作者: Feldman, Tatyana ; Cheah, Chan Y ; Lugtenburg, Pieternella J. ; Cheah, Chan Y. ; Sureda, Anna ; Poon, Michelle Limei ; Kim, Tae Min ; Thieblemont, Catherine ; Jurczak, Wojciech ; Mark, Thomas ; Dinh, Minh H. ; Linton, Kim M. ; Gasiorowski, Robin ; Cunningham, David ; Lugtenburg, Pieternella J ; Hutchings, Martin ; Karimi, Yasmin H ; van der Poel, Marjolein ; Phillips, Tycel ; Lewis, David John ; Soong, David ; Dinh, Minh H ; Do, Young Rok ; Karimi, Yasmin H. ; Clausen, Michael Roost ; Kilavuz, Nurgul ; Linton, Kim M ; Sacchi, Mariana ; Ghesquieres, Herve

Primary results (median follow-up, 10.7 months) from the pivotal EPCORE^® NHL-1 study in relapsed or refractory (R/R) large B-cell lymphoma (LBCL) demonstrated deep, durable responses with epcoritamab, a CD3xCD20 bispecific antibody, when used as monotherapy. We report long-term efficacy and safety results in patients with LBCL (N = 157; 25.1-month median follow-up). As of April 21, 2023, overall response rate was 63.1% and complete response (CR) rate was 40.1%. Estimated 24-month progression-free survival (PFS) and overall survival (OS) rates were 27.8% and 44.6%, respectively. An estimated 64.2% of complete responders remained in CR at 24 months. Estimated 24-month PFS and OS rates among complete responders were 65.1% and 78.2%, respectively. Of 119 minimal residual disease (MRD)-evaluable patients, 45.4% had MRD negativity, which correlated with longer PFS and OS. CR rates were generally consistent across predefined subgroups: 36% prior chimeric antigen receptor (CAR) T-cell therapy, 32% primary refractory disease, and 37% International Prognostic Index ≥3. The most common treatment-emergent adverse events were cytokine release syndrome (51.0%), pyrexia (24.8%), fatigue (24.2%), and neutropenia (23.6%). These results underscore the long-term benefit of epcoritamab for treating R/R LBCL with deep responses across subgroups, including patients with hard-to-treat disease and expected poor prognosis (ClinicalTrials.gov Registration: NCT03625037).

2024-11-05·Blood

3-Year Update from the Epcore NHL-1 Trial: Epcoritamab Leads to Deep and Durable Responses in Relapsed or Refractory Large B-Cell Lymphoma

作者: Soong, David ; Steele, Andrew J. ; Linton, Kim ; Li, Zhu ; Hutchings, Martin ; Clausen, Michael Roost ; Cheah, Chan Y. ; Vose, Julie M. ; Jurczak, Wojciech ; Eskelund, Christian ; Kim, Won Seog ; Cunningham, David ; Karimi, Yasmin H. ; Phillips, Tycel J. ; D'Angelo Månsson, Barbara ; Thieblemont, Catherine ; Feldman, Tatyana ; Ghesquieres, Herve ; Jafarinasabian, Pegah ; Farooq, Umar

