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★中国抗癌协会乳腺癌专业委员会主任委员 ★上海抗癌协会乳腺癌专业委员会主任委员。 ★上海医学会靶分子专业委员会主任委员 ★中华医学会肿瘤分会常委 ★上海市乳腺疾病防治委员会副主任委员 ★第七届亚洲乳腺癌协会主席  行政职务:复旦大学附属肿瘤医院外科主任、乳腺外科主任、乳腺癌多学科综合治疗组首席专家    获奖情况:1.2009年1月 教育部科学技术进步奖一等奖 《乳腺癌肺转移机制的研究和临床应用》 邵志敏（第一完成人） 2. 2009年11月 上海市科技进步奖二等奖 《乳腺癌肺转移机制的揭示及其临床应用》 邵志敏（第一完成人） 3. 2008.12 中华医学科技奖三等奖 《乳腺癌肺转移机制的研究和临床应用》 邵志敏（第一完成人） 4.2011年获上海市科技进步一等奖 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生物制剂初治银屑病患者的治疗历程对后续生物制剂药物留存率的影响","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002Fe9407aadc9176d6ff5fb1723518eec87\u002F2024\u002F12\u002F02\u002F104e6f0172a2c11d90a97a1a35291e677e0a3bc9_img_thumb_540_auto.jpg",[],{"type":372,"data":637,"needLogin":44,"reload":44},{"id":632},{"id":639,"title":640,"cover":641,"price_type":61,"price":59,"original_price":59,"learn_count":642,"learn_count_show":59,"series_id":59,"is_banner":59,"sort":59,"view_full_screen":59,"course_updated_count":59,"course_count":59,"course_type":61,"is_show":61,"buy_count":59,"tag":643,"action":644},701,"长春瑞滨基础信息及临床应用","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002Fd2d1de9e65e242bfa63574ae8516a36b\u002F2024\u002F01\u002F12\u002F47780249533a8015fb692502f74adb6d576b173b_img_thumb_540_auto.jpg",53,[],{"type":372,"data":645,"needLogin":44,"reload":44},{"id":639},["Reactive",647],[648,708,771,822,907,970,1038,1094,1137,1202],{"score":649,"jcr":650,"q":651,"uuid":652,"full_author":653,"abstract_text":654,"title":655,"file_path":656,"file_id":657,"snippet":658,"type":659,"year_jcr":660,"abstract":654,"pmcid":689,"id":690,"journal":691,"doi":692,"full_journal":693,"link":694,"free":61,"keyword":63,"imf":695,"pmid":696,"author":697,"doi_source_url":706,"is_favorite":59,"is_lib":59,"file_status":39,"path":707,"pdf_url":706},0.176,"MEDICINE","Q2","0025a541-3d43-3bc8-9fe9-87c6e826dac2","MingFeng Xue,Gang Chen,XingGuang Chen,JunYu Hu","Abstract The objective of the current study is to analyze the clinical and demographic characteristics of patients with bone metastasis of small cell lung cancer (SCLC) and explore their survival predictors.We retrospectively extracted patients with bone metastasis of SCLC from the Surveillance, Epidemiology, and End Results database. We applied Cox regression analyses to identify independent survival predictor of overall survival (OS) and cancer-specific survival (CSS). Only significant predictors from univariable analysis were included for multivariable Cox analysis. Kaplan-Meier method was used to evaluate survival differences between groups by the log-rank test.A total of 5120 patients with bone metastasis of SCLC were identified and included for survival analysis. The 1-year OS and CSS rates of bone metastasis of SCLC were 19.8% and 21.4%, respectively. On multivariable analysis, gender, age, radiotherapy, chemotherapy, liver metastasis, brain metastasis, insurance status, and marital status independently predicted OS and CSS. There was no significant difference of OS and CSS in terms of race and tumor size.Independent predictors of survival were identified among patients with bone metastasis of SCLC, which could be valuable to clinicians in treatment decision. Patients with bone metastasis of SCLC may benefit from radiotherapy and chemotherapy.","Predictors for survival in patients with bone metastasis of small cell lung cancer: A population-based study","https:\u002F\u002Fcdn-tap.talkmed.com\u002F202611130556\u002Faff49be21a7c75381950297212fb0650\u002F2025\u002F01\u002F13\u002Fd133ff910a1266cef087a8bec6f5eaa3237ba419.pdf","109687","Abstract The objective of the current study is to analyze the clinical and demographic characteristics of patients with bone metastasis of small cell lung cancer (SCLC) and explore their survival predictors.","pubmed",[661,669,674,679,684],{"jcrYear":662,"jif":663,"quartile":664,"category":665},2020,1.889,"Q3",[666],{"category":667,"source":668,"quartile":664},"MEDICINE, GENERAL & INTERNAL","SCIE",{"jcrYear":670,"jif":671,"quartile":664,"category":672},2021,1.817,[673],{"category":667,"source":668,"quartile":664},{"jcrYear":675,"jif":676,"quartile":664,"category":677},2022,1.6,[678],{"category":667,"source":668,"quartile":664},{"jcrYear":680,"jif":681,"quartile":651,"category":682},2023,1.3,[683],{"category":667,"quartile":651},{"jcrYear":685,"jif":686,"quartile":651,"category":687},2024,1.4,[688],{"category":667,"quartile":651},"PMC8389941","267887","Medicine (Baltimore)","10.1097\u002FMD.0000000000027070","Medicine (Baltimore). 2021 Aug 27;100(34):e27070.doi: 10.1097\u002FMD.0000000000027070.","https:\u002F\u002Fdoi.org\u002F10.1097\u002FMD.0000000000027070,https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F34449503\u002F","1.4","34449503",[698,700,702,704],{"name":699},"MingFeng Xue",{"name":701},"Gang Chen",{"name":703},"XingGuang Chen",{"name":705},"JunYu Hu","https:\u002F\u002Fdoi.org\u002F10.1097\u002Fmd.0000000000027070","2025\u002F01\u002F13\u002Fd133ff910a1266cef087a8bec6f5eaa3237ba419.pdf",{"score":649,"jcr":709,"q":651,"uuid":710,"full_author":711,"abstract_text":712,"title":713,"file_path":714,"file_id":715,"snippet":716,"type":659,"year_jcr":717,"abstract":712,"pmcid":738,"id":739,"journal":740,"doi":741,"full_journal":742,"link":743,"free":61,"keyword":63,"imf":744,"pmid":745,"author":746,"doi_source_url":769,"is_favorite":59,"is_lib":59,"file_status":39,"path":770,"pdf_url":769},"Targeted Oncology","003ce6bb-35fc-303f-b59e-aaace071a684","Chang Liu,Hui Yu,Jianhua Chang,Haiquan Chen,Yuan Li,Weixin Zhao,Kuaile Zhao,Zhengfei Zhu,Si Sun,Min Fan,Jialei Wang","Abstract Background: Approximately 1-2% of patients with non‒small-cell lung cancer (NSCLC) harbor ROS1 rearrangements. Crizotinib, an oral small-molecule tyrosine kinase inhibitor (TKI) that targets anaplastic lymphoma kinase (ALK), MET, and ROS1, has shown marked antitumor activity in patients with ROS1-positive advanced NSCLC. Objective: Our objective was to analyze the efficacy and safety of crizotinib treatment in Chinese patients with advanced NSCLC with ROS1 rearrangement in real-world clinical practice. Methods: We included 35 patients with ROS1-positive NSCLC in this retrospective analysis. All received crizotinib 250 mg twice daily between March 2016 and April 2018 at the Fudan University Shanghai Cancer Center. All had histologically or cytologically confirmed locally advanced or metastatic NSCLC with ROS1 rearrangements, which were identified by fluorescence in situ hybridization, reverse transcriptase polymerase chain reaction, or next-generation sequencing. The main outcome measures were progression-free survival (PFS), overall survival (OS), objective response rate (ORR), disease control rate (DCR), and adverse events. Results: The median age of the patients was 51.0 years; 23 (65.7%) were female and 28 (80.0%) were never smokers. All were diagnosed as having adenocarcinoma; eight patients (22.9%) had brain metastases at baseline. The ORR and DCR were 71.4% and 94.3%, respectively. The estimated median PFS was 11.0 months (95% confidence interval [CI] 7.8-14.2). The estimated median OS was 41.0 months (95% CI 22.5-59.5). Elevated transaminases (54.3%), vision disorder (25.7%), elevated blood creatinine (22.9%), diarrhea (20.0%), and vomiting (20.0%) were the most commonly reported adverse effects. Conclusion: Crizotinib was effective and well tolerated in Chinese patients with ROS1-positive advanced NSCLC in real-world clinical practice. The progression sites and patterns, as well as treatments after first disease progression on crizotinib were diverse. Crizotinib beyond progressive disease and local therapy after failure of crizotinib treatment were feasible and effective in clinical practice.","Crizotinib in Chinese Patients with ROS1-Rearranged Advanced Non‒Small-Cell Lung Cancer in Routine Clinical Practice","https:\u002F\u002Fcdn-tap.talkmed.com\u002F202611130556\u002Fe9a6f659b57f76cd2f4655c2435fbdc9\u002F2024\u002F12\u002F19\u002Fd22eeafb94c07c766cd0165094926213026e7d73.pdf","68096","Abstract Background: Approximately 1-2% of patients with non‒small-cell lung cancer (NSCLC) harbor ROS1 rearrangements.",[718,723,727,731,735],{"jcrYear":662,"jif":719,"quartile":651,"category":720},4.493,[721],{"category":722,"source":668,"quartile":651},"ONCOLOGY",{"jcrYear":670,"jif":724,"quartile":651,"category":725},4.897,[726],{"category":722,"source":668,"quartile":651},{"jcrYear":675,"jif":728,"quartile":651,"category":729},5.4,[730],{"category":722,"source":668,"quartile":651},{"jcrYear":680,"jif":732,"quartile":651,"category":733},4.4,[734],{"category":722,"quartile":651},{"jcrYear":685,"jif":139,"quartile":651,"category":736},[737],{"category":722,"quartile":651},"PMC6602983","159176","Target Oncol","10.1007\u002Fs11523-019-00636-6","Target Oncol. 2019 Jun;14(3):315-323.doi: 10.1007\u002Fs11523-019-00636-6.","https:\u002F\u002Fdx.doi.org\u002F10.1007\u002Fs11523-019-00636-6,https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F30976989\u002F","4.0","30976989",[747,749,751,753,755,757,759,761,763,765,767],{"name":748},"Chang Liu",{"name":750},"Hui Yu",{"name":752},"Jianhua Chang",{"name":754},"Haiquan Chen",{"name":756},"Yuan Li",{"name":758},"Weixin Zhao",{"name":760},"Kuaile Zhao",{"name":762},"Zhengfei Zhu",{"name":764},"Si Sun",{"name":766},"Min Fan",{"name":768},"Jialei Wang","https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs11523-019-00636-6","2024\u002F12\u002F19\u002Fd22eeafb94c07c766cd0165094926213026e7d73.pdf",{"score":649,"jcr":772,"q":651,"uuid":773,"full_author":774,"abstract_text":775,"title":776,"file_path":777,"file_id":778,"snippet":779,"type":659,"year_jcr":780,"abstract":775,"pmcid":800,"id":801,"journal":802,"doi":803,"full_journal":804,"link":805,"free":61,"keyword":806,"imf":807,"pmid":808,"author":809,"doi_source_url":820,"is_favorite":59,"is_lib":59,"file_status":39,"path":821,"pdf_url":820},"BMC CANCER","05218a5c-c5ec-3ff8-9ed4-0320e879addc","Shizhao Cheng,Lei Yang,Xin Dai,Jing Wang,Xingpeng Han","Abstract Background: Brain metastases were rare in esophageal cancer patients. Using the Surveillance, Epidemiology, and End Results (SEER) database, the present study investigated the incidence, risk and prognostic factors of brain metastases in esophageal cancer patients. Methods: Retrieving esophageal cancer patients diagnosed between 2010 and 2018 from the SEER database, univariable and multivariable logistic and cox regression models were used to investigate the risk factors for brain metastases development and prognosis, respectively. The brain metastases predicting nomogram was constructed, evaluated and validated. The overall survival (OS) of patients with brain metastases was analyzed by Kaplan-Meier method. Results: A total of 34,107 eligible esophageal cancer patients were included and 618 of them were diagnosed with brain metastases (1.8%). The median survival of the brain metastatic esophageal cancer patients was 5 (95% CI: 5-7) months. The presence of bone metastases and lung metastases were the homogeneously associated factors for the development and prognosis of brain metastases in esophageal cancer patients. Patients younger than 65 years, American Indian\u002FAlaska Native race (vs. White), overlapping lesion (vs. Upper third), esophageal adenocarcinoma histology subtype, higher N stage, and liver metastases were positively associated with brain metastases occurrence. The calibration curve, ROC curve, and C-index exhibited good performance of the nomogram for predicting brain metastases. Conclusions: Homogeneous and heterogeneous factors were found for the development and prognosis of brain metastases in esophageal cancer patients. The nomogram had good calibration and discrimination for predicting brain metastases. Keywords: Brain metastases; Esophageal cancer; Prognosis factor; Risk factor; SEER.","The risk and prognostic factors for brain metastases in esophageal cancer patients: an analysis of the SEER database","https:\u002F\u002Fcdn-tap.talkmed.com\u002F202611130556\u002F3fe0b0a5923a59a5db32d9ad14f1c27d\u002F2025\u002F01\u002F13\u002F4da70f15987dbcbc13ab54e9b996953689285b00.pdf","109689","Abstract Background: Brain metastases were rare in esophageal cancer patients.",[781,785,789,793,797],{"jcrYear":662,"jif":782,"quartile":651,"category":783},4.43,[784],{"category":722,"source":668,"quartile":651},{"jcrYear":670,"jif":786,"quartile":651,"category":787},4.638,[788],{"category":722,"source":668,"quartile":651},{"jcrYear":675,"jif":790,"quartile":651,"category":791},3.8,[792],{"category":722,"source":668,"quartile":651},{"jcrYear":680,"jif":794,"quartile":651,"category":795},3.4,[796],{"category":722,"quartile":651},{"jcrYear":685,"jif":794,"quartile":651,"category":798},[799],{"category":722,"quartile":651},"PMC8465786","267880","BMC Cancer","10.1186\u002Fs12885-021-08802-8","BMC Cancer. 