更新于：2024-05-01

TYRO3

TYRO3蛋白酪氨酸激酶

更新于：2024-05-01

基本信息

别名

Brt、BYK、DTK

+ [13]

简介

(Microbial infection) Acts as a receptor for Ebolavirus, possibly through GAS6 binding to phosphatidyl-serine at the surface of virion envelope. Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to several ligands including TULP1 or GAS6. Regulates many physiological processes including cell survival, migration and differentiation. Ligand binding at the cell surface induces dimerization and autophosphorylation of TYRO3 on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with PIK3R1 and thereby enhances PI3-kinase activity. Activates the AKT survival pathway, including nuclear translocation of NF-kappa-B and up-regulation of transcription of NF-kappa-B-regulated genes. TYRO3 signaling plays a role in various processes such as neuron protection from excitotoxic injury, platelet aggregation and cytoskeleton reorganization. Also plays an important role in inhibition of Toll-like receptors (TLRs)-mediated innate immune response by activating STAT1, which selectively induces production of suppressors of cytokine signaling SOCS1 and SOCS3. (Microbial infection) Acts as a receptor for lassa virus and lymphocytic choriomeningitis virus, possibly through GAS6 binding to phosphatidyl-serine at the surface of virion envelope.

关联

项与 TYRO3 相关的药物

Cabozantinib (s)-Malate

苹果酸卡博替尼

靶点

AXL x RET x ROS1 x TYRO3 x Tie-2 x TrkB x VEGFR1 x VEGFR2 x VEGFR3 x c-Kit x c-Met

作用机制

AXL抑制剂 [+10]

在研机构

原研机构

在研适应症

非在研适应症

最高研发阶段批准上市

首次获批国家/地区

美国

首次获批日期2012-11-29

Merestinib

靶点

AXL x NTRK x ROS1 x TYRO3 x Tie-2 x c-Met

作用机制

AXL抑制剂 [+5]

在研机构

原研机构

在研适应症

非在研适应症

最高研发阶段临床2期

首次获批国家/地区-

首次获批日期1800-01-20

RXDX-106

靶点

AXL x MerTK x TYRO3

作用机制

AXL抑制剂 [+2]

在研机构

Teva Pharmaceutical Industries Ltd. [+2]

原研机构

Teva Pharmaceutical Industries Ltd.

在研适应症

肿瘤

非在研适应症

晚期恶性实体瘤 [+1]

最高研发阶段临床1期

首次获批国家/地区-

首次获批日期1800-01-20

290

项与 TYRO3 相关的临床试验

NCT06341712 / Not yet recruiting临床2期

A Phase II, Randomized, Open-label Study to Assess the Efficacy, Safety, and Pharmacokinetics (PK) of Maintenance Cabozantinib (XL184) Plus Best Supportive Care (BSC) Versus BSC in Children, Adolescents and Young Adults (AYA) With Unresectable Residual Osteosarcoma Either at Diagnosis or at First Relapse After Standard Treatment

The participants of this study will be children, adolescents, and young adults with residual osteosarcoma, which cannot be removed completely through surgery.
Participants will have achieved a partial response or stable disease at the end of conventional chemotherapy. Osteosarcoma is cancer of the bone. The cancer cells make immature bone cells, known as osteoid.
Osteosarcoma is very rare, but it is the most common type of bone cancer in children and teens. It is most common in teens and young adults.
In this study, participants will receive either cabozantinib and best supportive care or the best supportive care alone. Best supportive care will be provided at the investigator's discretion and according to institutional guidelines.
It includes antibiotics, nutritional support, correction of metabolic disorders, optimal symptom control and pain management (including radiotherapy), etc. but does not include tumor specific therapy.
Cabozantinib will be taken by mouth (orally), as a tablet, once a day. Cabozantinib will be provided to participants who tolerate it for as long as their disease does not progress. Participants in the study receiving best supportive care alone may switch to treatment with cabozantinib and best supportive care if their disease progresses and if other eligibility criteria are met.
Participants may withdraw consent to participate at any time.
The estimated duration of the study for participants is 24 months, however a participant could remain in the study longer if demonstrating treatment benefit.