Introduction: Epcoritamab monotherapy resulted in deep, durable responses with a manageable safety profile in patients with challenging-to-treat relapsed or refractory (R/R) large B-cell lymphoma (LBCL) in the pivotal phase 2 EPCORE® NHL-1 trial (NCT03625037). Here, we report 3-y follow-up results, including long-term efficacy and safety.Methods: Adults with R/R CD20+ LBCL (including diffuse LBCL [DLBCL], high-grade B-cell lymphoma, primary mediastinal large B-cell lymphoma, and follicular lymphoma [FL] grade [G] 3B) and ≥2 prior lines of systemic therapy were enrolled in the expansion phase of the study and treated with subcutaneous epcoritamab (0.16 mg and 0.8 mg step-up doses followed by 48-mg full doses) in 28-d cycles according to the approved dosing schedule: QW, cycles 1-3; Q2W, cycles 4-9; Q4W, cycles ≥10, until progressive disease or unacceptable toxicity. Corticosteroid prophylaxis was given during cycle 1. The primary endpoint was overall response rate (ORR) per Lugano criteria. Efficacy results presented here are based on investigators' assessment. Minimal residual disease (MRD) was assessed based on the clonoSEQ® (Adaptive Biotechnologies) ctDNA assay.Results: A total of 157 patients were treated with epcoritamab monotherapy. Median age was 64 y, 60% of patients were male, median number of prior lines of therapy was 3 (range, 2-11), and 61% had primary refractory disease; additional baseline characteristics have been presented previously. At data cutoff (May 3, 2024), 19 patients (12%) remained on treatment. Primary reasons for treatment discontinuation included progressive disease in 91 patients (58%) and adverse events (AEs) in 26 patients (17%); few patients who remained on epcoritamab ≥1 y progressed: 5/47 patients from >12 to ≤24 mo and 2/29 patients beyond 24 mo. The ORR and complete response (CR) rate per investigators were 59% and 41%; median follow-up was 37.1 mo (range, 0.3+ to 45.5). Median duration of response was 20.8 mo (95% CI, 13.0-32.0). Median duration of CR was 36.1 mo (95% CI, 20.2 to not reached [NR]). Median progression-free survival (PFS) was 4.2 mo (95% CI, 2.8-5.5); among complete responders, it was 37.3 mo (95% CI, 26.0-NR). Median overall survival (OS) was 18.5 mo (95% CI, 11.7-27.7); among complete responders, it was NR (95% CI, 36.4-NR). At 36 mo, an estimated 63% of complete responders remained alive. For patients with FL G3B (n=5) and patients with DLBCL transformed from FL (n=32), ORR/CR rates were 60%/60% and 50%/44%, respectively. Of the 119 overall patients who were MRD evaluable, 54 (45%) were MRD negative. In a cycle 3 day 1 landmark analysis, 36-mo rates of PFS/OS were 52%/55% among MRD-negative patients, and 18%/30% among MRD-positive patients. In an exploratory cycle 13 day 1 evaluation, 98% (40/41) of MRD-evaluable patients were MRD negative. There were 15 patients with CR who had a temporary epcoritamab hold for >6 wk (primarily due to AEs; median, 70.5 d, range, 48-257 d); all maintained their response at their next imaging assessment following treatment reinitiation. Of these patients, 6 had post-reinitiation MRD samples available, all of which were MRD negative. The most common treatment-emergent AEs (TEAEs) remained CRS (51%; 32% G1, 16% G2, 3% G3), fatigue (25%), and pyrexia (25%); CRS rates remained unchanged since prior reports. Fatal TEAEs were reported in 20 patients; 10 patients had G5 COVID-19 (including COVID-19 pneumonia). Rates of G≥3 infections were stable over time with rates within 3%-17% for 12-wk study intervals up to wk 144. Incidence of G≥3 cytopenias was highest (27%) during the first 8 wks of treatment and rates were within 0%-13% in subsequent 12-wk time periods up to wk 144. Immunoglobulin G levels decreased by a median of ~20% after the start of epcoritamab treatment (baseline median, 540.0 mg/dL) and remained stable over time.Conclusions: With a 3-year follow-up, epcoritamab continued to show deep and durable responses, with more than half of complete responders remaining in remission at 3 years: median duration of CR, 36.1 mo. Sustained MRD negativity was observed. Long-term safety was consistent with prior reports. These results with extended follow-up support the value of epcoritamab monotherapy as an effective and potentially curative therapy for patients with challenging-to-treat R/R LBCL.

2024-11-05·Blood

Examining Ras/MAP Kinase Signaling in Primary Myelofibrosis May Yield Insight into the Mechanisms of JAK Inhibitor Resistance and Provide New Therapeutic Targets

作者: Kandarpa, Malathi ; Ribick, Mark ; Talpaz, Moshe ; Reynolds, Samuel B ; Li, Qing