2021 Sep 26;21(1):1057.doi: 10.1186\u002Fs12885-021-08802-8.","https:\u002F\u002Fbmccancer.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12885-021-08802-8,https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F34563149\u002F","Keywords: Brain metastases; Esophageal cancer; Prognosis factor; Risk factor; SEER.","3.4","34563149",[810,812,814,816,818],{"name":811},"Shizhao Cheng",{"name":813},"Lei Yang",{"name":815},"Xin Dai",{"name":817},"Jing Wang",{"name":819},"Xingpeng Han","https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs12885-021-08802-8","2025\u002F01\u002F13\u002F4da70f15987dbcbc13ab54e9b996953689285b00.pdf",{"score":649,"jcr":823,"q":824,"uuid":825,"full_author":826,"abstract_text":827,"title":828,"snippet":829,"file_path":830,"file_id":831,"list_abstract_url":832,"type":659,"year_jcr":833,"abstract":827,"pmcid":855,"id":856,"journal":857,"full_journal":858,"doi":859,"free":61,"link":63,"keyword":63,"imf":860,"pmid":861,"author":862,"doi_source_url":905,"is_favorite":59,"is_lib":59,"file_status":39,"path":906,"pdf_url":905},"HAEMATOLOGICA","Q1","0543f2f8-bdd8-3bbf-bffa-88af8a5c9449","Yang Yunfan, Liu Yuntao, Sun Hui, Meng Li, Lin Hai, Chen Chunyan, Hu Jianda, Shen Xuliang, Duan Minghui, Zhang Yanli, Abulaiti Dilinazi, Wang Jinghua, Zhu Hongqian, Hua Luoming, Leng Qing, Zhang Chun, Sun Lili, Li Weiming, Zhu Huanling, Liu Bingcheng, Wang Jianxiang","The aim of this study was to evaluate the efficacy and safety of flumatinib in later-line treatment of Chinese patients with Philadelphia chromosome-positive chronic-phase chronic myeloid leukemia ((CP-CML) previously treated with tyrosine kinase inhibitors (TKI). Patients with CML-CP were evaluated for probabilities of responses, including complete hematologic response (CHR), cytogenetic response, and molecular response (MR), and adverse events after the later-line flumatinib therapy. Of 336 enrolled patients with a median age 50 years, the median duration of treatment with flumatinib was 11.04 months (range, 2-25.23). Patients who achieved clinical responses at baseline showed maintenance of CHR, complete cytogenetic response (CCyR) or 2-log molecular response (MR2), major molecular response (MMR), and 4-log molecular response or deep molecular response (MR4\u002FDMR) in 100%, 98.9%, 98.6%, and 92.9% of patients, respectively. CHR, CCyR\u002FMR2, MMR, and MR4\u002FDMR were achieved in 86.4%, 52.7%, 49.6%, and 23.5% of patients, respectively, who lacked the respective clinical responses at baseline. The patients without response at baseline, treated with flumatinib as a second-line TKI, having no resistance to prior TKI or only resistance to imatinib, with response to last TKI, and with BCR::ABL ≤10% had higher CCyR\u002FMR2, MMR, or MR4\u002FDMR rates. The adverse events observed during the later-line flumatinib treatment were tolerable and consistent with those reported with the first-line therapy. Flumatinib was effective and safe in patients who were resistant or intolerant to other TKI. In particular, second-line flumatinib treatment induced high response rates and was more beneficial to patients without previous second-generation TKI resistance, thus serving as a probable treatment option for these patients.","Safety and efficacy of flumatinib as later-line therapy in patients with chronic myeloid leukemia.","The aim of this study was to evaluate the efficacy and safety of flumatinib in later-line treatment of Chinese patients with Philadelphia chromosome-positive chronic-phase chronic myeloid leukemia ((CP-CML) previously treated with tyrosine kinase inhibitors (TKI).","https:\u002F\u002Fcdn-tap.talkmed.com\u002F202611130556\u002Ff858ba6db3ca62a7c1d6bdd895650e3b\u002F2024\u002F10\u002F30\u002F98e34f9ba5535d8fe64dfbf86031baf2da5d29c2.pdf","34501","https:\u002F\u002Fpubmed-ncbi-nlm-nih.talkmed.com\u002F?term=Flumatinib&page=1&size=10&format=abstract",[834,839,843,847,851],{"jcrYear":662,"jif":835,"quartile":824,"category":836},9.941,[837],{"category":838,"source":668,"quartile":824},"HEMATOLOGY",{"jcrYear":670,"jif":840,"quartile":824,"category":841},11.049,[842],{"category":838,"source":668,"quartile":824},{"jcrYear":675,"jif":844,"quartile":824,"category":845},10.1,[846],{"category":838,"source":668,"quartile":824},{"jcrYear":680,"jif":848,"quartile":824,"category":849},8.2,[850],{"category":838,"quartile":824},{"jcrYear":685,"jif":852,"quartile":824,"category":853},7.9,[854],{"category":838,"quartile":824},"PMC11609796","86681","Haematologica","Haematologica. 2024 Dec 01;109(12):3965-3974. doi: 10.3324\u002Fhaematol.2023.284892.","10.3324\u002Fhaematol.2023.284892","7.9","38934064",[863,865,867,869,871,873,875,877,879,881,883,885,887,889,891,893,895,897,899,901,903],{"name":864},"Yang Yunfan",{"name":866},"Liu Yuntao",{"name":868},"Sun Hui",{"name":870},"Meng Li",{"name":872},"Lin Hai",{"name":874},"Chen Chunyan",{"name":876},"Hu Jianda",{"name":878},"Shen Xuliang",{"name":880},"Duan Minghui",{"name":882},"Zhang Yanli",{"name":884},"Abulaiti Dilinazi",{"name":886},"Wang Jinghua",{"name":888},"Zhu Hongqian",{"name":890},"Hua Luoming",{"name":892},"Leng Qing",{"name":894},"Zhang Chun",{"name":896},"Sun Lili",{"name":898},"Li Weiming",{"name":900},"Zhu Huanling",{"name":902},"Liu Bingcheng",{"name":904},"Wang Jianxiang","https:\u002F\u002Fdoi.org\u002F10.3324\u002Fhaematol.2023.284892","2024\u002F10\u002F30\u002F98e34f9ba5535d8fe64dfbf86031baf2da5d29c2.pdf",{"score":649,"jcr":908,"q":824,"uuid":909,"full_author":910,"abstract_text":911,"title":912,"file_path":913,"file_id":914,"snippet":915,"type":659,"year_jcr":916,"abstract":911,"pmcid":943,"id":944,"journal":945,"doi":946,"full_journal":947,"link":948,"free":61,"keyword":949,"imf":950,"pmid":951,"author":952,"doi_source_url":968,"is_favorite":59,"is_lib":59,"file_status":39,"path":969,"pdf_url":968},"OncoImmunology","06554bb7-cab6-30a5-abe7-a27f891321cf","Meichen Li,Jing Chen,Hui Yu,Baishen Zhang,Xue Hou,Honghua Jiang,Dan Xie,Likun Chen","Abstract Background: Immunotherapy has shown intracranial efficacy in non-small cell lung cancer (NSCLC) patients with brain metastases. However, predictive biomarkers for intracranial response to immunotherapy are lacking. This post-hoc analysis aimed to explore the potential of immunological cytokines in cerebrospinal fluid (CSF) to predict intracranial tumor response to immunotherapy in patients with brain metastases. Methods: Treatment-naive NSCLC patients with brain metastases who received camrelizumab plus chemotherapy were enrolled. Paired plasma and CSF samples were prospectively collected at baseline and the first treatment assessment. All samples were analyzed for 92 immuno-oncology cytokines using Olink's panels. Results: A total of 28 patients were included in this analysis. At baseline, most immunological cytokines were significantly lower in CSF than in plasma, whereas a subset comprising CD83, PTN, TNFRSF21, TWEAK, ICOSLG, DCN, IL-8, and MCP-1, was increased in CSF. Baseline CSF levels of LAMP3 were significantly higher in patients with intracranial tumor response, while the levels of CXCL10, IL-12, CXCL11, IL-18, TIE2, HGF, and PDCD1 were significantly lower. Furthermore, the CXCL10, CXCL11, TIE2, PDCD1, IL-18, HGF, and LAMP3 in CSF were also significantly associated with intracranial progression-free survival for immunotherapy. The identified cytokines in CSF were decreased at the first treatment evaluation in patients with intracranial tumor response. The logistic CSF immuno-cytokine model yielded an AUC of 0.91, as compared to PD-L1 expression (AUC of 0.72). Conclusions: Immunological cytokines in CSF could predict intracranial tumor response to immunotherapy in NSCLC patients with brain metastases, and the findings warrant validation in a larger prospective cohort study. Trial registration: ClinicalTrials.gov identifier: NCT04211090. Keywords: Brain metastases; cerebrospinal fluid; immunological cytokines; immunotherapy; tumor response.","Cerebrospinal fluid immunological cytokines predict intracranial tumor response to immunotherapy in non-small cell lung cancer patients with brain metastases","https:\u002F\u002Fcdn-tap.talkmed.com\u002F202611130556\u002F65170d2694162f1299e541a400275ea0\u002F2024\u002F12\u002F16\u002F70a901665c285d3f7df247d530a6fab671991ea7.pdf","44003","Abstract Background: Immunotherapy has shown intracranial efficacy in non-small cell lung cancer (NSCLC) patients with brain metastases.",[917,923,928,933,938],{"jcrYear":662,"jif":918,"quartile":824,"category":919},8.11,[920,922],{"category":921,"source":668,"quartile":824},"IMMUNOLOGY",{"category":722,"source":668,"quartile":824},{"jcrYear":670,"jif":924,"quartile":824,"category":925},7.723,[926,927],{"category":921,"source":668,"quartile":824},{"category":722,"source":668,"quartile":824},{"jcrYear":675,"jif":929,"quartile":824,"category":930},7.2,[931,932],{"category":921,"source":668,"quartile":824},{"category":722,"source":668,"quartile":824},{"jcrYear":680,"jif":934,"quartile":824,"category":935},6.5,[936,937],{"category":921,"quartile":824},{"category":722,"quartile":824},{"jcrYear":685,"jif":939,"quartile":824,"category":940},6.3,[941,942],{"category":921,"quartile":824},{"category":722,"quartile":824},"PMC10761018","107503","Oncoimmunology","10.1080\u002F2162402X.2023.2290790","Oncoimmunology. 2023 Dec 7;13(1):2290790.doi: 10.1080\u002F2162402X.2023.2290790.","https:\u002F\u002Fwww.tandfonline.com\u002Fdoi\u002Fabs\u002F10.1080\u002F2162402X.2023.2290790?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub  0pubmed,https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F38169917\u002F","Keywords: Brain metastases; cerebrospinal fluid; immunological cytokines; immunotherapy; tumor response.","6.3","38169917",[953,955,957,958,960,962,964,966],{"name":954},"Meichen Li",{"name":956},"Jing Chen",{"name":750},{"name":959},"Baishen Zhang",{"name":961},"Xue Hou",{"name":963},"Honghua Jiang",{"name":965},"Dan Xie",{"name":967},"Likun Chen","https:\u002F\u002Fdoi.org\u002F10.1080\u002F2162402x.2023.2290790","2024\u002F12\u002F16\u002F70a901665c285d3f7df247d530a6fab671991ea7.pdf",{"score":649,"jcr":971,"q":824,"uuid":972,"full_author":973,"abstract_text":974,"title":975,"file_path":976,"file_id":977,"snippet":978,"type":659,"year_jcr":979,"abstract":974,"pmcid":1012,"id":1013,"journal":1014,"doi":1015,"full_journal":1016,"link":1017,"free":61,"keyword":1018,"imf":1019,"pmid":1020,"author":1021,"doi_source_url":1036,"is_favorite":59,"is_lib":59,"file_status":39,"path":1037,"pdf_url":1036},"MOLECULAR MEDICINE","06672ee4-6867-37ab-b06b-69e65b49c601","Dantong Sun,Yan Zhu,Jingjuan Zhu,Junyan Tao,Xiaojuan Wei,Yang Wo,Helei Hou","Abstract Introduction: Targeted therapy for NSCLC is rapidly evolving. EGFR-TKIs benefit NSCLC patients with sensitive EGFR mutations and significantly prolong survival. However, 20-30% of patients demonstrate primary resistance to EGFR-TKIs, which leads to the failure of EGFR-TKI treatment. The mechanisms of primary resistance to EGFR-TKIs require further study. Methods: Targeted sequencing was used for the detection of genomic alterations among patients in our center. Regular cell culture and transfection with plasmids were used to establish NSCLC cell lines over-expressing MDM2 and vector control. We used the MTT assays to calculate the inhibition rate after exposure to erlotinib. Available datasets were used to determine the role of MDM2 in the prognosis of NSCLC. Results: Four patients harboring concurrent sensitive EGFR mutations and MDM2 amplifications demonstrated insensitivity to EGFR-TKIs in our center. In vitro experiments suggested that MDM2 amplification induces primary resistance to erlotinib. Over-expressed MDM2 elevated the IC50 value of erlotinib in HCC2279 line and reduced the inhibition rate. In addition, MDM2 amplification predicted a poor prognosis in NSCLC patients and was associated with a short PFS in those treated with EGFR-TKIs. The ERBB2 pathway was identified as a potential pathway activated by MDM2 amplification could be the focus of further research. Conclusion: MDM2 amplification induces the primary resistance to EGFR-TKIs and predicts poor prognosis in NSCLC patients. MDM2 may serve as a novel biomarker and treatment target for NSCLC. Further studies are needed to confirm the mechanism by which amplified MDM2 leads to primary resistance to EGFR-TKIs. Keywords: EGFR-TKIs; MDM2 amplification; NSCLC; Primary resistance; Prognosis.","Primary resistance to first-generation EGFR-TKIs induced by MDM2 amplification in NSCLC","https:\u002F\u002Fcdn-tap.talkmed.com\u002F202611130556\u002F2a729d00725f199ef9ae20d2f0ac9008\u002F2024\u002F12\u002F19\u002Fcbe75f25af6a187b68e260d51013498fdf6324bb.pdf","63372","Abstract Introduction: Targeted therapy for NSCLC is rapidly evolving.",[980,989,995,1001,1006],{"jcrYear":662,"jif":981,"quartile":824,"category":982},6.354,[983,985,987],{"category":984,"source":668,"quartile":824},"BIOCHEMISTRY & MOLECULAR BIOLOGY",{"category":986,"source":668,"quartile":651},"CELL BIOLOGY",{"category":988,"source":668,"quartile":824},"MEDICINE, RESEARCH & EXPERIMENTAL",{"jcrYear":670,"jif":990,"quartile":824,"category":991},6.382,[992,993,994],{"category":984,"source":668,"quartile":824},{"category":986,"source":668,"quartile":651},{"category":988,"source":668,"quartile":651},{"jcrYear":675,"jif":996,"quartile":824,"category":997},5.7,[998,999,1000],{"category":984,"source":668,"quartile":824},{"category":986,"source":668,"quartile":651},{"category":988,"source":668,"quartile":651},{"jcrYear":680,"jif":41,"quartile":824,"category":1002},[1003,1004,1005],{"category":984,"quartile":824},{"category":986,"quartile":824},{"category":988,"quartile":824},{"jcrYear":685,"jif":1007,"quartile":824,"category":1008},6.4,[1009,1010,1011],{"category":984,"quartile":824},{"category":986,"quartile":824},{"category":988,"quartile":824},"PMC7329552","148989","Mol Med","10.1186\u002Fs10020-020-00193-z","Mol Med. 2020 Jul 1;26(1):66.doi: 10.1186\u002Fs10020-020-00193-z.","https:\u002F\u002Fmolmed.