开始日期2024-06-13

申办/合作机构

Ipsen SA

NCT06364631 / Recruiting临床3期IIT

First Line Randomised Study Platform to Optimize Treatment in Patients With Metastatic Renal Cell Carcinoma

Systemic therapy for renal cell carcinoma (RCC) relies on 2 classes of agents: anti-angiogenic targeted therapy (Vascular endothelial growth factor Tyrosine Kinase Inhibitor- VEGFR TKI) and immune checkpoint inhibitor (ICI), targeting either PD1/PDL1 axis or CTLA4. Combination therapy is SOC for clear cell RCC in all guidelines with either ICI-ICI or ICI-VEGFR TKI. However, no head-to-head comparison have been performed between the 2 approaches and patients are treated based on physician decision without clinical /biomarker factors to guide treatment selection. PDL1 staining is, to date, the biomarker that has demonstrated its ability to enrich for overall survival benefit favoring ICI-ICI strategy in PDL1(+) and ICI-VEGFR TKI in PDL1(-) patients.
Study design has been developed to demonstrate that ICI-ICI is superior to ICI-VEGFR TKI in prolonging Overall Survival (OS) for PDL1(+) patients and to demonstrate that ICI-VEGFR TKI is superior to ICI-ICI in prolonging Progression Free Survival (PFS) and OS for PDL1(-) patients.

开始日期2024-04-12

申办/合作机构

Gustave Roussy, Cancer Campus, Grand Paris

[+9]

NCT06006013 / Not yet recruiting临床2期IIT

Phase II Open Label, Single-Arm Study of Cabozantinib in Combination With Atezolizumab in the Treatment of Locally Advanced or Metastatic Adrenocortical Carcinoma

This phase II trial tests how well cabozantinib in combination with atezolizumab works in treating patients with adrenocortical cancer that has spread to nearby tissue or lymph nodes (locally advanced), that has spread from where it first started (primary site) to other places in the body (metastatic), or that cannot be removed by surgery (unresectable). Cabozantinib inhibits receptor tyrosine kinases, which are receptors commonly over-expressed by tumor cells. This may result in an inhibition of both tumor growth and blood vessel formation, eventually leading to a decrease in tumor size or extent in the body. Immunotherapy with monoclonal antibodies, such as atezolizumab, may help the body's immune system attack the cancer and may interfere with the ability of tumor cells to grow and spread. Adding cabozantinib to atezolizumab may be more effective at treating patients with adrenal cortical cancer than giving these drugs alone.

开始日期2024-04-01

申办/合作机构

Emory University

[+1]

100 项与 TYRO3 相关的临床结果

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100 项与 TYRO3 相关的转化医学

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0 项与 TYRO3 相关的专利（医药）

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980

项与 TYRO3 相关的文献（医药）

2024-02-23·Clinical science (London, England : 1979)

Intervention treatment reducing cellular senescence inhibits tubulointerstitial fibrosis in diabetic mice following acute kidney injury.

Article

作者: Gregory H Tesch ; Frank Y Ma ; Elyce Ozols ; David J Nikolic-Paterson

Senescence of kidney tubules leads to tubulointerstitial fibrosis (TIF). Proximal tubular epithelial cells undergo stress-induced senescence during diabetes and episodes of acute kidney injury (AKI), and combining these injuries promotes the progression of diabetic kidney disease (DKD). Since TIF is crucial to progression of DKD, we examined the therapeutic potential of targeting senescence with a senolytic drug (HSP90 inhibitor) and/or a senostatic drug (ASK1 inhibitor) in a model of TIF in which AKI is superimposed on diabetes. After 8 weeks of streptozotocin-induced diabetes, mice underwent bilateral clamping of renal pedicles to induce mild AKI, followed by 28 days of reperfusion. Groups of mice (n=10-12) received either vehicle, HSP90 inhibitor (alvespimycin), ASK1 inhibitor (GS-444217), or both treatments. Vehicle-treated mice displayed tubular injury at day 3 and extensive tubular cell senescence at day 10, which remained unresolved at day 28. Markers of senescence (Cdkn1a, Cdkn2a), inflammation (Cd68, Tnf, Ccl2) and TIF (Col1a1, Col4a3, α-Sma/Acta2, Tgfb1) were elevated at day 28, coinciding with renal function impairment. Treatment with alvespimycin alone reduced kidney senescence and levels of Col1a1, Acta2, Tgfb1, and Cd68; however, further treatment with GS-444217 also reduced Col4a3, Tnf, Ccl2 and renal function impairment. Senolytic therapy can inhibit TIF during DKD, but its effectiveness can be improved by follow-up treatment with a senostatic inhibitor, which has important implications for treating progressive DKD.

