Ma John E.Pawlowski Mei Sheng Duh Eric D.Morris Francesca Devine Francis A.Farraye | 2023 | Gastroenterology Report2023，11，1： | 0 |
| 2 | KDELR2 promotes breast cancer proliferation via HDAC3-mediated cell cycle progression显示文摘Background:Histone deacetylases(HDACs)engage in the regulation of various cellular processes by controlling global gene expression.The dysregulation of HDACs leads to carcinogenesis,making HDACs ideal targets for cancer therapy.However,the use of HDAC inhibitors(HDACi)as single agents has been shown to have limited success in treating solid tumors in clinical studies.This study aimed to identify a novel downstream effector of HDACs to provide a potential target for combination therapy.Methods:Transcriptome sequencing and bioinformatics analysis were performed to screen for genes responsive toHDACi in breast cancer cells.The effects of HDACi on cell viability were detected using the MTT assay.The mRNA and protein levels of genes were determined by quantitative reverse transcription-PCR(qRT-PCR)andWestern blotting.Cell cycle distribution and apoptosis were analyzed by flow cytometry.The binding of CREB1(cAMP-response element binding protein 1)to the promoter of the KDELR(The KDEL(Lys-Asp-Glu-Leu)receptor)gene was validated by the ChIP(chromatin immunoprecipitation assay).The association between KDELR2 and protein of centriole 5(POC5)was detected by immunoprecipitation.A breast cancer-bearing mouse model was employed to analyze the effect of the HDAC3-KDELR2 axis on tumor growth.Results:KDELR2 was identified as a novel target of HDAC3,and its aberrant expression indicated the poor prognosis of breast cancer patients.We found a strong correlation between the protein expression patterns of HADC3 and KDELR2 in tumor tissues from breast cancer patients.The results of the ChIP assay and qRT-PCR analysis validated that HDAC3 transactivated KDELR2 via CREB1.The HDAC3-KDELR2 axis accelerated the cell cycle progression of cancer cells by protecting the centrosomal protein POC5 from proteasomal degradation.Moreover,the HDAC3-KDELR2 axis promoted breast cancer cell proliferation and tumorigenesis in vitro and in vivo.Conclusion:Our results uncovered a previously unappreciated function of KDELR2 in tumorigenesis,linking a critical Golgi-the endoplasmic reticulum traffic transport protein to HDAC-controlled cell cycle progression on the path of cancer development and thus revealing a potential therapeutical target for breast cancer. | Haoran Wei Wenhao Ma Xiaofei Lu Haiying Liu Kashuai Lin Yinghui Wang Zijian Ye Linchong Sun Zhitong Huang Tingting Pan Zilong Zhou Eric Y.Cheng Huafeng Zhang Ping Gao Xiuying Zhong | 2021 | Cancer Communications2021，41，9： | 0 |
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