Primary myelofibrosis (PMF) is a myeloproliferative neoplasm (MPN) arising from a clonal expansion in myeloid-committed hematopoietic stem and progenitor cells (HSPCs). Aberrant cytokine signaling and the acquisition of additional mutations then collectively induce a recruitment of fibroblasts to the bone marrow, leading to collagen fibrosis. Hematopoietic stem cell transplantation remains the only curative therapy. In non-transplant candidates, JAK2-inhibitors are most commonly utilized for symptomatic relief and reduction in splenomegaly but are in general not considered to be disease-modifying therapies and may lead to worsening cytopenias themselves. Recent studies, accordingly, have begun exploring alternative signaling mechanisms in PMF beyond JAK/STAT. Amongst these, mutations activating Ras signaling are frequently detected in PMF and have been associated with shortened overall survival, progression to AML and advanced disease features.Ras-activating mutations are common in myelofibrosis and many other pathways, including those involved in cytokine signaling, also activate Ras. In order to directly evaluate this process, we examined the levels of Ras activity, measured by the binding of effector Ras binding domain (RBD) via ELISA, in peripheral blood mononuclear cells from 27 PMF patients and compared it to 13 healthy donors and 12 patients with pre-MF conditions, including polycythemia vera (PV) or essential thrombocytopenia (ET). This revealed that Ras activity was significantly higher in patients with PMF as compared to healthy donors (1.74 fold, p=0.0304) and to these other MPNs (1.64 fold, 0.0462). In addition to Ras activating mutations (NRAS, KRAS, CBL, NF1), 8 of 27 samples with no detectable Ras activating mutations also demonstrated higher Ras activity as compared to patients with PV, ET and healthy donors. Interestingly, we also observed a significant increase in Ras activity from 1.594 to 5.105 (absolute difference of 3.511, p=0.0115) in patients not on treatment (5) compared to those on JAK inhibitors (11).To directly evaluate the relationship between Jak inhibition and Ras activation, we treated a JAK2 homozygous human erythroleukemia (HEL) cell line with ruxolitinib at 0.5 µM over a 7-day time course alongside a vehicle (DMSO) control. Here, we observed a significant increase in Ras activity, measured by RBD binding, at nearly all timepoints from 4 hours to 7 days, with a range of percentage increase from 28.4 to 146.6 (p value range 0.0002 to 0.003). Activation of downstream MAP Kinase pathway signaling, measured by pERK levels, in cells exposed to ruxolitinib was also elevated relative to vehicle. Ras activity notably increased with longer periods of exposure to ruxolitinib, suggesting that the induction of Ras/MAP Kinase by JAK inhibition occurs in a time-dependent manner.Our preliminary data, which requires additional confirmation, suggests that JAK2 inhibition leads to activation of Ras in JAK2 mutant cells, raising the possibility that Ras activation conveys resistance to JAK inhibitors. Targeting Ras in PMF, therefore, may improve the efficacy of JAK inhibitors. To begin testing this theory, we examined the effects of combining JAK and Ras pathway inhibitors in MF cells. Here, whole bone marrow from 4 different patients with PMF was plated in methylcellulose-enriched media formulated for the growth of CD34+ cells under 4 therapeutic conditions in colony forming assays: Ruxolitinib, cobimetinib, ruxolitinib + cobimetinib and an unstimulated control. While all four patients were variably sensitive to individual therapies, the combination of ruxolitinib and cobimetinib yielded a more significant reduction in colony formation. Specifically, treatment with ruxolitinib monotherapy resulted in a reduction in colony number to 73.93% of that of untreated marrow (p=0.0025) and cobimetinib monotherapy to 79.3% (p=0.0092). Combination therapy, however, resulted in an even more substantial reduction to 45.8% (p<0.0001). While expansion is required in a larger cohort, our findings suggest that MAP Kinase pathway modulation may serve as a therapeutic strategy to overcome JAK inhibitor resistance in PMF.