2024-01-29·Scientific reports

Prognostic DNA mutation and mRNA expression analysis of perineural invasion in oral squamous cell carcinoma.

Article

作者: Su Kyung Kuk ; Kitae Kim ; Jae Il Lee ; KangMi Pang

This study analyzed oral squamous cell carcinoma (OSCC) genomes and transcriptomes in relation to perineural invasion (PNI) and prognosis using Cancer Genome Atlas data and validated these results with GSE41613 data. Gene set enrichment analysis (GSEA), gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes were conducted. We identified 22 DNA mutations associated with both overall survival (OS) and PNI. Among them, TGFBR1 and RPS6KA4 mRNAs were overexpressed, while TYRO3 and GPR137 mRNAs were underexpressed in PNI patients. Among the 141 mRNA genes associated with both OS and PNI, we found overlap with PNI-related DNA mutations, including ZNF43, TEX10, TPSD1, and PSD3. In GSE41613 data, TGFBR1, RPS6KA4, TYRO3, GPR137, TEX10 and TPSD1 mRNAs were expressed differently according to the prognosis. The 22 DNA-mutated genes clustered into nervous system development, regulation of DNA-templated transcription, and transforming growth factor beta binding. GSEA analysis of mRNAs revealed upregulation of hallmarks epithelial mesenchymal transition (EMT), TNFα signaling via NF-κB, and IL2 STAT5 signaling. EMT upregulation aligned with the TGFBR1 DNA mutation, supporting its significance in PNI. These findings suggest a potential role of PNI genes in the prognosis of OSCC, providing insights for diagnosis and treatment of OSCC.

2024-01-18·European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery

Aberrant expressions of TAM receptors are associated with postoperative recurrence in chronic rhinosinusitis with nasal polyps.

Article

作者: Yandan Zhou ; Zhili Feng ; Jie Wen ; Chi Yang ; Qiancheng Jing

OBJECTIVES:

TAM receptors (TYRO3, AXL, and MER) play important roles in inflammatory responses, but their effects in chronic rhinosinusitis with nasal polyps (CRSwNP) remain elucidated. We aim to evaluate the values of TAM receptors in disease severity and postoperative recurrence of CRSwNP.

METHODS:

We initially enrolled 160 patients with CRSwNP who were treated with functional endoscopic sinus surgery (FESS) and postoperative recurrence was evaluated during the follow-up period. Circulating TAM receptor levels were detected by enzyme-linked immunosorbent assay (ELISA), and tissue expressions were measured by real-time polymerase chain reaction (RT-PCR) and immunohistochemical (IHC). The relationships between TAM receptor levels and postoperative recurrence were examined.

RESULTS:

A total of 150 patients completed the follow-up schedule, 49 patients experienced postoperative recurrence and the remaining 101 patients were non-recurrent. In recurrent CRSwNP patients, serum levels of TAM receptors were increased compared to those in non-recurrent patients and were positively correlated with disease severity scores (P < 0.05). Circulating TYRO3 and MER were identified as potential predictors of postoperative recurrence based on receiver operating characteristics (ROC) and Kaplan-Meier plots (P < 0.05). Furthermore, tissue TAM receptor levels, as determined by both RT-PCR and IHC, were enhanced in the recurrent group than in the non-recurrent group (P < 0.05) and were predictive of postoperative recurrence (P < 0.05). Interestingly, circulating TYRO3 and MER concentrations, as well as tissue TYRO3 expression, were found to be significantly increased in patients who experienced postoperative recurrence (P < 0.05). IHC images from the same patients revealed that TAM expressions were enhanced in the recurrent tissues compared to their baseline tissue levels.

CONCLUSIONS:

Our laboratory results demonstrated that TAM receptors were increased in recurrent CRSwNP patients and associated with postoperative recurrence. Moreover, the new laboratory findings suggested that measuring circulating levels of TAM receptors might serve as a promising new approach to assess disease progression and predict the risk of postoperative recurrence.