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs10020-020-00193-z,https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F32611363\u002F","Keywords: EGFR-TKIs; MDM2 amplification; NSCLC; Primary resistance; Prognosis.","6.4","32611363",[1022,1024,1026,1028,1030,1032,1034],{"name":1023},"Dantong Sun",{"name":1025},"Yan Zhu",{"name":1027},"Jingjuan Zhu",{"name":1029},"Junyan Tao",{"name":1031},"Xiaojuan Wei",{"name":1033},"Yang Wo",{"name":1035},"Helei Hou","https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs10020-020-00193-z","2024\u002F12\u002F19\u002Fcbe75f25af6a187b68e260d51013498fdf6324bb.pdf",{"score":649,"jcr":1039,"q":651,"uuid":1040,"full_author":1041,"abstract_text":1042,"title":1043,"file_path":1044,"file_id":1045,"snippet":1046,"list_abstract_url":1047,"type":659,"year_jcr":1048,"abstract":1042,"pmcid":1068,"id":1069,"journal":1070,"doi":1071,"full_journal":1072,"link":1073,"free":61,"keyword":1074,"imf":1075,"pmid":1076,"author":1077,"doi_source_url":1092,"is_favorite":59,"is_lib":59,"file_status":39,"path":1093,"pdf_url":1092},"Cancer Research and Treatment","0ced28d3-680d-332a-b493-68b4e9fc357a","Kim H, Park S, Jung HA, Sun JM, Lee SH, Ahn JS, Ahn MJ.","Abstract Purpose: The impact of epidermal growth factor receptor (EGFR) mutation in locally advanced non-small cell lung cancer (NSCLC) remains controversial. This study was conducted to investigate the clinical outcomes and recurrence patterns after definitive chemoradiotherapy (CRT) in patients with unresectable stage III non-squamous-cell lung cancer according to EGFR mutation status. Materials and methods: We retrospectively reviewed 604 patients with pathologically confirmed stage III NSCLC who were treated with definitive CRT and were examined for EGFR mutation at Samsung Medical Center, Korea, from January 2013 to December 2018. Among them, we identified 236 patients with stage III non-squamous-cell lung cancer who were treated with definitive CRT and were examined for EGFR mutation status. We analyzed the frequency of EGFR mutation, progression-free survival (PFS), overall survival (OS), objective response rate (ORR), and recurrence pattern. Results: Among 236 patients, EGFR mutation was detected in 71 patients (30.1%) and the median follow-up duration was 41.7 months. There were no significant differences in PFS (9.9 vs. 10.9 months, p=0.236), and ORR to CRT (93.0% vs. 90.3%, p=0.623) according to EGFR mutation status. However, the EGFR mutant group showed significantly higher recurrence (88.7% vs. 75.2%, p=0.022), distant metastasis (76.1% vs. 61.2%, p=0.036) rates, especially brain (38.0% vs. 12.7%, p \u003C 0.001), and better median OS (59.2 vs. 41.3 months, p=0.037) compared with patients without EGFR mutation. Conclusion: Patients with EGFR mutation-positive unresectable stage III non-squamous lung cancer exhibited higher recurrence and distant metastasis rates, especially brain metastasis. Keywords: Chemoradiotherapy; EGFR mutation; Metastasis; Non-small-cell lung carcinoma; Survival.","\u003Cb>EGFR\u003C\u002Fb> Mutation-Positive \u003Cb>Unresectable\u003C\u002Fb> \u003Cb>Stage\u003C\u002Fb> \u003Cb>III\u003C\u002Fb> Non-Squamous \u003Cb>Lung\u003C\u002Fb> Cancer Is Associated with a High Incidence of Brain Metastasis.","https:\u002F\u002Fcdn-tap.talkmed.com\u002F202611130556\u002Fca3035b954a61bd0e4db734c651b7592\u002F2024\u002F12\u002F17\u002F6172eec3561ae7b1d9d0af6a81fcead025e5590c.pdf","46762","PURPOSE: The impact of epidermal growth factor receptor (\u003Cb>EGFR\u003C\u002Fb>) mutation in locally advanced \u003Cb>non\u003C\u002Fb>-\u003Cb>small\u003C\u002Fb> \u003Cb>cell\u003C\u002Fb> \u003Cb>lung\u003C\u002Fb> cancer (\u003Cb>NSCLC\u003C\u002Fb>) remains controversial. ...CONCLUSION: Patients with \u003Cb>EGFR\u003C\u002Fb> mutation-positive \u003Cb>unresectable\u003C\u002Fb> \u003Cb>stage\u003C\u002Fb> …","https:\u002F\u002Fpubmed-ncbi-nlm-nih.talkmed.com\u002F?term=EGFR+mutant+stage+III+unresectable+NSCLC&page=1&size=10&format=abstract",[1049,1053,1057,1061,1065],{"jcrYear":662,"jif":1050,"quartile":651,"category":1051},4.679,[1052],{"category":722,"source":668,"quartile":651},{"jcrYear":670,"jif":1054,"quartile":651,"category":1055},5.036,[1056],{"category":722,"source":668,"quartile":651},{"jcrYear":675,"jif":1058,"quartile":651,"category":1059},4.6,[1060],{"category":722,"source":668,"quartile":651},{"jcrYear":680,"jif":1062,"quartile":651,"category":1063},4.1,[1064],{"category":722,"quartile":651},{"jcrYear":685,"jif":790,"quartile":651,"category":1066},[1067],{"category":722,"quartile":651},"PMC10101774","114379","Cancer Res Treat","10.4143\u002Fcrt.2022.388","Cancer Res Treat. 2023 Apr;55(2):498-505. doi: 10.4143\u002Fcrt.2022.388. Epub 2022 Oct 4.","https:\u002F\u002Fdx.doi.org\u002F10.4143\u002Fcrt.2022.388,https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F36228655\u002F","Keywords: Chemoradiotherapy; EGFR mutation; Metastasis; Non-small-cell lung carcinoma; Survival.","3.8","36228655",[1078,1080,1082,1084,1086,1088,1090],{"name":1079},"Kim H",{"name":1081},"Park S",{"name":1083},"Jung HA",{"name":1085},"Sun JM",{"name":1087},"Lee SH",{"name":1089},"Ahn JS",{"name":1091},"Ahn MJ.","https:\u002F\u002Fdoi.org\u002F10.4143\u002Fcrt.2022.388","2024\u002F12\u002F17\u002F6172eec3561ae7b1d9d0af6a81fcead025e5590c.pdf",{"score":649,"uuid":1095,"jcr":63,"q":63,"full_author":1096,"abstract_text":1097,"title":1098,"file_path":1099,"file_id":1100,"snippet":1101,"list_abstract_url":1102,"type":659,"year_jcr":63,"abstract":1103,"pmcid":1104,"id":1105,"journal":1106,"doi":1107,"full_journal":1108,"link":1109,"free":61,"keyword":1110,"imf":63,"pmid":1111,"author":1112,"doi_source_url":1135,"is_favorite":59,"is_lib":59,"file_status":39,"path":1136,"pdf_url":1135},"18aa0d93-a7c3-3ad0-894c-60c62b1e4f5c","H F Zhao,Y F Yang,B C Liu,W M Li,N Xu,X L Liu,Q Jiang,H B Dang,L X Liang,Yanli Zhang,Y P Song","Abstract in English, Chinese Objective: This study aimed to observe whether the treatment-free remission (TFR) of second-generation tyrosine kinase inhibitors (TKI) in chronic myeloid leukemia (CML) is better than imatinib (IM) . Methods: The clinical data of 274 CML patients who discontinued treatment and with complete clinical data were retrospectively studied from June 2013 to March 2021. Using both univariate and multivariate Cox proportional hazards regression models, risk factors influencing TFR outcomes after drug withdrawal in CML patients were assessed. Results: A total of 274 patients were enrolled, 140 patients were women (51.1%) , with a median age of 48 (9-84) years at the time of TKI discontinuation. Prior to TKI discontinuation, 172 (62.8%) patients were treated with IM, and 102 (37.2%) had received second-generation TKI treatment, including 73 patients who had shifted from IM to a second-generation TKI and 29 patients who used second-generation TKI as the first-line treatment. The rationale for converting to a second-generation TKI are as follows: 37 patients aimed deep molecular response (DMR) to achieve TFR, seven patients changed due to IM intolerance, and 29 patients changed because of failure to achieve the optimal treatment response. The use of the last type of TKI included 96 patients (94.1%) with nilotinib, three patients (2.9%) with dasatinib, and two patients (2%) with flumatinib, including one patient who changed to IM due to second-generation TKI intolerance. No statistical differences were found in the median age at diagnosis and TKI discontinuation, sex, Sokal score, IFN treatment before TKI, median time of TKI treatment to achieve DMR, and the reasons for TKI discontinuation between the second TKI and IM (P>0.05) .The median cumulative treatment time of TKI (71.5 months vs 88 months, P\u003C0.001) , the last TKI median treatment time (60 months vs 88 months, P\u003C0.001) , and the median duration of DMR (58 months vs 66 months, P=0.002) were significantly shorter in the second-generation TKI compared with IM. In the median follow-up of 22 (6-118) months after TKI discontinuation, 88 patients (32.1%) had lost their MMR at a median of 6 (1-91) months; of the 53 patients (60.2%) who lost MMR within 6 months, the overall TFR rate was 67.9%, and the cumulative TFR rates at 12 and 24 months were 70.5% and 67.5%, respectively. Withdrawal syndrome occurred in 26 patients (9.5%) . For patients who restarted TKI treatment, 72 patients (83.7%) achieved DMR again at a median treatment of 4 (1 to 18) months. The univariate analysis showed that the TFR rate of patients treated with second-generation TKI was significantly higher than those who were treated with IM (77.5% vs 62.2%, P=0.041) . A further subgroup analysis found that the TFR rate of the second-generation TKI patients was significantly higher than those treated with IM (80.8% vs 62.2%, P=0.026) . No significant difference was found in the second-generation TKI used as the first line treatment compared with those who were treated with IM (69.0% vs 62.2%, P=0.599) . The multivariate analysis results showed that second-generation TKI treatment was an independent prognostic factor affecting TFR in patients who discontinued TKI (RR=1.827, 95%CI 1.015-3.288, P=0.044) . Conclusion: In the clinical setting, more CML patients rapidly achieved TFR using second-generation TKI than IM treatment. 目的： 观察真实世界中酪氨酸激酶抑制剂（TKI）治疗慢性髓性白血病（CML）停药患者的无治疗缓解（treatment free remission, TFR）情况，及二代TKI在TFR方面是否优于伊马替尼（IM）。 方法： 对来自国内8家血液病治疗中心的自2013年6月至2021年3月期间停用TKI且有明确停药结局和相对完整临床资料的274例CML患者进行回顾性分析，使用单因素分析和多因素Cox比例风险回归模型评估影响CML患者停药后TFR结局的危险因素。 结果： 274例患者，女性140例（51.1%），停药时中位年龄48（9~84）岁。停药前，172例（62.8%）患者应用IM治疗，102例（37.2%）接受过二代TKI治疗，包括73例IM转换二代TKI者和29例一线二代TKI治疗者。转换二代TKI的原因包括：37例因追求TFR在IM治疗获得深层分子学反应（DMR）期间转换二代TKI、7例因IM不良反应不耐受、29例因TKI治疗未达最佳治疗反应。接受过二代TKI者末次应用TKI类型包括：尼洛替尼96例（94.1%），达沙替尼3例（2.9%），氟马替尼2例（2.0%），1例为二代TKI不耐受再次更换为IM治疗。IM治疗组和二代TKI治疗组在确诊时中位年龄、停药时中位年龄、性别、Sokal评分、TKI治疗前是否应用干扰素、TKI治疗至获得DMR中位时间、停药原因等基线特征差异均无统计学意义（P值均>0.05）。停药前TKI中位累积治疗时间（71.5个月对88个月，P\u003C0.001）、末次TKI中位治疗时间（60个月对88个月，P\u003C0.001）、DMR中位持续时间（58个月对66个月，P=0.002），二代TKI治疗组均较IM治疗组显著缩短。停药后中位随访22（6~118）个月，88例（32.1%）患者在中位6（1~91）个月失去主要分子学反应（MMR），其中53例（60.2%）患者在≤6个月内失去MMR，总体的TFR率67.9%，12个月和24个月的累积TFR率分别为70.5%和67.5%。26例（9.5%）患者发生停药综合征。72例（83.7%）重启TKI治疗患者在中位治疗4（1~18）个月再次获得DMR。单因素分析结果显示，停药前应用二代TKI治疗组患者的TFR率显著高于IM治疗组（77.5%对62.2%，P=0.041）。进一步亚组分析发现，IM转换二代TKI治疗组患者的TFR率显著高于IM治疗组（80.8%对62.2%，P=0.026），二代TKI一线治疗组和IM治疗组TFR率差异无统计学意义（69.0%对62.2%，P=0.599）。多因素分析结果显示，应用二代TKI治疗是影响停药患者TFR的独立预后因素（RR=1.827，95%CI 1.015~3.288，P=0.044）。 