项与 University of Michigan Comprehensive Cancer Center 相关的新闻（医药）

2022-08-26

·药时代

200万天价疗法硬扛寒冬

CAR-T细胞疗法正对国内的支付能力做压力测试。单针120万元或129万元为药品费，加上配套医疗费，总价200万元左右。CAR-T商业化意义超越自身，寒蝉凄切，总要有一个勇士去摸天花板，试探环境对前沿疗法，甚至对医药行业创新探索的包容度。到本月，复星凯特阿基仑赛注射液累计治疗超过200位患者，药明巨诺瑞基奥仑赛注射液完成260位患者的回输治疗（包含临床研究及商业化阶段）。国产CAR-T商业化逾一年，完成回输的患者还不足500人，这一届富人不行。药明巨诺生产基地可满足每2500例自体CAR-T细胞治疗的需求，大部分产能闲置。在下游CAR-T厂商亏损死扛且不放量的情况下，上游CGT（细胞基因疗法）CDMO也承受着压力。细胞疗法产业链当下活在寒气中，不过未来被治愈癌症的曙光照耀着。 01 30万元支付天花板由于支付环境差异，美中药物经济学存在一个换算比例，约为1/7，CAR-T疗法在美国的定价，诺华Kymriah为47.5万美元、吉利德Yescarta为37.3万美元，疗法在中国进入47.5万~37.3万人民币区间，才能达到一个各方可以接受的均衡价位。据《international journal of cancer》文献，单人份CAR-T生产成本约为8万美元。药明巨诺瑞基奥仑赛商业化初期，毛利率仅为29.4%，单人份CAR-T生产成本约为70万人民币，加上研发、销售、管理费用，其实是亏损的。预计今年下半年成本预计能降低到50万-55万元，毛利率提升到35%以上，中期（2-3年）通过国内供应品替代进口材料，进一步降低成本到45万元左右，长期（3-5年）则实施新技术，简化/替代/合并单元操作，使得下一代CAR-T产品具有更低成本。医保支付的天花板是多少？现在医保目录中近3000个药品，医保基金最高支付额为30万元。2021年医保谈判结束后，测算专家组组长表示：“不能再高，否则，医保基金就难以承受了。”今年医保谈判一大悬念，在于30万元天花板能否被打破？美国医保是如何支持前沿疗法的？CMS（美国医疗保险与医疗服务中心）通过医疗保险B部分，为接受吉利德CAR-T治疗的患者支付40万美元，为接受诺华CAR-T治疗的患者支付50万美元。CAR-T已纳入超过国内30个城市惠民保。沪惠保最高赔付金额50万元，不限既往症人群。今年3月到5月，4位CAR-T疗法患者通过浙江宁波惠民保产品“天一甬宁保”，分别获赔50.8万元、100万元、94.4万元和47.2万元。杭州市惠民保产品“西湖益联保”、重庆渝快保和北京京惠保也分别完成一次CAR-T疗法患者的理赔，金额分别为50万元、36万元和100万元。商保有崛起之势，大为缓解支付焦虑，但上述患者仍需自费100万元以上，对普通家庭是不可承受之重。细胞疗法的效果又是如此惊艳。截至7月，上海瑞金医院有超过30位患者接受复星凯特CAR-T治疗，其中22位患者已完成首次疗效评估，客观缓解率（ORR）高达95.5%，完全缓解率（CR）高达68.1%，即其中有15位患者获得完全缓解。 02 国内细胞疗法企业全景破解可及性问题，需要支付环境和技术迭代共同努力。自体CAR-T高度定制化，局限性愈发明显。