项与 TYRO3 相关的新闻（医药）

2024-03-26

·生物谷

Nature Communications：科学家们揭示了Axl/MerTK是一个受滑膜细胞特征、疾病分期和治疗调节的动态轴

在本研究中，研究者利用与疾病分期和治疗暴露相匹配的RA患者独特的滑膜组织生物资源，评估了Axl和MerTK与滑膜组织病理学和疾病活动性的关系，以及它们的地形表达和靶向治疗的纵向调节。 Tyro3、Axl和MerTK是TAM酪氨酸激酶受体家族的三个成员。从历史上看，三敲除小鼠中所有三种TAM受体的缺失导致广谱自身免疫的发展，包括爪的破坏性炎症性关节炎。从那时起，Axl和MerTK，特别是，已涉及人类自身免疫性疾病的发病机制，包括类风湿关节炎(RA);然而，个体tam对炎症调节和临床治疗反应的确切贡献仍有待阐明。图片来源：https://doi.org/10.1038/s41467-024-46564-6 近日，来自伦敦玛丽女王大学和英国国家卫生研究院的研究者们在Nature Communications杂志上发表了题为“Axl and MerTK regulate synovial inflammation and are modulated by IL-6 inhibition in rheumatoid arthritis”的文章，该研究揭示了Axl和MerTK调节滑膜炎症，并通过IL-6抑制调节类风湿关节炎。 TAM酪氨酸激酶Axl和MerTK在类风湿关节炎(RA)中起重要作用。在本研究中，研究者利用与疾病分期和治疗暴露相匹配的RA患者独特的滑膜组织生物资源，评估了Axl和MerTK与滑膜组织病理学和疾病活动性的关系，以及它们的地形表达和靶向治疗的纵向调节。研究者发现，在未接受治疗的患者中，高AXL水平与缺乏免疫组织学和低疾病活动性相关，并与促炎基因的表达水平呈负相关。研究者使用免疫组织化学/荧光和数字空间分析确定了Axl/MerTK在类风湿滑膜中的位置，并表明Axl优先表达在衬里层。此外，它的外畴在滑膜液中释放，与滑膜组织病理学有关。研究者还发现，来自RA患者的toll样受体4刺激的滑膜成纤维细胞通过巨噬细胞调节MerTK的脱落。最后，Axl/MerTK滑膜表达受疾病分期和治疗干预的影响，尤其是IL-6的抑制。这些发现表明Axl/MerTK是一个受滑膜细胞特征、疾病分期和治疗调节的动态轴。数字空间剖面(DSP)确定了AXL和MERTK的位置同一性图片来源：https://doi.org/10.1038/s41467-024-46564-6 总之，由于动物模型中TAM受体激活的总体作用是改善关节炎，因此更好地了解这些酪氨酸激酶的个体特征是如何在RA关节的炎症环境中被调节的，以及它们之间的相互作用，将有助于确定对当前药物无反应的患者的潜在治疗方法和机制/靶点。（生物谷 Bioon.com）参考文献: Alessandra Nerviani et al. Axl and MerTK regulate synovial inflammation and are modulated by IL-6 inhibition in rheumatoid arthritis. Nat Commun. 2024 Mar 16;15(1):2398. doi: 10.1038/s41467-024-46564-6.