结论： 真实世界中，二代TKI治疗较IM治疗使更多的CML患者更早获得更好的TFR。. Keywords: Deprescriptions; Imatinib; Leukemia, myeloid, chronic; Second-generation tyrosine kinase inhibitors; Treatment free remission.","[Observational study of chronic myeloid leukemia Chinese patients who discontinued tyrosine kinase inhibitors in the real-world]","https:\u002F\u002Fcdn-tap.talkmed.com\u002F202611130556\u002F13b3cc2e58e3c758cb70c47049a94bf6\u002F2026\u002F01\u002F08\u002Fca05df16be2aa5ca6db32eacc8ad2e0ce0b79087.pdf","168644","\u003Cspan>\u003Cb>Objective:\u003C\u002Fb> This study aimed to observe whether the treatment-free remission (TFR) of second-generation tyrosine kinase inhibitors (TKI) in chronic myeloid leukemia (CML) is better than imatinib (IM) . \u003Cb>Methods:\u003C\u002Fb> The clinical data of 274 CML patients who discontinued treatment and with co\u003C\u002Fspan> …","https:\u002F\u002Fpubmed-ncbi-nlm-nih.talkmed.com\u002F?term=Flumatinib+as+first-line+treatment+for+chronic+myeloid+leukemia&page=2&size=10&format=abstract","\u003Cp>\n      \n      \u003Cb>Objective:\u003C\u002Fb> This study aimed to observe whether the treatment-free remission (TFR) of second-generation tyrosine kinase inhibitors (TKI) in chronic myeloid leukemia (CML) is better than imatinib (IM) . \u003Cb>Methods:\u003C\u002Fb> The clinical data of 274 CML patients who discontinued treatment and with complete clinical data were retrospectively studied from June 2013 to March 2021. Using both univariate and multivariate Cox proportional hazards regression models, risk factors influencing TFR outcomes after drug withdrawal in CML patients were assessed. \u003Cb>Results:\u003C\u002Fb> A total of 274 patients were enrolled, 140 patients were women (51.1%) , with a median age of 48 (9-84) years at the time of TKI discontinuation. Prior to TKI discontinuation, 172 (62.8%) patients were treated with IM, and 102 (37.2%) had received second-generation TKI treatment, including 73 patients who had shifted from IM to a second-generation TKI and 29 patients who used second-generation TKI as the first-line treatment. The rationale for converting to a second-generation TKI are as follows: 37 patients aimed deep molecular response (DMR) to achieve TFR, seven patients changed due to IM intolerance, and 29 patients changed because of failure to achieve the optimal treatment response. The use of the last type of TKI included 96 patients (94.1%) with nilotinib, three patients (2.9%) with dasatinib, and two patients (2%) with flumatinib, including one patient who changed to IM due to second-generation TKI intolerance. No statistical differences were found in the median age at diagnosis and TKI discontinuation, sex, Sokal score, IFN treatment before TKI, median time of TKI treatment to achieve DMR, and the reasons for TKI discontinuation between the second TKI and IM (\u003Ci>P\u003C\u002Fi>>0.05) .The median cumulative treatment time of TKI (71.5 months \u003Ci>vs\u003C\u002Fi> 88 months, \u003Ci>P\u003C\u002Fi><0.001) , the last TKI median treatment time (60 months \u003Ci>vs\u003C\u002Fi> 88 months, \u003Ci>P\u003C\u002Fi><0.001) , and the median duration of DMR (58 months \u003Ci>vs\u003C\u002Fi> 66 months, \u003Ci>P\u003C\u002Fi>=0.002) were significantly shorter in the second-generation TKI compared with IM. In the median follow-up of 22 (6-118) months after TKI discontinuation, 88 patients (32.1%) had lost their MMR at a median of 6 (1-91) months; of the 53 patients (60.2%) who lost MMR within 6 months, the overall TFR rate was 67.9%, and the cumulative TFR rates at 12 and 24 months were 70.5% and 67.5%, respectively. Withdrawal syndrome occurred in 26 patients (9.5%) . For patients who restarted TKI treatment, 72 patients (83.7%) achieved DMR again at a median treatment of 4 (1 to 18) months. The univariate analysis showed that the TFR rate of patients treated with second-generation TKI was significantly higher than those who were treated with IM (77.5% \u003Ci>vs\u003C\u002Fi> 62.2%, \u003Ci>P\u003C\u002Fi>=0.041) . A further subgroup analysis found that the TFR rate of the second-generation TKI patients was significantly higher than those treated with IM (80.8% \u003Ci>vs\u003C\u002Fi> 62.2%, \u003Ci>P\u003C\u002Fi>=0.026) . No significant difference was found in the second-generation TKI used as the first line treatment compared with those who were treated with IM (69.0% \u003Ci>vs\u003C\u002Fi> 62.2%, \u003Ci>P\u003C\u002Fi>=0.599) . The multivariate analysis results showed that second-generation TKI treatment was an independent prognostic factor affecting TFR in patients who discontinued TKI (\u003Ci>RR\u003C\u002Fi>=1.827, 95%\u003Ci>CI\u003C\u002Fi> 1.015-3.288, \u003Ci>P\u003C\u002Fi>=0.044) . \u003Cb>Conclusion:\u003C\u002Fb> In the clinical setting, more CML patients rapidly achieved TFR using second-generation TKI than IM treatment.\n    \u003C\u002Fp>","PMC9593009","402053","Zhonghua Xue Ye Xue Za Zhi","10.3760\u002Fcma.j.issn.0253-2727.2022.08.004","Zhonghua Xue Ye Xue Za Zhi. 2022 Aug 14;43(8):636-643. doi: 10.3760\u002Fcma.j.issn.0253-2727.2022.08.004.","[\"https:\u002F\u002Fwww.yiigle.com\u002FLinkIn.do?linkin_type=pubmed&DOI=10.3760\u002Fcma.j.issn.0253-2727.2022.08.004\",\"https:\u002F\u002Feuropepmc.org\u002Fabstract\u002FMED\u002F36709147\",\"https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F36709147\u002F\",false]","Keywords: Deprescriptions; Imatinib; Leukemia, myeloid, chronic; Second-generation tyrosine kinase inhibitors; Treatment free remission.","36709147",[1113,1115,1117,1119,1121,1123,1125,1127,1129,1131,1133],{"name":1114},"H F Zhao",{"name":1116},"Y F Yang",{"name":1118},"B C Liu",{"name":1120},"W M Li",{"name":1122},"N Xu",{"name":1124},"X L Liu",{"name":1126},"Q Jiang",{"name":1128},"H B Dang",{"name":1130},"L X Liang",{"name":1132},"Yanli Zhang",{"name":1134},"Y P Song","https:\u002F\u002Fdoi.org\u002F10.3760\u002Fcma.j.issn.0253-2727.2022.08.004","2026\u002F01\u002F08\u002Fca05df16be2aa5ca6db32eacc8ad2e0ce0b79087.pdf",{"score":649,"jcr":1138,"q":651,"uuid":1139,"full_author":1140,"abstract_text":1141,"title":1142,"file_path":1143,"file_id":1144,"snippet":1145,"type":659,"year_jcr":1146,"abstract":1141,"pmcid":1172,"id":1173,"journal":1174,"doi":1175,"full_journal":1176,"link":1177,"free":61,"keyword":1178,"imf":1179,"pmid":1180,"author":1181,"doi_source_url":1200,"is_favorite":59,"is_lib":59,"file_status":39,"path":1201,"pdf_url":1200},"Thoracic Cancer","191dfba1-05c4-3a23-a98e-0032dfe85cb0","Bora Lee,Wonjun Ji,Jae Cheol Lee,Si Yeol Song,Young Seob Shin,Young Hyun Cho,Ji Eun Park,Hyungjun Park,Chang-Min Choi","Abstract Introduction: Non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) mutation has a higher incidence of brain metastases than wild-type EGFR mutations. Osimertinib, a third-generation EGFR tyrosine kinase inhibitor (TKI), targets both EGFR-TKI sensitizing and T790M-resistance mutations and has a higher brain penetration rate relative to first- and second-generation EGFR-TKIs. Therefore, osimertinib has become a preferred first-line therapy for advanced EGFR mutation-positive NSCLC. However, lazertinib, an emerging EGFR-TKI, has shown higher selectivity toward EGFR mutations and improved penetration of the blood-brain barrier compared to osimertinib in preclinical studies. This trial will evaluate the efficacy of lazertinib as a first-line therapy in patients with EGFR mutation-positive NSCLC who have brain metastases, with or without additional local therapy. Methods: This is a single-center, open-label, single-arm phase II trial. A total of 75 patients with advanced EGFR mutation-positive NSCLC will be recruited. Eligible patients will receive oral lazertinib 240 mg, once daily until disease progression or intolerable toxicity is detected. Patients with moderate to severe symptoms related to brain metastasis will simultaneously receive local therapy for the brain. The primary endpoints are progression-free survival and intracranial progression-free survival. Discussion: Lazertinib, in combination with local therapy for the brain, if necessary, is expected to improve the clinical benefit in advanced EGFR mutation-positive NSCLC with brain metastases, as a first-line treatment. Keywords: brain metastases; epidermal growth factor receptor; lazertinib; non-small cell lung cancer.","Efficacy of lazertinib for symptomatic or asymptomatic brain metastases in treatment-naive patients with advanced EGFR mutation-positive non-small cell lung cancer: Protocol of an open-label, single-arm phase II trial","https:\u002F\u002Fcdn-tap.talkmed.com\u002F202611130556\u002Fbc52d7b5d64920dc683bae56e60d9029\u002F2024\u002F12\u002F17\u002F097a73b2d8ddf3d5899cd461193f9920d3f3f319.pdf","47700","Abstract Introduction: Non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) mutation has a higher incidence of brain metastases than wild-type EGFR mutations.",[1147,1153,1158,1163,1168],{"jcrYear":662,"jif":1148,"quartile":651,"category":1149},3.5,[1150,1151],{"category":722,"source":668,"quartile":664},{"category":1152,"source":668,"quartile":651},"RESPIRATORY SYSTEM",{"jcrYear":670,"jif":1154,"quartile":664,"category":1155},3.223,[1156,1157],{"category":722,"source":668,"quartile":664},{"category":1152,"source":668,"quartile":664},{"jcrYear":675,"jif":1159,"quartile":664,"category":1160},2.9,[1161,1162],{"category":722,"source":668,"quartile":664},{"category":1152,"source":668,"quartile":664},{"jcrYear":680,"jif":1164,"quartile":651,"category":1165},2.3,[1166,1167],{"category":722,"quartile":664},{"category":1152,"quartile":651},{"jcrYear":685,"jif":1164,"quartile":651,"category":1169},[1170,1171],{"category":722,"quartile":664},{"category":1152,"quartile":651},"PMC10396779","116570","Thorac Cancer","10.1111\u002F1759-7714.15018","Thorac Cancer. 2023 Aug;14(22):2233-2237.doi: 10.1111\u002F1759-7714.15018.","https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002F1759-7714.15018,https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F37365915\u002F","Keywords: brain metastases; epidermal growth factor receptor; lazertinib; non-small cell lung cancer.","2.3","37365915",[1182,1184,1186,1188,1190,1192,1194,1196,1198],{"name":1183},"Bora Lee",{"name":1185},"Wonjun Ji",{"name":1187},"Jae Cheol Lee",{"name":1189},"Si Yeol Song",{"name":1191},"Young Seob Shin",{"name":1193},"Young Hyun Cho",{"name":1195},"Ji Eun Park",{"name":1197},"Hyungjun Park",{"name":1199},"Chang-Min Choi","https:\u002F\u002Fdoi.org\u002F10.1111\u002F1759-7714.15018","2024\u002F12\u002F17\u002F097a73b2d8ddf3d5899cd461193f9920d3f3f319.pdf",{"score":649,"jcr":1203,"q":824,"uuid":1204,"full_author":1205,"abstract_text":1206,"title":1207,"file_path":1208,"file_id":1209,"snippet":1210,"type":659,"year_jcr":1211,"abstract":1206,"pmcid":1243,"id":1244,"journal":1245,"doi":1246,"full_journal":1247,"link":1248,"free":61,"keyword":1249,"imf":1250,"pmid":1251,"author":1252,"doi_source_url":1277,"is_favorite":59,"is_lib":59,"file_status":39,"path":1278,"pdf_url":1277},"JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM","1b82518a-3c73-322e-946e-2113a951372a","Andrea Varrone,Katarina Varnäs,Aurelija Jucaite,Zsolt Cselényi,Peter Johnström,Magnus Schou,Ana Vazquez-Romero,Mohammad M Moein,Christer Halldin,Andrew P Brown,Karthick Vishwanathan,Lars Farde","Abstract Osimertinib is a tyrosine kinase inhibitor (TKI) of the mutated epidermal growth factor receptor (EGFRm) with observed efficacy in patients with brain metastases. Brain exposure and drug distribution in tumor regions are important criteria for evaluation and confirmation of CNS efficacy. The aim of this PET study was therefore to determine brain distribution and exposure of 11C-labelled osimertinib administered intravenously in subjects with an intact blood-brain barrier. Eight male healthy subjects (age 52 ± 8 years) underwent one PET measurement with 11C-osimertinib. The pharmacokinetic parameters Cmax(brain) (standardized uptake value), Tmax(brain) and AUC0-90 minbrain\u002Fblood ratio were calculated. The outcome measure for 11C-osimertinib brain exposure was the total distribution volume (VT). 