第一款CAR -T疗法诺华Kymriah上市5年，已经触到自己的天花板，今年上半年销售额2.63亿美元，同比下降近12%。据密歇根大学综合癌症中心Samuel Silver博士介绍，美国CAR-T疗法的总费用至少为75万美元，非药品的费用为40万美元至45万美元，与药品费用大致相当。通用型CAR-T（UCAR-T）可实现生产流程的规模化和标准化，有望将生产成本降低90%。国产主要厂家为亘喜生物、北恒生物、科济生物，传奇生物、邦耀生物、安科生物参股公司博生吉、茂行生物、克睿基因、森朗生物对通用型CAR-T也有布局。亘喜生物UCAR-T管线有3个。靶向CD19的细胞疗法GC007g使用供者来源CAR技术，是国内第一款进入临床阶段的通用型CAR-T疗法，已在国内完成IIT临床试验。GC502是靶向CD19/CD7的双靶向UCAR-T产品，用于治疗急性B淋巴细胞白血病。GC027是靶向CD7的UCAR-T产品，用于治疗急性T淋巴细胞白血病。北恒生物UCAR-T管线达到7个，进度最快的TA101今年3月获得CDE临床试验默示许可，是国内首个基于CRISPR基因编辑技术的免疫细胞治疗产品，也是第二款进入临床阶段的通用型CAR-T疗法。科济生物UCAR-T管线有3个，KJ-C2111靶向BCMA，用于治疗多发性骨髓瘤（MM），目前处于IIT实验阶段，KJ-C2114目前还在临床前研究阶段。实体瘤CAR-T疗法覆盖面更广，也可通过规模化生产降低成本。2019年，全球癌症患者有1850万人，其中1730万是实体瘤患者，占比高达93%。科济药业核心产品CT041靶向Claudin18.2，用于治疗胃癌/食管胃结合部腺癌及胰腺癌，是全球首个且唯一进入到关键2期临床试验的实体瘤CAR-T，计划于2024年上半年向国内提交NDA，并计划今年下半年在北美启动一项2期临床试验。科济药业上半年亏损3.76亿元，现金储备27.4亿元，可支持4年以上的研发活动，控制成本能力比传奇生物更强。从市场表现看，其国内一线CAR-T企业的地位已得到认同。相比成熟的CAR-T疗法，NK细胞疗法还在早期阶段，但潜在优势突出，工业化量产潜力更大，适应症范围更广，安全性更好，成本更低，杀伤速度快，且可作为通用型现货产品。国内企业进行布局的有百济神州、优凯瑞、呈诺医学、重庆精准生物、阿思科力、科伦博泰、英百瑞、博生吉、再凌生物、星奕昂、贝斯生物、启函生物、恩凯赛药、景达生物、河络新图、昕传生物和济因生物。2021年11月，国家药监局审批通过国健呈诺现货型同种异体CAR-NK细胞产品的临床试验申请，为国内第一款进入临床阶段的NK细胞疗法。英百瑞用ADC思路开发细胞免疫疗法，在今年上半年NK细胞疗法领域融资金额以2.3亿元位列第一，2款产品即将进入IND。03 CGT CDMO等待爆发契机下游CAR-T商业化缓慢，上游CGT CDMO仍处于培育期，需等到通用型CAR-T上市才能实现工业化放量。和元生物可能是国内唯一盈利的CGT CDMO，一度受到质疑，被担忧上市后财务数据变脸。今年Q2营收6178万元，同比增长17.9%，环比下降15.6%，净利润796万元，环比下降34%，虽受疫情影响，但业绩与二级市场的炒作热度严重不匹配。和元生物半年报也在淡化细胞疗法的概念，更突出自身聚焦基因治疗的定位，主要客户深圳亦诺微、上海复诺健、康华生物、北恒生物中，仅有一家是CAR-T企业。