临床研究

2024-03-23

·生物探索

Cell Reports Medicine | 复旦大学董琼珠/钦伦秀/陆录发现提高检查点抑制剂疗效的潜在新策略

引言免疫检查点抑制剂，特别是PD-1/PD-L1抑制剂，已被批准用于不可切除的肝细胞癌(HCC)。然而，高耐药率仍然限制了它们的疗效，这突出表明迫切需要了解潜在的机制并制定克服耐药性的策略。2024年3月20日，复旦大学董琼珠、钦伦秀及陆录共同通讯在Cell Reports Medicine 在线发表题为“Disruption of MerTK increases the efficacy of checkpoint inhibitor by enhancing ferroptosis and immune response in hepatocellular carcinoma”的研究论文，该研究证明了高MER原癌基因酪氨酸激酶(MerTK)表达的HCC在两种同基因小鼠模型和接受抗PD-1/PD-L1治疗的患者中表现出抗PD-1/PD-L1耐药。在机制上，MerTK通过ERK/SP1途径通过SLC7A11的上调来限制铁死亡，并通过募集髓源性抑制细胞(MDSCs)促进免疫抑制性肿瘤微环境(TME)的发展，从而使HCC对抗PD-1/PD-L1产生耐药性。Sitravatinib是MerTK的一种抑制剂，通过促进肿瘤铁死亡和减少MDSC向TME的浸润，使耐药HCC对抗PD-L1治疗增敏。肝细胞癌(HCC)仍然是一个全球性的健康挑战，其发病率在全球范围内不断增加临床上，大多数HCC患者被诊断为晚期，治疗选择有限。最近，免疫疗法，如免疫检查点抑制剂(ICIs)抗CTLA4、抗PD-1/PD-L1、它们的联合或与其他药物的联合，在癌症患者中取得了无与伦比的成功。此外，nivolumab、pembrolizumab和atezolizumab等ICIs目前已被美国食品和药物管理局(FDA)批准用于HCC的全身治疗。然而，由于抗PD-1/PD-L1治疗经常出现耐药，反应率仍远不能令人满意，目前仅在约15% - 20%的HCC患者中观察到总体获益率。因此，迫切需要确定最佳患者选择的生物标志物，并确定克服这种耐药性的有效靶点。MER原癌基因酪氨酸激酶(MerTK)是酪氨酸受体激酶TAM家族(TYRO3、AXL和MerTK)的一员，在包括HCC在内的多种恶性肿瘤中高度表达6 (the Human Protein Atlas: proteinatlas.org)。同源蛋白生长抑制特异性蛋白6 (Gas6)和蛋白S (Pros1)都是MerTK活化的天然配体，可诱导MerTK的同二聚化和自磷酸化，激活MEK/ERK、PI3K/AKT、JAK/STAT等下游通路，从而达到肿瘤细胞增殖、抗凋亡、抑制炎症和肿瘤生长的目的。最近的研究表明，MerTK作为一种代谢调节剂，通过整合有氧糖酵解和氧化磷酸化，在调节HCC生长中起着关键作用。此外，MerTK的受体/配体活性已在多种免疫细胞类型中得到证实，并增强抗肿瘤免疫，这对癌症免疫治疗具有重要意义。模式图（Credit: Cell Reports Medicine）铁死亡作为一种代谢调节的细胞死亡形式，在癌症生物学中起着重要的作用。近年来，越来越多的证据表明，对铁死亡的抑制与对常规癌症治疗的耐药性有关，并且靶向铁死亡可能为癌症提供治疗潜力。最近，研究表明，在免疫治疗过程中，对铁死亡的调节可以重塑肿瘤生态位，从而导致T细胞介导的肿瘤根除。在HCC中，铁死亡已被证明在全身治疗(如靶向治疗和化疗)中具有耐药性。该研究发现MerTK是抵抗PD-1/PD-L1阻断的主要机制，通过增加髓源性抑制细胞(MDSC)的浸润，限制肿瘤细胞铁死亡并引起免疫抑制性肿瘤微环境(TME)。MerTK阻断可能有效对抗这种耐药，并使HCC对抗PD-L1治疗敏感。此外，MerTK可作为sitravatinib，联合抗PD-L1联合治疗筛查HCC患者的生物标志物。总之，该研究发现MerTK可以作为患者分层的预测性生物标志物，并且是克服HCC中抗PD-1/PD-L1耐药的有希望的靶点。原文链接https://doi.org/10.1016/j.xcrm.2024.101420责编|探索君排版|探索君文章来源|“iNature”End往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文Nature | 破除传统：为何我们需要重新思考肿瘤的命名方式热文Nature | 2024年值得关注的七项技术热文Nature | 自身免疫性疾病能被治愈吗？科学家们终于看到了希望热文CRISPR技术进化史 | 24年Cell综述