11C-osimertinib distributed rapidly to the brain, with higher uptake in grey than in white matter. Mean Cmax, Tmax and AUC0-90 minbrain\u002Fblood ratio were 1.5 (range 1-1.8), 13 min (range 5-30 min), and 3.8 (range 3.3-4.1). Whole brain and white matter VT were 14 mL×cm-3 (range 11-18) and 7 mL×cm-3 (range 5-12). This study in healthy volunteers shows that 11C-osimertinib penetrates the intact blood-brain barrier. The approach used further illustrates the role of molecular imaging in facilitating the development of novel drugs for the treatment of malignancies affecting the brain. Keywords: Brain metastasis; PET; blood–brain barrier; epidermal growth factor receptor; microdose.","A PET study in healthy subjects of brain exposure of 11C-labelled osimertinib - A drug intended for treatment of brain metastases in non-small cell lung cancer","https:\u002F\u002Fcdn-tap.talkmed.com\u002F202611130556\u002F9253e703204001bb69769f5169c54807\u002F2024\u002F12\u002F19\u002F502eaad1d86f78d4205dc1c900d9d3bd31e9df4c.pdf","62455","Abstract Osimertinib is a tyrosine kinase inhibitor (TKI) of the mutated epidermal growth factor receptor (EGFRm) with observed efficacy in patients with brain metastases.",[1212,1220,1226,1231,1237],{"jcrYear":662,"jif":1213,"quartile":824,"category":1214},6.2,[1215,1217,1218],{"category":1216,"source":668,"quartile":824},"ENDOCRINOLOGY & METABOLISM",{"category":838,"source":668,"quartile":824},{"category":1219,"source":668,"quartile":824},"NEUROSCIENCES",{"jcrYear":670,"jif":1221,"quartile":824,"category":1222},6.597,[1223,1224,1225],{"category":1216,"source":668,"quartile":824},{"category":838,"source":668,"quartile":651},{"category":1219,"source":668,"quartile":824},{"jcrYear":675,"jif":939,"quartile":824,"category":1227},[1228,1229,1230],{"category":1216,"source":668,"quartile":824},{"category":838,"source":668,"quartile":824},{"category":1219,"source":668,"quartile":824},{"jcrYear":680,"jif":1232,"quartile":824,"category":1233},4.9,[1234,1235,1236],{"category":1216,"quartile":824},{"category":838,"quartile":824},{"category":1219,"quartile":824},{"jcrYear":685,"jif":1238,"quartile":824,"category":1239},4.5,[1240,1241,1242],{"category":1216,"quartile":651},{"category":838,"quartile":824},{"category":1219,"quartile":824},"PMC7168784","146893","J Cereb Blood Flow Metab","10.1177\u002F0271678X19843776","J Cereb Blood Flow Metab. 2020 Apr;40(4):799-807.doi: 10.1177\u002F0271678X19843776.","https:\u002F\u002Fjournals.sagepub.com\u002Fdoi\u002F10.1177\u002F0271678X19843776?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub  0pubmed,https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F31006308\u002F","Keywords: Brain metastasis; PET; blood–brain barrier; epidermal growth factor receptor; microdose.","4.5","31006308",[1253,1255,1257,1259,1261,1263,1265,1267,1269,1271,1273,1275],{"name":1254},"Andrea Varrone",{"name":1256},"Katarina Varnäs",{"name":1258},"Aurelija Jucaite",{"name":1260},"Zsolt Cselényi",{"name":1262},"Peter Johnström",{"name":1264},"Magnus Schou",{"name":1266},"Ana Vazquez-Romero",{"name":1268},"Mohammad M Moein",{"name":1270},"Christer Halldin",{"name":1272},"Andrew P Brown",{"name":1274},"Karthick Vishwanathan",{"name":1276},"Lars Farde","https:\u002F\u002Fdoi.org\u002F10.1177\u002F0271678x19843776","2024\u002F12\u002F19\u002F502eaad1d86f78d4205dc1c900d9d3bd31e9df4c.pdf",["Reactive",1280],[1281,1441,1511,1595,1695,1771,1878,1986,2099,2192],{"id":1282,"content":1283,"user_id":1284,"type":61,"is_draft":59,"doc_id":1285,"view_count":1286,"like_count":59,"created_at":1287,"publish_at":1288,"uuid":1289,"company_id":59,"ask_content":1290,"user":1295,"department":1298,"doc":1303,"like":278,"favor":278,"follow_user":278,"tag":1429},343,"PARTNER试验评估了奥拉帕利在gBRCA野生型的三阴性乳腺癌（TNBC）患者中的疗效，研究表明，奥拉帕利与卡铂\u002F紫杉醇和蒽环类药物化疗联合使用时，并未改善病理完全缓解率（pCR）、无事件生存期（EFS）或总生存期（OS），即在gBRCA野生型TNBC患者的标准化疗中加入奥拉帕利没有提供额外的益处。",3834260,44647,364,"1712814100",1712814100,"4965e3f6-10c4-4a6e-b91b-0cb641d8395f",[1291],{"id":1292,"is_history":65,"is_question":44,"message":1293,"created_at":1294},"ai_3951","关键信息：\n-\tPARTNER试验评估了奥拉帕利在gBRCA野生型的三阴性乳腺癌（TNBC）患者中的疗效。\n-\t在gBRCA野生型的TNBC患者中，奥拉帕利与卡铂\u002F紫杉醇和蒽环类药物化疗联合使用时，并未改善病理完全缓解率（pCR）、无事件生存期（EFS）或总生存期（OS）。\n-\t该研究强调了基于TNBC患者遗传特征的治疗反应的潜在差异。\n\n背景及方法：\n-\t奥拉帕利可有效治疗具有BRCA1或BRCA2（gBRCAm）种系致病变异的女性乳腺癌患者。\n-\tPARTNER试验纳入gBRCA野生型的基底样型TNBC患者。\n-\tTNBC的标准治疗方法是蒽环类药物和紫杉烷类化疗，卡铂在新辅助治疗试验中显示出对标准治疗的潜在前景。\n-\t奥拉帕利在卡铂和紫杉醇之后进行新辅助治疗，然后在手术前进行含蒽环类药物的化疗。\n\n主要发现：\n-\t研究组（添加奥拉帕利）和对照组的病理完全缓解率（pCR）、无事件生存期（EFS）和总生存期（OS）相似。\n-\t与未达到pCR的患者相比，达到pCR的患者的EFS和OS显著更高。\n-\t该研究表明，奥拉帕利在gBRCA野生型TNBC患者的标准化疗中加入时没有提供额外的益处。\n\n意义：\n-\t结果表明，奥拉帕利治疗的潜在益处可能因TNBC患者的遗传特征而异。\n-\t了解TNBC肿瘤的分子特征，包括同源重组修复缺陷（HRD），对于识别可能受益于多腺苷二磷酸核糖聚合酶（PARP）抑制剂等靶向治疗的患者至关重要。\n-\t需要进一步的研究来探索基于TNBC患者的基因组成和肿瘤特征的个性化治疗方法。","1712734343",{"id":1284,"nickname":1296,"avatar":1297,"is_me":59},"TAP Voice 肿瘤","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002F4bab8184a0230c85905751a50ca57812\u002F2024\u002F03\u002F22\u002F6d9cba7e92f2d3a3c0bee8968c781d613b951e95.jpg",[1299],{"id":1300,"title":1301,"icon":1302},59,"肿瘤科","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002Fa18068a2ae510b95a243a3c52e9554b5\u002F2023\u002F03\u002F29\u002F49feeec84c0a85fc6be5f64d01e0aac482c4ebd5.png",{"jcr":1304,"q":824,"uuid":1305,"full_author":1306,"abstract_text":1307,"title":1308,"year_jcr":1309,"pmcid":1331,"id":1332,"full_journal":1333,"doi":1334,"link":1335,"free":61,"keyword":63,"imf":1336,"author":1337,"doi_source_url":1428},"NATURE","5f2b0888-cb44-39e9-9afe-c6086ac767c1","Jean E Abraham,Karen Pinilla,Alimu Dayimu,Louise Grybowicz,Nikolaos Demiris,Caron Harvey,Lynsey M Drewett,Rebecca Lucey,Alexander Fulton,Anne N Roberts,Joanna R Worley,Anita Chhabra,Wendi Qian,Anne-Laure Vallier,Richard M Hardy,Steve Chan,Tamas Hickish,Devashish Tripathi,Ramachandran Venkitaraman,Mojca Persic,Shahzeena Aslam,Daniel Glassman,Sanjay Raj,Annabel Borley,Jeremy P Braybrooke,Stephanie Sutherland,Emma Staples,Lucy C Scott,Mark Davies,Cheryl A Palmer,Margaret Moody,Mark J Churn,Jacqueline C Newby,Mukesh B Mukesh,Amitabha Chakrabarti,Rebecca R Roylance,Philip C Schouten,Nicola C Levitt,Karen McAdam,Anne C Armstrong,Ellen R Copson,Emma McMurtry,Marc Tischkowitz,Elena Provenzano,Helena M Earl","Abstract PARTNER is a prospective, phase II-III, randomized controlled clinical trial that recruited patients with triple-negative breast cancer1,2, who were germline BRCA1 and BRCA2 wild type3. Here we report the results of the trial. Patients (n = 559) were randomized on a 1:1 basis to receive neoadjuvant carboplatin-paclitaxel with or without 150 mg olaparib twice daily, on days 3 to 14, of each of four cycles (gap schedule olaparib, research arm) followed by three cycles of anthracycline-based chemotherapy before surgery. The primary end point was pathologic complete response (pCR)4, and secondary end points included event-free survival (EFS) and overall survival (OS)5. pCR was achieved in 51% of patients in the research arm and 52% in the control arm (P = 0.753). Estimated EFS at 36 months in the research and control arms was 80% and 79% (log-rank P > 0.9), respectively; OS was 90% and 87.2% (log-rank P = 0.8), respectively. In patients with pCR, estimated EFS at 36 months was 90%, and in those with non-pCR it was 70% (log-rank P \u003C 0.001), and OS was 96% and 83% (log-rank P \u003C 0.001), respectively. Neoadjuvant olaparib did not improve pCR rates, EFS or OS when added to carboplatin-paclitaxel and anthracycline-based chemotherapy in patients with triple-negative breast cancer who were germline BRCA1 and BRCA2 wild type. ClinicalTrials.gov ID: NCT03150576 .","The PARTNER trial of neoadjuvant olaparib with chemotherapy in triple-negative breast cancer",[1310,1315,1319,1323,1327],{"jcrYear":662,"jif":1311,"quartile":824,"category":1312},49.962,[1313],{"category":1314,"source":668,"quartile":824},"MULTIDISCIPLINARY SCIENCES",{"jcrYear":670,"jif":1316,"quartile":824,"category":1317},69.504,[1318],{"category":1314,"source":668,"quartile":824},{"jcrYear":675,"jif":1320,"quartile":824,"category":1321},64.8,[1322],{"category":1314,"source":668,"quartile":824},{"jcrYear":680,"jif":1324,"quartile":824,"category":1325},50.5,[1326],{"category":1314,"quartile":824},{"jcrYear":685,"jif":1328,"quartile":824,"category":1329},48.5,[1330],{"category":1314,"quartile":824},"PMC11136660","44647","Nature. 2024 May;629(8014):1142-1148.doi: 10.1038\u002Fs41586-024-07384-2.","10.1038\u002Fs41586-024-07384-2","https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41586-024-07384-2,https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F38588696\u002F","48.5",[1338,1340,1342,1344,1346,1348,1350,1352,1354,1356,1358,1360,1362,1364,1366,1368,1370,1372,1374,1376,1378,1380,1382,1384,1386,1388,1390,1392,1394,1396,1398,1400,1402,1404,1406,1408,1410,1412,1414,1416,1418,1420,1422,1424,1426],{"name":1339},"Jean E Abraham",{"name":1341},"Karen Pinilla",{"name":1343},"Alimu Dayimu",{"name":1345},"Louise Grybowicz",{"name":1347},"Nikolaos Demiris",{"name":1349},"Caron Harvey",{"name":1351},"Lynsey M Drewett",{"name":1353},"Rebecca Lucey",{"name":1355},"Alexander Fulton",{"name":1357},"Anne N Roberts",{"name":1359},"Joanna R Worley",{"name":1361},"Anita Chhabra",{"name":1363},"Wendi Qian",{"name":1365},"Anne-Laure Vallier",{"name":1367},"Richard M Hardy",{"name":1369},"Steve Chan",{"name":1371},"Tamas Hickish",{"name":1373},"Devashish Tripathi",{"name":1375},"Ramachandran Venkitaraman",{"name":1377},"Mojca Persic",{"name":1379},"Shahzeena Aslam",{"name":1381},"Daniel Glassman",{"name":1383},"Sanjay Raj",{"name":1385},"Annabel Borley",{"name":1387},"Jeremy P Braybrooke",{"name":1389},"Stephanie Sutherland",{"name":1391},"Emma Staples",{"name":1393},"Lucy C Scott",{"name":1395},"Mark Davies",{"name":1397},"Cheryl A Palmer",{"name":1399},"Margaret Moody",{"name":1401},"Mark J Churn",{"name":1403},"Jacqueline C Newby",{"name":1405},"Mukesh B Mukesh",{"name":1407},"Amitabha Chakrabarti",{"name":1409},"Rebecca R Roylance",{"name":1411},"Philip C Schouten",{"name":1413},"Nicola C Levitt",{"name":1415},"Karen McAdam",{"name":1417},"Anne C Armstrong",{"name":1419},"Ellen R Copson",{"name":1421},"Emma McMurtry",{"name":1423},"Marc Tischkowitz",{"name":1425},"Elena Provenzano",{"name":1427},"Helena M Earl","https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41586-024-07384-2",[1430,1432,1435,1438],{"id":1431,"name":27},70,{"id":1433,"name":1434},11451,"奥拉帕利",{"id":1436,"name":1437},6751,"TNBC",{"id":1439,"name":1440},11452,"gBRCA野生型",{"id":1442,"content":1443,"user_id":1444,"type":61,"is_draft":59,"doc_id":1445,"view_count":1446,"like_count":59,"created_at":1447,"publish_at":1448,"uuid":1449,"company_id":59,"ask_content":1450,"user":1455,"department":1458,"doc":1459,"like":278,"favor":278,"follow_user":278,"tag":1510},25,"最新的一项单中心研究，PP的生物制剂治疗的drug survival rate高于非生物制剂",3101419,10656,272,"1704428576",1704428576,"047a2434-bb33-4a82-be70-2655b90d1f45",[1451],{"id":1452,"is_history":65,"is_question":44,"message":1453,"created_at":1454},"ai_652","The document titled \"Drug survival of biologics and non-biologics in patients affected by palmoplantar psoriasis: a 'real-world', mono-center experience\" discusses the treatment and drug survival rates of biologic and non-biologic drugs in patients with palmoplantar psoriasis (PP). The study aims to evaluate the clinical and demographic characteristics of patients with PP and compare the drug survival rates between biologic and non-biologic drugs. The analysis includes data from 233 psoriasis patients with palmoplantar involvement. The main findings of the study are as follows:\n\n- Biologic drugs are associated with higher persistence in treatment compared to non-biologic drugs.\n- Anti-IL23 drugs have the best overall drug survival rate, with 67.94% of patients still on these drugs at 60 months.\n- Non-biologic drugs are associated with an increased risk of treatment discontinuation compared to biological drugs.\n- The study confirms the difficulty of treating PP and suggests that biologic drugs have better treatment persistence due to their better safety profile, rather than their higher effectiveness.\n\nKey Points:\n- Limited data is available on the treatment of palmoplantar psoriasis (PP) as these patients are often excluded from clinical trials.\n- PP is often resistant to treatment, making its clinical management complex.\n- Biologic drugs have higher treatment persistence compared to non-biologic drugs in patients with PP.\n- Anti-IL23 drugs have the best overall drug survival rate.\n- Non-biologic drugs are associated with an increased risk of treatment discontinuation.