上半年CDMO业务累计新增订单超1.3亿元，在手未执行订单超3.5亿元，开拓干细胞、NK细胞和mRNA新型业务种类。博腾股份上半年CGT CDMO收入1127万元，同比增长80%，是唯一增速较快的，但规模尚小。服务客户32家，同比增长167%；新项目31个，同比增长244%；新签订单约9208万元，同比增长68%。博腾生物B轮融资5.2亿元，现有4000平方米的研发与生产基地稳健运营中，今年Q4预计新增16000平方米的大规模产业化基地，将拥有10条GMP病毒载体生产线、10条GMP细胞治疗生产线以及上百个洁净车间。启动海外市场拓展，部署在北美的工艺开发和分析检测实验室能力。药明康德上半年CGT CDMO收入6.15亿元，同比增长35.7%，经调整Non-IFRS毛利-0.43亿元，毛利率为-6.9%，处于亏损状态。毛利下跌主要由于新启用的上海临港运营基地较低的利用率导致。拥有51个临床前和I期临床试验项目，9个II期临床试验项目，7个III期临床试验项目（其中4个项目处于上市申请准备阶段）。康龙化成CGT CDMO处于整合和投入阶段，海外运营成本过高，暂时亏损。金斯瑞生物科技CGT CDMO平台（蓬勃生物）接近盈亏平衡，2021年新增6400平方米质粒GMP厂房，2022年、2023年国内分别新增6400平方米，2024年美国生产基地将增加3.1万平方米质粒及病毒GMP厂房。质粒方面，蓬勃生物是国内最大的质粒CDMO供应商，有9个中国、美国、韩国IND申报成功经验，超过70个IND申报用质粒CMC项目进行中；病毒载体方面，成功为多个细胞治疗以及Genetherapy提供慢病毒及AAV载体，累计有3个中国、美国IND申报成功经验，超过20个IND申报用病毒载体CMC项目进行中；mRNA质粒方面，几乎与国内所有的mRNA疫苗企业建立合作，与韩国和美国公司合作的mRNA疫苗项目也相继在韩国和日本获临床批件；DNA疫苗方面，提供质粒的CMC研究。药明生基、蓬勃生物是领先优势较大的国际化CGT CDMO龙头。封面图来源：123rf版权声明/免责声明本文为授权转载文章，版权归拥有者。仅供感兴趣的个人谨慎参考，非商用，非医用、非投资用。欢迎朋友们批评指正！衷心感谢！文中图片、视频为授权正版作品，或来自微信公共图片库，或取自公司官网/网络根据CC0协议使用，版权归拥有者。任何问题，请与我们联系（电话：13651980212。微信：27674131。邮箱：contact@drugtimes.cn）。衷心感谢！推荐阅读优时比就左乙拉西坦注射用浓溶液暂停进口进行回应眼内给药迎来新格局｜脉络膜上腔微注射开启糖尿病性黄斑水肿治疗新时代谢雨礼博士 | 药物创新：more is different罗氏旗下基因泰克首次从中国创新药企获得潜在药物全球开发及商业化权益海阔凭药去，大道创新行! 2022第三届中国新药CMC高峰论坛与您再约上海！（第一轮通知）半年营收超10亿，复宏汉霖半年报业绩亮眼，彰显Biopharma实力中国需要自己的Flagship，多玛医药能做到吗？——专访多玛医药首席运营官黄蕤博士手握创新药项目的你，需要帮助吗？诺和诺德携手ATLATL为你点亮「星起点」...云顶退货，里面的「热闹」与「门道」在雷尼替丁的相关争议中，GSK放弃与Ideaya的一项实体瘤合作点击这里，报名参加第三届中国新药CMC高峰论坛！