免疫疗法

2024-02-24

·生物探索

Cell Rep Med | 复旦大学董琼珠/钦伦秀/陆录发现提高肝癌免疫检查点抑制剂疗效的潜在新策略

引言近年来，以免疫检查点抑制剂(ICIs)为代表的肿瘤免疫治疗被认为是癌症治疗领域最成功的方法之一，但病人获益有限，甚至病人获益之后仍可出现耐药问题。2024年2月20日，复旦大学董琼珠、钦伦秀及陆录共同通讯在Cell Reports Medicine 在线发表题为“Disruption of MerTK increases the efficacy of checkpoint inhibitor by enhancing ferroptosis and immune response in hepatocellular carcinoma”的研究论文，该研究表明靶向MerTK可通过增强肝细胞癌的铁死亡和免疫应答来提高免疫检查点抑制剂的疗效。在这项研究中，研究人员证明了MER原癌基因酪氨酸激酶(MerTK)在两种ICI耐药的肝癌小鼠模型和接受抗PD-1/PDL1治疗的肝癌患者中高表达，MerTK是导致肝癌ICIs耐药的“元凶”之一。机制上，MerTK通过ERK/SP1通路上调SLC7A11的表达抑制肝癌细胞铁死亡，并通过募集髓源性抑制细胞(MDSCs)促进肝癌免疫抑制性肿瘤微环境(TME)的形成，从而使肝癌对抗PD-1/PD-L1产生耐药性。Sitravatinib是MerTK的一种抑制剂，通过促进肿瘤细胞铁死亡和减少MDSC向TME的浸润，使耐药HCC对抗PD-L1治疗增敏。肝细胞癌(HCC)仍然是一个全球性的健康挑战，其发病率在全球范围内不断增加。临床上，大多数HCC患者被诊断为晚期，治疗选择有限。最近，免疫疗法，如ICIs抗CTLA4、抗PD-1/PD-L1、它们的联合或与其他药物的联合，在癌症患者中取得了无与伦比的成功。此外，nivolumab、pembrolizumab和atezolizumab等ICIs目前已被FDA批准用于HCC的全身治疗。然而，由于抗PD-1/PD-L1治疗经常出现耐药，反应率仍远不能令人满意，目前仅在约15% - 20%的HCC患者中观察到总体获益率。因此，迫切需要确定最佳患者选择的生物标志物，并确定克服这种耐药性的有效靶点。MerTK是酪氨酸受体激酶TAM家族(TYRO3、AXL和MerTK)的一员，在包括HCC在内的多种恶性肿瘤中高度表达(the Human Protein Atlas: proteinatlas.org)。同源蛋白生长抑制特异性蛋白6 (Gas6)和蛋白S (Pros1)都是MerTK活化的天然配体，可诱导MerTK的同二聚化和自磷酸化，激活MEK/ERK、PI3K/AKT、JAK/STAT等下游通路，从而促进肿瘤细胞增殖、抗凋亡、抑制炎症和肿瘤恶性进程。最近的研究表明，MerTK作为一种代谢调节剂，通过整合有氧糖酵解和氧化磷酸化，在调节HCC生长中起着关键作用。此外，MerTK的受体/配体活性已在多种免疫细胞类型中得到证实，对癌症的免疫治疗具有重要意义。模式图（Credit: Cell Reports Medicine）铁死亡作为一种代谢调节的细胞死亡形式，在癌症生物学中起着重要作用。近年来，越来越多的证据表明，抑制铁死亡与传统癌症治疗的耐药性密切相关，靶向铁死亡可能为癌症治疗提供潜力。最近，研究表明，在免疫治疗过程中，调节铁死亡可以重塑肿瘤免疫微环境，从而导致T细胞介导的肿瘤消除。在HCC中，铁死亡已被证明与肿瘤治疗(如靶向治疗和化疗)耐药相关。该研究表明，MerTK上调SLC7A11表达抑制肿瘤细胞铁死亡，同时通过在HCC微环境中募集MDSCs促进肿瘤TME，从而导致抗PD-L1治疗耐药。靶向MerTK是提高PD-L1抗体治疗效果的有效策略。在PD-L1耐药肝癌中，MerTK抑制剂Sitravatinib和ICIs联合使用可有效增加肿瘤细胞铁死亡，减少肝癌微环境中MDSCs募集，促进CD8+ T细胞活化。该研究表明MerTK可作为ICB疗效预测标志物，并且是克服HCC中抗PD-1/PD-L1耐药的潜在靶点。原文链接https://doi.org/10.1016/j.xcrm.2024.101415责编|探索君排版|探索君文章来源|“iNature”End往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文Nature | 破除传统：为何我们需要重新思考肿瘤的命名方式热文Nature | 2024年值得关注的七项技术热文Nature | 自身免疫性疾病能被治愈吗？科学家们终于看到了希望热文Nature | 癌症与神经系统的致命舞蹈

免疫疗法