\n- Biologic drugs have better treatment persistence due to their better safety profile, rather than their higher effectiveness.","1704428083",{"id":1444,"nickname":1456,"avatar":1457,"is_me":59},"阿钟","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002F87cc54b53c9ca9b348fe424d612fb09a\u002F2025\u002F03\u002F24\u002Fc9fe8d26-e8ec-79c3-7511-a39ee20c3e7b.jpg",[],{"jcr":1460,"q":824,"uuid":1461,"full_author":1462,"abstract_text":1463,"title":1464,"year_jcr":1465,"pmcid":63,"id":1486,"full_journal":1487,"doi":1488,"link":1489,"free":59,"keyword":63,"imf":1490,"author":1491,"doi_source_url":1489},"INTERNATIONAL JOURNAL OF DERMATOLOGY","29073f00-7e59-3274-a811-95c9734f4f42","Giacomo Caldarola,Gennaro Marco Falco,Laura Calabrese,Alessandra D'Amore,Andrea Chiricozzi,Marco Mariani,Gerardo Palmisano,Clara De Simone,Ketty Peris","Abstract Background: Data on the treatment of palmoplantar psoriasis (PP) are very limited as these patients are often excluded from clinical trials. Moreover, this form of psoriasis is often resistant to treatment, making its clinical management complex. Methods: Primary endpoint was to evaluate the clinical and demographic characteristics and the drug survival of both biological and non-biological drugs in a population affected by PP. Secondary endpoint was to highlight any differences between the hyperkeratotic and pustular variant. We analyzed data from 233 psoriasis patients with palmoplantar involvement, with or without chronic plaque psoriasis. We performed a drug-survival analysis with the aid of Kaplan-Meier survival and a multivariate analysis to highlight the influence of certain variables on treatment persistence using a Cox regression model. Results: The drug-survival analysis revealed that biologic drugs compared to non-biologic drugs are associated with a higher persistence in treatment (59.73 vs. 43.56%); in particular, anti-IL23 drugs were found to be the drugs with the best drug-survival overall (67.94% of patients at 60 months are still on these drugs). Furthermore, our multivariate analysis shows that when compared with biological drugs, non-biological drugs are associated with an increased risk of treatment discontinuation (HR = 1.95 [95% CI: 1.41-2.68], P = 0.001). Conclusions: Our study confirms the difficulty of treating PP and shows that biologic drugs are associated with longer persistence in treatment than non-biologics in both PP's variants, not because of their higher effectiveness but because of their better safety profile.","Drug survival of biologics and non-biologics in patients affected by palmoplantar psoriasis: a \"real-world\", mono-center experience",[1466,1471,1475,1479,1482],{"jcrYear":662,"jif":1467,"quartile":664,"category":1468},2.736,[1469],{"category":1470,"source":668,"quartile":664},"DERMATOLOGY",{"jcrYear":670,"jif":1472,"quartile":651,"category":1473},3.204,[1474],{"category":1470,"source":668,"quartile":651},{"jcrYear":675,"jif":1476,"quartile":824,"category":1477},3.6,[1478],{"category":1470,"source":668,"quartile":824},{"jcrYear":680,"jif":1148,"quartile":824,"category":1480},[1481],{"category":1470,"quartile":824},{"jcrYear":685,"jif":1483,"quartile":824,"category":1484},3.2,[1485],{"category":1470,"quartile":824},"10656","Int J Dermatol. 2024 Jan;63(1):51-58.doi: 10.1111\u002Fijd.16917.","10.1111\u002Fijd.16917","https:\u002F\u002Fdoi.org\u002F10.1111\u002Fijd.16917","3.2",[1492,1494,1496,1498,1500,1502,1504,1506,1508],{"name":1493},"Giacomo Caldarola",{"name":1495},"Gennaro Marco Falco",{"name":1497},"Laura Calabrese",{"name":1499},"Alessandra D'Amore",{"name":1501},"Andrea Chiricozzi",{"name":1503},"Marco Mariani",{"name":1505},"Gerardo Palmisano",{"name":1507},"Clara De Simone",{"name":1509},"Ketty Peris",[],{"id":1512,"content":1513,"user_id":1514,"type":61,"is_draft":59,"doc_id":1515,"view_count":1516,"like_count":59,"created_at":1517,"publish_at":1518,"uuid":1519,"company_id":59,"ask_content":1520,"user":1525,"department":1528,"doc":1533,"like":278,"favor":278,"follow_user":278,"tag":1586},555,"本研究表明：不同年龄组患者使用类固醇类药物的情况存在显著差异；研究还指出需要为老年IBD患者提供相应的治疗指南。",3834258,62059,117,"1718848366",1718848366,"f5d18fc3-dc5d-4f98-92cb-258e61e7aca6",[1521],{"id":1522,"is_history":65,"is_question":44,"message":1523,"created_at":1524},"ai_5624","■ 本研究探讨了儿童和老年炎症性肠病（IBD）患者在第一疗程和第二疗程全身类固醇治疗后的治疗模式，并将其与成人IBD进行了比较。\n\n■ 本研究使用丹麦医疗保健登记系统来识别2000-2018年间诊断为克罗恩病（CD，N=14404）或溃疡性结肠炎（UC，N=25735）的患者，将其划分为不同年龄组，并分析用药和手术情况。\n\n■ 本研究发现：①儿童患者使用免疫调节剂和生物制剂的频率较高，而老年患者使用上述药物的频率较低；②即使在接受两个疗程的全身类固醇治疗后，老年患者接受的类固醇保留药物仍然较少；③高度虚弱与老年患者发病时药物使用量较低相关。\n\n■ 本研究表明：不同年龄组患者使用类固醇类药物的情况存在显著差异；研究还指出需要为老年IBD患者提供相应的治疗指南。\n\n\nNordestgaard RLM, Wewer MD, Malham M, Wewer V, Boysen T, Burisch J. Treatment of inflammatory bowel disease with steroid-sparing medications is age-dependent - Results from a Danish nationwide cohort study, 2000-2018. Aliment Pharmacol Ther. Published online June 10, 2024. doi:10.1111\u002Fapt.18106","1718777829",{"id":1514,"nickname":1526,"avatar":1527,"is_me":59},"TAP Voice IBD","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002F44e3cfd6e6472a73080a3a134057f7dc\u002F2024\u002F03\u002F18\u002Fefab46dc3ea151fac501d3c243a9485ef22701b3.jpg",[1529],{"id":1530,"title":1531,"icon":1532},31,"消化内科","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002Fb4285a9bf7558817b93e3ac27ba57c0b\u002F2023\u002F03\u002F29\u002F195b12b64e9fd6cf5ee4499aa5018d102e6dbb4d.png",{"jcr":1534,"q":824,"uuid":1535,"full_author":1536,"title":1537,"list_abstract_url":1538,"year_jcr":1539,"id":1567,"full_journal":1568,"doi":1569,"free":59,"keyword":1570,"imf":1571,"author":1572,"doi_source_url":1585},"ALIMENTARY PHARMACOLOGY & THERAPEUTICS","2b743972-e910-3aaf-9681-53f5ae4504ff","Nordestgaard RLM, Wewer MD, Malham M, Wewer V, Boysen T, Burisch J.","Treatment of \u003Cb>inflammatory\u003C\u002Fb> \u003Cb>bowel\u003C\u002Fb> \u003Cb>disease\u003C\u002Fb> with steroid-sparing medications is age-dependent - Results from a Danish nationwide cohort study, 2000-2018.","https:\u002F\u002Fpubmed.ncbi.nlm.nih.gov\u002F?term=Inflammatory+Bowel+Disease+AND+%22last+14+days%22%5Bdp%5D&page=1&size=100&format=abstract",[1540,1547,1552,1557,1562],{"jcrYear":662,"jif":1541,"quartile":824,"category":1542},8.171,[1543,1545],{"category":1544,"source":668,"quartile":824},"GASTROENTEROLOGY & HEPATOLOGY",{"category":1546,"source":668,"quartile":824},"PHARMACOLOGY & PHARMACY",{"jcrYear":670,"jif":1548,"quartile":824,"category":1549},9.524,[1550,1551],{"category":1544,"source":668,"quartile":824},{"category":1546,"source":668,"quartile":824},{"jcrYear":675,"jif":1553,"quartile":824,"category":1554},7.6,[1555,1556],{"category":1544,"source":668,"quartile":824},{"category":1546,"source":668,"quartile":824},{"jcrYear":680,"jif":1558,"quartile":824,"category":1559},6.6,[1560,1561],{"category":1544,"quartile":824},{"category":1546,"quartile":824},{"jcrYear":685,"jif":1563,"quartile":824,"category":1564},6.7,[1565,1566],{"category":1544,"quartile":824},{"category":1546,"quartile":824},"62059","Aliment Pharmacol Ther. 2024 Jun 10. doi: 10.1111\u002Fapt.18106. Online ahead of print.","10.1111\u002Fapt.18106","Keywords: Crohn’s disease; elderly; epidemiology; paediatrics; ulcerative colitis.","6.7",[1573,1575,1577,1579,1581,1583],{"name":1574},"Nordestgaard RLM",{"name":1576},"Wewer MD",{"name":1578},"Malham M",{"name":1580},"Wewer V",{"name":1582},"Boysen T",{"name":1584},"Burisch J.","https:\u002F\u002Fdoi.org\u002F10.1111\u002Fapt.18106",[1587,1590,1593],{"id":1588,"name":1589},6078,"皮质类固醇",{"id":1591,"name":1592},622,"炎症性肠病",{"id":1594,"name":7},531,{"id":1596,"content":63,"user_id":1597,"type":61,"is_draft":59,"doc_id":1598,"view_count":1599,"like_count":59,"created_at":1600,"publish_at":1601,"uuid":1602,"company_id":59,"ask_content":1603,"user":1608,"department":1610,"doc":1615,"like":278,"favor":278,"follow_user":278,"tag":1685},252,3834044,37798,278,"1711078362",1711078362,"952c4789-2c95-4211-b2ed-56a1ecc71462",[1604],{"id":1605,"is_history":65,"is_question":44,"message":1606,"created_at":1607},"ai_3047","The document discusses a study on the use of mepolizumab, an anti-interleukin-5 monoclonal antibody, in the treatment of eosinophilic granulomatosis with polyangiitis. The study was a multicenter, double-blind, phase 3 trial that aimed to evaluate the efficacy and safety of mepolizumab compared to a placebo in participants with relapsing or refractory eosinophilic granulomatosis with polyangiitis over a 52-week period. The key findings indicate that mepolizumab treatment led to significantly more weeks of remission, a higher proportion of participants in remission, and reduced glucocorticoid use compared to the placebo group. However, only about half of the participants treated with mepolizumab achieved protocol-defined remission. The study highlights the potential of mepolizumab as a treatment option for this condition, emphasizing the need for more effective therapies to reduce reliance on glucocorticoids and immunosuppressive agents.\n\n- Eosinophilic granulomatosis with polyangiitis (EGPA) is a condition characterized by eosinophilic vasculitis and various symptoms.\n- Mepolizumab, an anti-interleukin-5 monoclonal antibody, was studied for its efficacy in treating EGPA.\n- The study was a phase 3 trial involving 136 participants with relapsing or refractory EGPA.\n- Participants were randomized to receive mepolizumab or placebo in addition to standard care for 52 weeks.\n- Primary endpoints included accrued weeks of remission and the proportion of participants in remission at specific time points.\n- Mepolizumab treatment resulted in significantly more weeks of remission, a higher proportion of participants in remission, and reduced glucocorticoid use compared to placebo.\n- The safety profile of mepolizumab was similar to previous studies.\n- The study suggests mepolizumab as a potential treatment option for EGPA, emphasizing the need for more effective therapies to reduce reliance on glucocorticoids and immunosuppressive agents.","1711077919",{"id":1597,"nickname":1609,"avatar":63,"is_me":59},"cc",[1611],{"id":1612,"title":1613,"icon":1614},56,"风湿免疫科","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002F8e742c17b918713f1665d3f94fdf4945\u002F2023\u002F03\u002F29\u002F13ff367712d1baa5b2624ab921b8560c64dbe690.png",{"jcr":1616,"q":824,"uuid":1617,"full_author":1618,"title":1619,"list_abstract_url":1620,"year_jcr":1621,"pmcid":1642,"id":1643,"full_journal":1644,"doi":1645,"free":61,"keyword":63,"imf":1646,"author":1647,"doi_source_url":1684},"NEW ENGLAND JOURNAL OF MEDICINE","4655ffa0-ea51-328d-b018-5cc871bef4e9","Wechsler ME, Akuthota P, Jayne D, Khoury P, Klion A, Langford CA, Merkel PA, Moosig F, Specks U, Cid MC, Luqmani R, Brown J, Mallett S, Philipson R, Yancey SW, Steinfeld J, Weller PF, Gleich GJ; EGPA Mepolizumab Study Team.","\u003Cb>Mepolizumab\u003C\u002Fb> or Placebo for Eosinophilic Granulomatosis with Polyangiitis.","https:\u002F\u002Fpubmed-ncbi-nlm-nih.talkmed.com\u002F?term=Mepolizumab&page=1&size=10&format=abstract",[1622,1626,1630,1634,1638],{"jcrYear":662,"jif":1623,"quartile":824,"category":1624},91.253,[1625],{"category":667,"source":668,"quartile":824},{"jcrYear":670,"jif":1627,"quartile":824,"category":1628},176.082,[1629],{"category":667,"source":668,"quartile":824},{"jcrYear":675,"jif":1631,"quartile":824,"category":1632},158.5,[1633],{"category":667,"source":668,"quartile":824},{"jcrYear":680,"jif":1635,"quartile":824,"category":1636},96.2,[1637],{"category":667,"quartile":824},{"jcrYear":685,"jif":1639,"quartile":824,"category":1640},78.5,[1641],{"category":667,"quartile":824},"PMC5548295","37798","N Engl J Med. 2017 May 18;376(20):1921-1932. doi: 10.1056\u002FNEJMoa1702079.","10.1056\u002FNEJMoa1702079","78.5",[1648,1650,1652,1654,1656,1658,1660,1662,1664,1666,1668,1670,1672,1674,1676,1678,1680,1682],{"name":1649},"Wechsler ME",{"name":1651},"Akuthota P",{"name":1653},"Jayne D",{"name":1655},"Khoury P",{"name":1657},"Klion A",{"name":1659},"Langford CA",{"name":1661},"Merkel PA",{"name":1663},"Moosig F",{"name":1665},"Specks U",{"name":1667},"Cid MC",{"name":1669},"Luqmani R",{"name":1671},"Brown J",{"name":1673},"Mallett S",{"name":1675},"Philipson R",{"name":1677},"Yancey SW",{"name":1679},"Steinfeld J",{"name":1681},"Weller PF",{"name":1683},"Gleich GJ; EGPA Mepolizumab Study Team.","https:\u002F\u002Fdoi.org\u002F10.1056\u002Fnejmoa1702079",[1686,1689,1692],{"id":1687,"name":1688},8949,"免疫科",{"id":1690,"name":1691},162,"临床试验",{"id":1693,"name":1694},947,"未来研究方向",{"id":1696,"content":1697,"user_id":1444,"type":61,"is_draft":59,"doc_id":1698,"view_count":1699,"like_count":59,"created_at":1700,"publish_at":1701,"uuid":1702,"company_id":59,"ask_content":1703,"user":1708,"department":1709,"doc":1710,"like":278,"favor":278,"follow_user":278,"tag":1770},78,"与相邻正常组织相比，NSCLC组织中hsa_circ_0050386的表达水平较低。hsa_circ_0050386的表达水平较低与NSCLC的更晚期相关",16193,267,"1705489742",1705489742,"2d71c92e-193b-429f-b569-cdb1c9ede663",[1704],{"id":1705,"is_history":65,"is_question":44,"message":1706,"created_at":1707},"ai_1017","这篇文章是由Chen等人撰写的研究论文，题为《环状RNA hsa_circ_0050386通过调节SRSF3\u002FFN1轴抑制非小细胞肺癌的进展》。该研究调查了环状RNA hsa_circ_0050386在非小细胞肺癌（NSCLC）进展中的作用。作者发现，与相邻正常组织相比，NSCLC组织中hsa_circ_0050386的表达水平较低。hsa_circ_0050386的表达水平较低与NSCLC的更晚期相关。功能上，hsa_circ_0050386抑制了体外和体内NSCLC细胞的增殖和侵袭。研究还发现，hsa_circ_0050386与RNA结合蛋白SRSF3相互作用，导致Fibronectin 1（FN1）表达下调，从而抑制NSCLC的进展。