免疫疗法细胞疗法基因疗法信使RNA合作

2022-06-08

·BioSpace

Xilis Announces Breast Cancer Oncologist Dr. Daniel F. Hayes to Join Clinical Advisory Board

June 8, 2022 12:30 UTC Xilis expands CAB to five members to help company develop its MicroOrganoSphere™ technology DURHAM, N.C.--(BUSINESS WIRE)--Xilis, Inc., a pioneering company developing its MicroOrganoSphere™ (MOS™) technology to guide precision therapy for cancer patients and accelerate drug discovery and development, announced today that breast cancer oncologist Daniel F. Hayes, MD, FACP, FASCO, has joined the company’s Clinical Advisory Board (CAB). Dr. Hayes is a Professor of Internal Medicine, the Stuart B. Padnos Professor in Breast Cancer, and the Clinical Director of the Breast Oncology Program at the University of Michigan Comprehensive Cancer Center. He served as the past President of American Society of Clinical Oncology (ASCO) from 2015 to 2018 and is a world-recognized thought leader in the field of breast cancer. Dr. Hayes will become the fifth member of the Xilis CAB, joining leading gastrointestinal (GI) oncologists Scott Kopetz, MD, PhD, FACP, MD Anderson and Tanios Bekaii-Saab, MD, Mayo Clinic, along with Xilis’ lung and early clinical phase oncologists and investigators Gilberto de Lima Lopes, Jr., MD, MBA, FAMS, University of Miami and Scott Antonia, MD, PhD, Duke University. These leading oncologists are providing guidance to introduce Xilis’ MOS technology to the clinic. “The addition of Dan Hayes to our CAB highlights the excitement of building our MOS technology across important tumor types. To have five of the world’s leading oncologists recognize the potential of our MOS technology to revolutionize the way we approach cancer therapy is gratifying,” said David Hsu, MD, co-founder of Xilis. “The chance to improve patients’ treatments is what motivates each of the clinicians on our board, which aligns with the passion of every employee at Xilis. Dan’s impact on the field of oncology cannot be overstated.” Dr. Hayes joins an accomplished CAB with expertise in colon, breast, and lung cancers, as well as immuno-therapies. Other Xilis Clinical Advisory Board Members Scott Kopetz, MD, PhD, FACP: Dr. Kopetz is a Professor in the Department of Gastrointestinal (GI) Medical Oncology, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center. He is a physician-scientist who enjoys the intellectual challenges of the lab, the emotional engagement of the clinic and has the motivation to bridge the two. Tanios Bekaii-Saab, MD: Dr. Bekaii-Saab is a Professor of Medicine at the Mayo Clinic College of Medicine and Science, Leader of the Gastrointestinal Cancer Program at the Mayo Clinic Cancer Center, Medical Director of the Cancer Clinical Research Office, Vice Chair and Section Chief for Medical Oncology for the Division of Hematology/Oncology in the Department of Internal Medicine at the Mayo Clinic in Phoenix, Arizona, USA. He is the consortium chair for the Academic and Community Cancer Research United (ACCRU) network. He is also one of the leading clinician-scientists in the Alliance for Clinical Trials in Oncology, a National Cancer Institute (NCI)-supported cooperative research group. Dr. Bekaii-Saab conducts clinical and translational research focused on developing anti-cancer agents for patients with GI cancers. Dr. Bekaii-Saab collaborates extensively with various scientists and industry partners to design and execute innovative clinical trials, including many first-in-human studies. Gilberto de Lima Lopes, Jr., MD, MBA, FAMS: Dr. de Lima Lopes is Interim Chief of the division of medical oncology and Professor of Clinical Medicine at the University of Miami and works on developing new drugs and methods to treat cancer through designing, leading and participating in Phase I through IV clinical trials. He has helped bring several novel cancer therapies into the clinic. He is also a leader in the area known as Global Oncology and is the Editor-in-Chief for ASCO’s journal JCO Global Oncology. Scott Antonia, MD, PhD: Dr. Antonia is recognized as a global leader in the development of immunotherapy for lung cancer. While at Moffitt Cancer Center, he helped develop immunotherapies to fight lung cancer, including one that in June 2019 changed the standard of care for stage III non-small-cell lung cancer. Dr. Antonia now serves as director of the Duke Cancer Institute Center for Cancer Immunotherapy, a DCI Strategic Plan priority that aims to enhance the institute’s ability to develop and test novel immunotherapeutic approaches. About Xilis Based in Durham, North Carolina, Xilis, Inc. is a biotechnology company developing a precision oncology platform that guides treatment decisions for oncologists to improve cancer care outcomes for patients and supports drug discovery and development for pharmaceutical companies. Xilis’ proprietary MicroOrganoSphere™ (MOS) technology consists of miniature patient tumors that capture the full microenvironment and heterogeneity and provides an automated and scalable solution. Using MOS and AI-driven algorithms, Xilis is developing a Xilis Response Score™ for the clinic, enabling oncologists to make informed and timely treatment decisions. Additionally, the MOS technology is speeding up development and clinical trials of cancer drugs by enabling analysis of authentic tumor microenvironments, high-throughput preclinical modeling, and clinical patient selection capabilities. To learn more about Xilis, visit our website at Xilis.com or follow us on LinkedIn.

免疫疗法ASCO会议合作

2007-04-16

·BioSpace

University of Michigan Health System's New Imaging Method Shows Whether Treatment for Advanced Prostate Cancer is Working

ANN ARBOR, Mich. -- Researchers at the University of Michigan Comprehensive Cancer Center have identified a new imaging technique that can measure the effectiveness of treatment for prostate cancer that has spread to the bones. The technique involves measuring diffusion of water within tumors. >>> Discuss This Story

100 项与 University of Michigan Comprehensive Cancer Center 相关的药物交易

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100 项与 University of Michigan Comprehensive Cancer Center 相关的转化医学

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