这些发现表明，hsa_circ_0050386可能作为NSCLC治疗的潜在生物标志物和治疗靶点\n要点\n- 与相邻正常组织相比，NSCLC组织中hsa_circ_0050386的表达水平较低\n- hsa_circ_0050386的表达水平较低与NSCLC的更晚期相关\n- hsa_circ_0050386抑制了体外和体内NSCLC细胞的增殖和侵袭\n- hsa_circ_0050386与RNA结合蛋白SRSF3相互作用，导致FN1表达下调\n- hsa_circ_0050386可能作为NSCLC治疗的潜在生物标志物和治疗靶点。","1705489686",{"id":1444,"nickname":1456,"avatar":1457,"is_me":59},[],{"jcr":1711,"q":824,"uuid":1712,"full_author":1713,"abstract_text":1714,"title":1715,"year_jcr":1716,"pmcid":1737,"id":1738,"full_journal":1739,"doi":1740,"link":1741,"free":61,"keyword":1742,"imf":1743,"author":1744,"doi_source_url":1769},"Journal of Translational Medicine","9e817a3f-b9a2-3c74-8195-1ed435ea8a2f","Jinbin Chen,Boqi Rao,Zeqin Huang,Chen Xie,Yonghui Yu,Binyao Yang,Di Wu,Dedong Wang,Fuman Qiu,Yifeng Zhou,Yibin Deng,Jiachun Lu","Abstract Background: Lung cancer is the most prevalent cancer worldwide, with non-small cell lung cancer (NSCLC) accounting for 85% of all cases. Circular RNAs(circRNA) play crucial roles in regulating the progression of lung cancer. Despite the identification of a large number of circRNAs, their expression patterns, functions, and mechanisms of action in NSCLC development remain unclear.This study aims to investigate the transcriptional expressions, functions, and potential mechanisms of circRNA hsa_circ_0050386 in NSCLC. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized for the analysis of hsa_circ_0050386 expression. Cell proliferation was detected using the IncuCyte Live Cell Analysis System and clone formation assays. Migration and invasion of NSCLC cells were evaluated through Transwell assays. Flow cytometry was performed to assay cell cycle and apoptosis. Western blot was used to investigate protein expression. Protein binding analysis was conducted by employing pull-down assays, RNA immunoprecipitation (RIP), and mass spectrometry. The role of hsa_circ_0050386 in vivo was evaluated through the use of a xenograft model. Results: The study discovered that hsa_circ_0050386 displayed lower expression levels in NSCLC tissues when compared to adjacent normal tissues. Patients exhibiting lower levels of hsa_circ_0050386 expression exhibited an inverse correlation with the Clinical Stage, T-stage, and M-stage of NSCLC. Functionally, hsa_circ_0050386 suppressed the proliferation and invasion of NSCLC cells both in vitro and in vivo. A comprehensive examination exposed the interaction between hsa_circ_0050386 and RNA binding protein Serine and arginine-rich splicing factor 3 (SRSF3), resulting in the down-regulation of Fibronectin 1 (FN1) expression, which inhibits the progression of NSCLC. Conclusions: Our study shows that hsa_circ_0050386 suppresses the malignant biological behavior of NSCLC cells by down-regulating the expression of FN1, and may serve as a potential biomarker and therapeutic target for NSCLC treatment. Keywords: Circular RNA (circRNA); Fibronectin 1 (FN1); Non-small cell lung cancer (NSCLC); Serine and arginine-rich splicing factor 3 (SRSF3).","Circular RNA hsa_circ_0050386 suppresses non-small cell lung cancer progression via regulating the SRSF3\u002FFN1 axis",[1717,1721,1725,1729,1733],{"jcrYear":662,"jif":1718,"quartile":651,"category":1719},5.531,[1720],{"category":988,"source":668,"quartile":651},{"jcrYear":670,"jif":1722,"quartile":824,"category":1723},8.448,[1724],{"category":988,"source":668,"quartile":824},{"jcrYear":675,"jif":1726,"quartile":824,"category":1727},7.4,[1728],{"category":988,"source":668,"quartile":824},{"jcrYear":680,"jif":1730,"quartile":824,"category":1731},6.1,[1732],{"category":988,"quartile":824},{"jcrYear":685,"jif":1734,"quartile":824,"category":1735},7.5,[1736],{"category":988,"quartile":824},"PMC10785521","16193","J Transl Med. 2024 Jan 12;22(1):47.doi: 10.1186\u002Fs12967-023-04812-1.","10.1186\u002Fs12967-023-04812-1","https:\u002F\u002Ftranslational-medicine.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12967-023-04812-1,https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F38216996\u002F","Keywords: Circular RNA (circRNA); Fibronectin 1 (FN1); Non-small cell lung cancer (NSCLC); Serine and arginine-rich splicing factor 3 (SRSF3).","7.5",[1745,1747,1749,1751,1753,1755,1757,1759,1761,1763,1765,1767],{"name":1746},"Jinbin Chen",{"name":1748},"Boqi Rao",{"name":1750},"Zeqin Huang",{"name":1752},"Chen Xie",{"name":1754},"Yonghui Yu",{"name":1756},"Binyao Yang",{"name":1758},"Di Wu",{"name":1760},"Dedong Wang",{"name":1762},"Fuman Qiu",{"name":1764},"Yifeng Zhou",{"name":1766},"Yibin Deng",{"name":1768},"Jiachun Lu","https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs12967-023-04812-1",[],{"id":1772,"content":1773,"user_id":1284,"type":61,"is_draft":59,"doc_id":1774,"view_count":342,"like_count":61,"created_at":1775,"publish_at":1776,"uuid":1777,"company_id":59,"ask_content":1778,"user":1783,"department":1784,"doc":1786,"like":278,"favor":278,"follow_user":278,"tag":1859},20092,"这项研究评估了在既往接受雷莫西尤单抗治疗且出现疾病进展的晚期胃\u002F食管胃结合部癌患者中，雷莫西尤单抗联合伊立替康作为三线或更后线治疗的疗效和安全性，其结果发现，尽管PFS和DCR在联合治疗组有所改善，但OS与伊立替康单药治疗相比并无显著优势。",375978,"1748507710",1748507710,"fdf1fc09-8d09-4b22-8cd3-f18227ce9fe3",[1779],{"id":1780,"is_history":65,"is_question":44,"message":1781,"created_at":1782},"ai_42132","\n关键信息：\nRINDBeRG研究比较了对于既往接受雷莫西尤单抗且出现疾病进展的晚期或复发性胃\u002F食管胃结合部癌患者，雷莫西尤单抗联合伊立替康与伊立替康单药治疗作为三线或后线治疗方案的疗效和安全性。\n这是一项随机对照3期临床研究，共纳入402例在雷莫西尤单抗治疗期间出现疾病进展的患者，随机分配接受雷莫西尤单抗联合伊立替康治疗（n=202）或伊立替康单药治疗（n=200）。研究的主要终点为总生存期（OS），次要终点包括无进展生存期（PFS）、缓解率、疾病控制率（DCR）和安全性。\n研究结果显示，联合治疗组的中位OS为9.4个月，单药治疗组为8.5个月，校正HR为0.91（95% CI，0.74-1.12；P=0.49）。与单药治疗组相比，联合治疗组的PFS显著延长（中位PFS：2.8个月vs. 3.8个月；HR：0.72 [95% CI，0.59-0.89]；P=0.002），DCR显著改善（52.1% vs. 64.4%；P=0.03）。联合治疗组的不良事件可控。\n该研究表明，与伊立替康单药治疗相比，尽管PFS和DCR在联合治疗组有所改善，但未能带来显著的OS获益。\n\n\nSakai D, Kadowaki S, Kawabata R, et al. Randomized Phase III Trial of Ramucirumab Beyond Progression Plus Irinotecan in Patients With Ramucirumab-Refractory Advanced Gastric Cancer: RINDBeRG Trial. J Clin Oncol. Published online May 23, 2025. doi:10.1200\u002FJCO.24.01119","1748400151",{"id":1284,"nickname":1296,"avatar":1297,"is_me":59},[1785],{"id":1300,"title":1301,"icon":1302},{"q":824,"jcr":1787,"uuid":1788,"full_author":1789,"title":1790,"list_abstract_url":1791,"year_jcr":1792,"pmcid":1813,"id":1814,"doi":1815,"full_journal":1816,"free":61,"link":1817,"keyword":63,"imf":1818,"author":1819,"doi_source_url":1858},"JOURNAL OF CLINICAL ONCOLOGY","c9043c55-f199-3f52-b94c-47e9a81d89f1","Sakai D, Kadowaki S, Kawabata R, Hara H, Satake H, Takahashi M, Takeno A, Imai H, Minashi K, Kawakami T, Boku S, Matsuyama J, Sakamoto Y, Sawada K, Kataoka M, Kawakami H, Shimokawa T, Boku N, Satoh T.","Randomized Phase III Trial of Ramucirumab Beyond Progression Plus Irinotecan in Patients With Ramucirumab-Refractory Advanced \u003Cb>Gastric\u003C\u002Fb> \u003Cb>Cancer\u003C\u002Fb>: RINDBeRG Trial.","https:\u002F\u002Fpubmed-ncbi-nlm-nih.talkmed.com\u002F?term=Gastric+Cancer+AND+%28Clinical+Trial%5Bpt%5D%29&page=1&size=100&sort=date&format=abstract",[1793,1797,1801,1805,1809],{"jcrYear":662,"jif":1794,"quartile":824,"category":1795},44.544,[1796],{"category":722,"source":668,"quartile":824},{"jcrYear":670,"jif":1798,"quartile":824,"category":1799},50.739,[1800],{"category":722,"source":668,"quartile":824},{"jcrYear":675,"jif":1802,"quartile":824,"category":1803},45.3,[1804],{"category":722,"source":668,"quartile":824},{"jcrYear":680,"jif":1806,"quartile":824,"category":1807},42.1,[1808],{"category":722,"quartile":824},{"jcrYear":685,"jif":1810,"quartile":824,"category":1811},41.9,[1812],{"category":722,"quartile":824},"PMC12199805","375978","10.1200\u002FJCO.24.01119","J Clin Oncol. 2025 Jul;43(19):2196-2207. doi: 10.1200\u002FJCO.24.01119. Epub 2025 May 23.","[\"https:\u002F\u002Fascopubs.org\u002Fdoi\u002F10.1200\u002FJCO.24.01119?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub  0pubmed\",\"https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F40408613\u002F\"]","41.9",[1820,1822,1824,1826,1828,1830,1832,1834,1836,1838,1840,1842,1844,1846,1848,1850,1852,1854,1856],{"name":1821},"Sakai D",{"name":1823},"Kadowaki S",{"name":1825},"Kawabata R",{"name":1827},"Hara H",{"name":1829},"Satake H",{"name":1831},"Takahashi M",{"name":1833},"Takeno A",{"name":1835},"Imai H",{"name":1837},"Minashi K",{"name":1839},"Kawakami T",{"name":1841},"Boku S",{"name":1843},"Matsuyama J",{"name":1845},"Sakamoto Y",{"name":1847},"Sawada K",{"name":1849},"Kataoka M",{"name":1851},"Kawakami H",{"name":1853},"Shimokawa T",{"name":1855},"Boku N",{"name":1857},"Satoh T.","https:\u002F\u002Fdoi.org\u002F10.1200\u002Fjco.24.01119",[1860,1863,1866,1869,1872,1875],{"id":1861,"name":1862},5385,"胃癌",{"id":1864,"name":1865},18682,"胃食管交界癌",{"id":1867,"name":1868},105579,"抗血管生成治疗",{"id":1870,"name":1871},115592,"伊立替康",{"id":1873,"name":1874},12224,"雷莫西尤单抗",{"id":1876,"name":1877},115633,"跨线治疗",{"id":1879,"content":1880,"user_id":1284,"type":61,"is_draft":59,"doc_id":1881,"view_count":1882,"like_count":59,"created_at":1883,"publish_at":1884,"uuid":1885,"company_id":59,"ask_content":1886,"user":1891,"department":1892,"doc":1894,"like":278,"favor":278,"follow_user":278,"tag":1973},20334,"本研究作为PACE研究的一项辅助分析，将可评估基线CTC的203例患者分为Stage IVindolent组（\u003C5 CTCs\u002F7.5 mL）和Stage IVaggressive组（≥5 CTCs\u002F7.5 mL），并进行ctDNA分析。研究发现，Stage IVindolent组与Stage IVaggressive组的中位PFS分别为5.7个月和3.5个月（P\u003C0.001）。提示CTC检测具有指导治疗决策的潜在临床价值。",386818,126,"1756967373",1756967373,"8b12fbb7-29a6-4522-bed6-178eccc4f34f",[1887],{"id":1888,"is_history":65,"is_question":44,"message":1889,"created_at":1890},"ai_44429","-\t研究评估了循环肿瘤细胞（CTC）计数在细胞周期蛋白依赖性激酶（CDK）4\u002F6抑制剂治疗后进展的激素受体（HR）阳性\u002F人表皮生长因子受体2（HER2）阴性转移性乳腺癌（MBC）患者中的预后预测价值。\n-\t2期PACE研究纳入220例患者，按1:2:1的比例随机分配至氟维司群（F）组、氟维司群+哌柏西利（F+P）组或氟维司群+哌柏西利+avelumab（F+P+A）组。本研究作为PACE研究的一项辅助分析，203例患者可评估基线CTC，基于基线CTC计数将患者分为Stage IVindolent组（\u003C5 CTCs\u002F7.5 mL）和Stage IVaggressive组（≥5 CTCs\u002F7.5 mL），并进行同步循环肿瘤基因（ctDNA）分析。主要研究终点为无进展生存期（PFS）。\n-\t研究发现，Stage IVindolent组与Stage IVaggressive组的中位PFS分别为5.7个月和3.5个月（P\u003C0.001）。在Stage IVaggressive组中，相较F，F+P和F+P+A可改善PFS，而Stage IVindolent组未观察到联合治疗获益。\n-\t研究结果表明，基线CTC计数为HR+\u002FHER2-MBC提供重要预后信息，CTC检测具有指导治疗决策的潜在临床价值。\n\nGerratana L, Reduzzi C, Ren Y, et al. Circulating tumor cells dynamics after CDK4\u002F6 inhibitor for hormone-receptor positive metastatic breast cancer: a biomarker analysis from the PACE phase II study. Clin Cancer Res. Published online August 25, 2025. doi:10.1158\u002F1078-0432.CCR-25-0327","1756368900",{"id":1284,"nickname":1296,"avatar":1297,"is_me":59},[1893],{"id":1300,"title":1301,"icon":1302},{"uuid":1895,"jcr":1896,"q":824,"full_author":1897,"title":1898,"list_abstract_url":1899,"year_jcr":1900,"pmcid":63,"id":1920,"doi":1921,"full_journal":1922,"link":1923,"free":59,"keyword":63,"imf":1924,"author":1925,"doi_source_url":1972},"fc056c01-1765-3f1d-b322-b338d4caf9cb","CLINICAL CANCER RESEARCH","Lorenzo Gerratana,Carolina Reduzzi,Yue Ren,Rinath Jeselsohn,Reshma L Mahtani,Cynthia X Ma,Angela DeMichele,Jane L Meisel,Kathy Miller,Yara Abdou,Elizabeth C Riley,Rubina Qamar,Priyanka Sharma,Sonya A Reid,Naomi Ko,Yuan Liu,Eric Gauthier,Harold J Burstein,Michelle DeMeo,Sara M Tolaney,Meredith M Regan,Massimo Cristofanilli,Erica L Mayer","Circulating tumor cells dynamics after CDK4\u002F6 inhibitor for hormone-receptor positive metastatic breast cancer: a biomarker analysis from the PACE phase II study","https:\u002F\u002Fpubmed-ncbi-nlm-nih.talkmed.com\u002F?term=Breast+Cancer+AND+%22last+7+days%22%5Bdp%5D&page=2&size=100&sort=date&format=abstract",[1901,1905,1909,1913,1916],{"jcrYear":662,"jif":1902,"quartile":824,"category":1903},12.531,[1904],{"category":722,"source":668,"quartile":824},{"jcrYear":670,"jif":1906,"quartile":824,"category":1907},13.801,[1908],{"category":722,"source":668,"quartile":824},{"jcrYear":675,"jif":1910,"quartile":824,"category":1911},11.5,[1912],{"category":722,"source":668,"quartile":824},{"jcrYear":680,"jif":448,"quartile":824,"category":1914},[1915],{"category":722,"quartile":824},{"jcrYear":685,"jif":1917,"quartile":824,"category":1918},10.2,[1919],{"category":722,"quartile":824},"386818","10.1158\u002F1078-0432.CCR-25-0327","Clin Cancer Res. 2025 Aug 25. doi: 10.1158\u002F1078-0432.CCR-25-0327. Online ahead of print.","[\"https:\u002F\u002Faacrjournals.org\u002Fclincancerres\u002Farticle-lookup\u002Fdoi\u002F10.1158\u002F1078-0432.CCR-25-0327\",false,false]","10.2",[1926,1928,1930,1932,1934,1936,1938,1940,1942,1944,1946,1948,1950,1952,1954,1956,1958,1960,1962,1964,1966,1968,1970],{"name":1927},"Lorenzo Gerratana",{"name":1929},"Carolina Reduzzi",{"name":1931},"Yue Ren",{"name":1933},"Rinath Jeselsohn",{"name":1935},"Reshma L Mahtani",{"name":1937},"Cynthia X Ma",{"name":1939},"Angela DeMichele",{"name":1941},"Jane L Meisel",{"name":1943},"Kathy Miller",{"name":1945},"Yara Abdou",{"name":1947},"Elizabeth C Riley",{"name":1949},"Rubina Qamar",{"name":1951},"Priyanka Sharma",{"name":1953},"Sonya A Reid",{"name":1955},"Naomi Ko",{"name":1957},"Yuan Liu",{"name":1959},"Eric Gauthier",{"name":1961},"Harold J Burstein",{"name":1963},"Michelle DeMeo",{"name":1965},"Sara M Tolaney",{"name":1967},"Meredith M Regan",{"name":1969},"Massimo Cristofanilli",{"name":1971},"Erica L Mayer","https:\u002F\u002Fdoi.org\u002F10.1158\u002F1078-0432.ccr-25-0327",[1974,1977,1980,1983],{"id":1975,"name":1976},589,"转移性乳腺癌",{"id":1978,"name":1979},11140,"CDK4\u002F6抑制剂",{"id":1981,"name":1982},19000,"激素受体阳性",{"id":1984,"name":1985},10151,"HER2阴性",{"id":1987,"content":1988,"user_id":1989,"type":61,"is_draft":59,"doc_id":1990,"view_count":1991,"like_count":59,"created_at":1992,"publish_at":1993,"uuid":1994,"company_id":59,"ask_content":1995,"user":2000,"department":2003,"doc":2008,"like":278,"favor":278,"follow_user":278,"tag":2089},7456,"儿童时期和孕妇产前的日光暴露可能对儿童发病的MS疾病过程有保护作用，需要进一步研究以更好地了解日光暴露对相关人群的影响。",3834259,360126,144,"1740479050",1740479050,"24385952-b41f-4af9-8813-c6cbdcb70082",[1996],{"id":1997,"is_history":65,"is_question":44,"message":1998,"created_at":1999},"ai_20326","儿童发病的多发性硬化中日光暴露与复发风险之间的相关性\n●\t该研究评估了生命各阶段的日光暴露与儿童发病的多发性硬化（MS）复发风险之间的关联。\n●\t研究人员对来自美国18家儿童MS诊所的334名儿童MS患者进行了多中心队列研究。\n●\t研究发现，在儿童生命的第一个夏天和孕妇妊娠中期的较高日光暴露（每天≥30分钟）与儿童发病的MS复发风险较低有相关性；然而，近期的日光暴露与复发风险无显著相关。\n●\t研究表明，儿童时期和孕妇产前的日光暴露可能对儿童发病的MS疾病过程有保护作用，需要进一步研究以更好地了解日光暴露对相关人群的影响。\n\nChang G, Sebastian P, Virupakshaiah A, et al. Association Between Sun Exposure and Risk of Relapse in Pediatric-Onset Multiple Sclerosis. Neurol Neuroimmunol Neuroinflamm. 2025;12(2):e200375. doi:10.1212\u002FNXI.0000000000200375","1740463299",{"id":1989,"nickname":2001,"avatar":2002,"is_me":59},"TAP Voice 神经免疫","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002Fd32b2f7c942c573983e6395052619e35\u002F2024\u002F03\u002F26\u002Fcd67a692313740e914ecd4690aa8facc111956b9.jpg",[2004],{"id":2005,"title":2006,"icon":2007},32,"神经内科","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002F04e57411df91d31a60b61357905b959e\u002F2023\u002F03\u002F29\u002Fda5e684d7e9d367fc1b8be6ba9cf28260cfc31da.png",{"jcr":2009,"q":824,"uuid":2010,"full_author":2011,"title":2012,"list_abstract_url":2013,"year_jcr":2014,"pmcid":2040,"id":2041,"full_journal":2042,"doi":2043,"free":61,"link":2044,"keyword":63,"imf":1743,"author":2045,"doi_source_url":2088},"Neurology-Neuroimmunology & Neuroinflammation","74f2d648-bf32-37b8-9551-1794f08161ef","Chang G, Sebastian P, Virupakshaiah A, Schoeps VA, Cherbuin N, Casper TC, Gorman MP, Benson LA, Chitnis T, Rensel M, Abrams AW, Lotze T, Mar SS, Schreiner TL, Wheeler YS, Rose JW, Graves J, Krupp LB, Waldman AT, Lucas R, Waubant E; as the US Network of Pediatric Multiple Sclerosis Centers.","Association Between Sun Exposure and Risk of Relapse in Pediatric-Onset \u003Cb>Multiple\u003C\u002Fb> \u003Cb>Sclerosis\u003C\u002Fb>.","https:\u002F\u002Fpubmed.ncbi.nlm.nih.gov\u002F?term=Multiple+Sclerosis+AND+%22last+14+days%22%5Bdp%5D&page=5&size=10&format=abstract",[2015,2021,2026,2031,2036],{"jcrYear":662,"jif":2016,"quartile":824,"category":2017},8.485,[2018,2020],{"category":2019,"source":668,"quartile":824},"CLINICAL NEUROLOGY",{"category":1219,"source":668,"quartile":824},{"jcrYear":670,"jif":2022,"quartile":824,"category":2023},11.36,[2024,2025],{"category":2019,"source":668,"quartile":824},{"category":1219,"source":668,"quartile":824},{"jcrYear":675,"jif":2027,"quartile":824,"category":2028},8.8,[2029,2030],{"category":2019,"source":668,"quartile":824},{"category":1219,"source":668,"quartile":824},{"jcrYear":680,"jif":2032,"quartile":824,"category":2033},7.8,[2034,2035],{"category":2019,"quartile":824},{"category":1219,"quartile":824},{"jcrYear":685,"jif":1734,"quartile":824,"category":2037},[2038,2039],{"category":2019,"quartile":824},{"category":1219,"quartile":824},"PMC11820808","360126","Neurol Neuroimmunol Neuroinflamm. 2025 Mar;12(2):e200375. doi: 10.1212\u002FNXI.0000000000200375. Epub 2025 Feb 12.","10.1212\u002FNXI.0000000000200375","[\"https:\u002F\u002Fwww.neurology.org\u002Fdoi\u002F10.1212\u002FNXI.0000000000200375?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub  0pubmed\",\"https:\u002F\u002Fpmc.ncbi.nlm.nih.gov\u002Farticles\u002Fpmid\u002F39938013\u002F\"]",[2046,2048,2050,2052,2054,2056,2058,2060,2062,2064,2066,2068,2070,2072,2074,2076,2078,2080,2082,2084,2086],{"name":2047},"Chang G",{"name":2049},"Sebastian P",{"name":2051},"Virupakshaiah A",{"name":2053},"Schoeps VA",{"name":2055},"Cherbuin N",{"name":2057},"Casper TC",{"name":2059},"Gorman MP",{"name":2061},"Benson LA",{"name":2063},"Chitnis T",{"name":2065},"Rensel M",{"name":2067},"Abrams AW",{"name":2069},"Lotze T",{"name":2071},"Mar SS",{"name":2073},"Schreiner TL",{"name":2075},"Wheeler YS",{"name":2077},"Rose JW",{"name":2079},"Graves J",{"name":2081},"Krupp LB",{"name":2083},"Waldman AT",{"name":2085},"Lucas R",{"name":2087},"Waubant E; as the US Network of Pediatric Multiple Sclerosis Centers.","https:\u002F\u002Fdoi.org\u002F10.1212\u002Fnxi.0000000000200375",[2090,2093,2096],{"id":2091,"name":2092},394,"儿童",{"id":2094,"name":2095},110743,"日光照射",{"id":2097,"name":2098},11885,"多发性硬化症",{"id":2100,"content":2101,"user_id":2102,"type":61,"is_draft":59,"doc_id":2103,"view_count":2104,"like_count":59,"created_at":2105,"publish_at":2106,"uuid":2107,"company_id":59,"ask_content":2108,"user":2113,"department":2116,"doc":2121,"like":278,"favor":278,"follow_user":278,"tag":2182},794,"第16周，氘可来昔替尼组达到主要终点PASI 75（68.8% vs. 8.1%）和sPGA 0\u002F1（55.6% vs. 6.8%）的患者比例显著高于安慰剂组（P\u003C0.0001）。氘可来昔替尼的疗效维持至第52周，耐受性良好，严重不良事件发生率和停药率较低。",3828017,85516,146,"1729849939",1729849939,"72c2f00a-cba3-4932-b7c2-d883e5294e11",[2109],{"id":2110,"is_history":65,"is_question":44,"message":2111,"created_at":2112},"ai_7291","■ 这项研究评估了口服、选择性、变构酪氨酸激酶2（TYK2）抑制剂氘可来昔替尼在中重度斑块状银屑病患者中的疗效和安全性。\n■ 该3期随机临床研究招募了来自中国和韩国的患者（n=220），患者前16周随机（1∶2）分配至安慰剂组（n=74）或氘可来昔替尼组（n=146；每日1次，剂量为6 mg），第17-52周均使用氘可来昔替尼。主要终点包括第16周时达到银屑病面积和严重指数较基线减少≥75%（PASI 75）以及静态临床医师整体评估（sPGA）评分0（清除）或1（几乎清除）的患者比例。\n■ 第16周，氘可来昔替尼组达到主要终点PASI 75（68.8% vs. 8.1%）和sPGA 0\u002F1（55.6% vs. 6.8%）的患者比例显著高于安慰剂组（P\u003C0.0001）。氘可来昔替尼的疗效维持至第52周，耐受性良好，严重不良事件发生率和停药率较低。\n■ 上述结果表明，每日1次氘可来昔替尼或许是中重度斑块状银屑病患者的首选治疗方案。","1729840953",{"id":2102,"nickname":2114,"avatar":2115,"is_me":59},"TAP Voice 皮肤","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002F7054b2754c3071158452397fbf7045d2\u002F2024\u002F01\u002F25\u002F6e5db2763a46c2edbb4c09d8a2d78285ebdfcd5a.jpg",[2117],{"id":2118,"title":2119,"icon":2120},50,"皮肤性病科","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002F33c0ff41f45518906064b8058d583b2a\u002F2023\u002F03\u002F29\u002F19d645d21856639c32f7c200d0c24cf314de056a.png",{"jcr":2122,"q":824,"uuid":2123,"full_author":2124,"title":2125,"list_abstract_url":2126,"year_jcr":2127,"pmcid":63,"id":2147,"full_journal":2148,"doi":2149,"link":2150,"free":59,"keyword":63,"imf":2151,"author":2152,"doi_source_url":2181},"BRITISH JOURNAL OF DERMATOLOGY","ea68a725-bd69-3f13-8689-ceec6b7b2581","Jianzhong Zhang,Yangfeng Ding,Ping Wang,Linfeng Li,Weili Pan,Yan Lu,Hao Cheng,Xian Jiang,Ji-Chen Ho,Shuping Guo,Leona Liu,Arkendu Chatterjee,Renata M Kisa,Subhashis Banerjee","Deucravacitinib, an oral selective allosteric tyrosine kinase 2 inhibitor, in patients from China mainland, Taiwan and South Korea with moderate-to-severe plaque psoriasis: a phase III randomized clinical trial","https:\u002F\u002Fpubmed.ncbi.nlm.nih.gov\u002F?term=Psoriasis&page=2&size=10&sort=date&format=abstract",[2128,2132,2136,2140,2143],{"jcrYear":662,"jif":2129,"quartile":824,"category":2130},9.302,[2131],{"category":1470,"source":668,"quartile":824},{"jcrYear":670,"jif":2133,"quartile":824,"category":2134},11.113,[2135],{"category":1470,"source":668,"quartile":824},{"jcrYear":675,"jif":2137,"quartile":824,"category":2138},10.3,[2139],{"category":1470,"source":668,"quartile":824},{"jcrYear":680,"jif":387,"quartile":824,"category":2141},[2142],{"category":1470,"quartile":824},{"jcrYear":685,"jif":2144,"quartile":824,"category":2145},9.6,[2146],{"category":1470,"quartile":824},"85516","Br J Dermatol. 2025 Feb 18;192(3):402-409. doi: 10.1093\u002Fbjd\u002Fljae406.","10.1093\u002Fbjd\u002Fljae406","[\"http:\u002F\u002Fovidsp.ovid.com\u002Fovidweb.cgi?T=JS&PAGE=linkout&SEARCH=39437312.ui\",\"https:\u002F\u002Facademic.oup.com\u002Fbjd\u002Farticle-lookup\u002Fdoi\u002F10.1093\u002Fbjd\u002Fljae406\",false]","9.6",[2153,2155,2157,2159,2161,2163,2165,2167,2169,2171,2173,2175,2177,2179],{"name":2154},"Jianzhong Zhang",{"name":2156},"Yangfeng Ding",{"name":2158},"Ping Wang",{"name":2160},"Linfeng Li",{"name":2162},"Weili Pan",{"name":2164},"Yan Lu",{"name":2166},"Hao Cheng",{"name":2168},"Xian Jiang",{"name":2170},"Ji-Chen Ho",{"name":2172},"Shuping Guo",{"name":2174},"Leona Liu",{"name":2176},"Arkendu Chatterjee",{"name":2178},"Renata M Kisa",{"name":2180},"Subhashis Banerjee","https:\u002F\u002Fdoi.org\u002F10.1093\u002Fbjd\u002Fljae406",[2183,2186,2189],{"id":2184,"name":2185},16895,"氘可来昔替尼",{"id":2187,"name":2188},8679,"斑块状银屑病",{"id":2190,"name":2191},20675,"TYK2",{"id":2193,"content":2194,"user_id":2195,"type":61,"is_draft":59,"doc_id":2196,"view_count":2197,"like_count":59,"created_at":2198,"publish_at":2199,"uuid":2200,"company_id":59,"ask_content":2201,"user":2214,"department":2216,"doc":278,"like":278,"favor":278,"follow_user":278,"tag":2221},112,"很强大的AI工具",3679610,20002,325,"1706696079",1706696079,"c361e786-93f7-435c-abcc-b57ec4033453",[2202,2206,2210],{"id":2203,"is_history":65,"is_question":44,"message":2204,"created_at":2205},"ai_1355","This document discusses a study that compares the speed of kill of two parasiticides, sarolaner (Simparica™) and afoxolaner (NexGard®), against Ixodes scapularis ticks on dogs. The study found that a single oral dose of sarolaner provided over 99% efficacy within 24 hours of treatment and over 95% efficacy against subsequent weekly re-infestations of ticks for 35 days. Sarolaner had a faster speed of kill against I. scapularis than afoxolaner, particularly towards the end of the monthly treatment period. The study suggests that sarolaner provides highly effective and reliable control of ticks and reduces the risk of tick-borne diseases. \n\nMain points:\n- The study compares the speed of kill of sarolaner and afoxolaner against Ixodes scapularis ticks on dogs.\n- Sarolaner provided over 99% efficacy within 24 hours of treatment and over 95% efficacy against subsequent weekly re-infestations of ticks for 35 days.\n- Sarolaner had a faster speed of kill against I. scapularis than afoxolaner, particularly towards the end of the monthly treatment period.\n- Sarolaner provides highly effective and reliable control of ticks and reduces the risk of tick-borne diseases.","1706695932",{"id":2207,"is_history":65,"is_question":44,"message":2208,"created_at":2209},"ai_1356","关键信息：\n- 杀灭寄生虫剂的速度对于最大限度地减少蜱虫感染的影响和降低蜱传病原体传播的风险至关重要。\n- Sarolaner 咀嚼片在治疗后 24 小时内提供 >99% 的疗效，对随后每周一次的蜱虫再感染持续 35 天提供 >95% 的疗效。\n- Afoxolaner在第0天和第14天的8小时以及第0天的12小时仅显着低于安慰剂。\n- Sarolaner 对肩胛蜱的杀灭速度比 afoxolaner 快，尤其是在每月治疗期结束时。\n\n背景和方法：\n- 肩胛硬蜱在北美通常感染狗和猫，是导致莱姆病病原体的主要媒介。\n- 该研究评估了单次口服剂量后 5 周内 sarolaner 和 afoxolaner 对狗肩胛骨的杀灭速度。\n- 根据治疗前的蜱虫计数，将 24 只狗随机分配到安慰剂、sarolaner 或 afoxolaner 治疗组。\n- 对狗进行检查，并在治疗和随后的再次感染后的不同时间点计算活蜱虫。\n\n主要发现\u002F结果：\n- Sarolaner在治疗后24小时内提供了>99%的疗效，对随后每周一次的蜱虫再次感染的疗效为>95%，持续35天。\n- 与安慰剂相比，Sarolaner在第0天至第21天的8小时和12小时以及第35天的12小时显著减少了蜱虫计数。\n- Afoxolaner在第0天和第14天的8小时以及第0天的12小时仅显着低于安慰剂。\n- 在第 14 天至第 35 天感染后 24 小时，从 afoxolaner 处理的狗中回收的活蜱虫多于从 sarolaner 处理的狗中回收的活蜱虫。\n- 从第21天到研究结束，afoxolaner的疗效下降到80%以下，而sarolaner的疗效在35天内为>95%。\n\n影响：\n- Sarolaner 对肩胛蜱的杀灭速度比 afoxolaner 快，尤其是在每月治疗期结束时。\n- Sarolaner在整个治疗期间对蜱虫进行高效可靠的控制，并降低蜱传疾病（包括莱姆病）的风险。","1706695990",{"id":2211,"is_history":65,"is_question":44,"message":2212,"created_at":2213},"ai_1357","根据所提供的信息，研究结果表明，sarolaner对Ixodes scapularis的杀虫速度比afoxolaner更快。sarolaner在单次口服剂量后的24小时内提供了超过99%的杀虫效果，并且在连续五周的重新感染期间保持了超过95%的杀虫效果。与此相比，afoxolaner在早期时间点的杀虫效果较低，而且在治疗结束后的35天内，其杀虫效果下降至不到80%。因此，sarolaner在单次口服剂量后能够快速而持续地杀死Ixodes scapularis，从而有效控制蜱虫，并减少蜱传疾病的风险\n请注意，这是根据提供的信息进行的简要总结，具体细节和结果可能需要查看原始研究文章以获取更准确和详细的信息。","1706696006",{"id":2195,"nickname":2215,"avatar":63,"is_me":59},"clz187",[2217],{"id":2218,"title":2219,"icon":2220},54,"感染科","https:\u002F\u002Fcdn.edstatic.com\u002F202707160556\u002Fc3f4ea06c33abaf245b5ecb6b417cd3e\u002F2023\u002F03\u002F29\u002Fade264ac1556f13668165ef1775cd60380f6e519.png",[2222,2224,2227,2230,2233,2235],{"id":570,"name":2223},"Ixodes scapularis",{"id":2225,"name":2226},81,"sarolaner",{"id":2228,"name":2229},82,"afoxolaner",{"id":2231,"name":2232},83,"speed of kill",{"id":588,"name":2234},"tick infestation",{"id":144,"name":2236},"Lyme disease"]