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Immune checkpoint inhibitor-related myocarditis in thymic epithelial tumors: Recent progress and perspectives 胸腺上皮肿瘤免疫检查点抑制剂相关性心肌炎的研究进展与展望
Pub Date : 2023-05-17 DOI: 10.1002/mog2.31
Jianqiong Yin, Zhuoran Yao, Jing Pan, Lu Gan, Jianxin Xue

Thymic epithelial tumors (TETs) are rare anterior mediastinal malignancies originating in the thymus with poor outcomes, and standard platinum-based chemotherapy shows limited efficacy for treating metastatic or recurrent disease. In this setting, further improved novel treatment strategies are needed. Immune checkpoint inhibitors (ICIs) are widely applied in clinical practice for cancer therapy and early results of clinical trials have brought notable objective responses and lasting survival benefits to patients with TETs. However, the incidences of immune-related adverse events (irAEs), especially cardiac adverse events, are higher than those of other tumor types. Myocarditis is a rapidly progressive and life-threatening irAE in patients treated with ICIs, thereby hindering the further utilization of ICI in TETs patients. Therefore, this article aims to review the results of case series and clinical trials that evaluated ICIs for the treatment of TETs and to provide an overview of the clinical features of fatal ICI-related myocarditis in TETs. Furthermore, we approach insights into the immunobiology of thymic tumors and focus on revealing the mechanisms of cardiotoxicity in patients with TETs, hoping to provide several valuable insights for maximizing the therapeutic potential of ICIs in TETs.

胸腺上皮肿瘤(TETs)是一种罕见的前纵隔恶性肿瘤,起源于胸腺,预后较差,标准的铂类化疗对治疗转移性或复发性疾病的疗效有限。在这种情况下,需要进一步改进新的治疗策略。免疫检查点抑制剂(ICIs)在癌症治疗的临床实践中得到了广泛应用,临床试验的早期结果为TET患者带来了显著的客观反应和持久的生存益处。然而,免疫相关不良事件(irAE),特别是心脏不良事件的发生率高于其他肿瘤类型。在接受ICIs治疗的患者中,心肌炎是一种进展迅速且危及生命的irAE,从而阻碍了ICI在TETs患者中的进一步应用。因此,本文旨在回顾评估ICIs治疗TETs的病例系列和临床试验的结果,并概述TETs中致命的ICI相关心肌炎的临床特征。此外,我们深入了解胸腺肿瘤的免疫生物学,并专注于揭示TETs患者心脏毒性的机制,希望为最大限度地发挥ICIs在TETs中的治疗潜力提供一些有价值的见解。
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引用次数: 0
A new synthetic lethal strategy expands the application of PARP inhibitors/cisplatin 一种新的合成致死策略扩大了PARP抑制剂/顺铂的应用
Pub Date : 2023-05-09 DOI: 10.1002/mog2.28
Jinrui Wang, Daniel D. Billadeau, Ying Zheng, Da Jia

In a recent study published in Signal Transduction and Targeted Therapy, Zhang et al.1 identified a panel of genes that served as a novel predictor of response to poly adenosine diphosphate-ribose polymerase (PARP) inhibitors/cisplatin in HR proficient patients, which could guide a broader application of PARP inhibitors/cisplatin in cancer therapy.

Cancer cells differ from normal cells in their ability to repair damaged DNA—most cancer cells lose one or more DNA repair pathways, resulting in greater reliance on the remaining pathways.2 Thus, small molecules that can induce DNA damage have been used to treat various cancers. Among them, cisplatin/PARP inhibitors are well established cancer drugs and are used to target tumor cells with homologous recombination (HR) defects.2 Platinum salts (carboplatin, cisplatin, and oxaliplatin) are the commonly-used chemotherapeutic agents, which were historically thought to cause cell death by inducing DNA damage.2 Recent studies suggest that the mechanisms of action of platinum salts are more diverse3 (Figure 1A). Zhang et al.1 further showed that cisplatin promotes cell death through DNA damage-induced ribosomal stress, rather than failed DNA repair, in certain tumor cells. PARP inhibitors are approved for the treatment of ovarian and breast cancers with BRCA1/2 mutations, and act through synthetic lethality in DNA repair-deficient tumors.3-5 However, it is known that some HR-proficient patients also respond well to PARP inhibitors and cisplatin therapy.3 Consistently, Zhang et al.1 also identified patients who benefited from the treatment of PARP inhibitors, despite their normal HR functions. Therefore, it is necessary to identify biomarkers that can help to stratify the patients so they will benefit most from PARP inhibitors and cisplatin therapy.

To identify these biomarkers, the authors analyzed RNA-Seq data from the Cancer Cell Line Encyclopedia and drug sensitivity data (GDSC) from the extensive and Sanger cell line databases1 (Figure 1B). They used weighted gene co-expression network analysis to negatively correlate drug signatures with co-expressed gene modules.1 Through these analyses, the authors found that expression of genes in the ribosome biogenesis pathway could be used to predict cellular drug response to PARP inhibition or cisplatin-based chemotherapy.1 Ultimately, they obtained a panel of 8 genes involved in ribosome biogenesis for further analysis.1

In the following studies, the authors provided multiple lines of evidence suggesting that these eight genes could be used to predict PARP inhibitors/cisplatin sensitivity.1 First,

1提出了一种新的合成杀伤策略,该策略不同于Helladay和Ashwoth小组提出的经典策略。Helladay和Ashwoth的策略依赖于抑制两种不同的DNA修复途径,但未能解释为什么PARP抑制剂/顺铂在治疗许多HR功能正常的肿瘤患者方面仍然有效。1 Zhang等人1发现,PARP抑制剂和顺铂可以在八个基因高表达的细胞中诱导致死,即使它们的HR功能很熟练。1因此,他们提出了一种新的治疗策略,将PARP抑制剂/顺铂与增加八个基因表达的药物相结合。1最后但并非最不重要的是,作者报道了三种上市药物可以增强PARP抑制剂和顺铂在某些肿瘤细胞中的治疗效果。1未来的研究应该确定其他具有类似活性的药物。当然,他们的工作也提出了一些重要的问题。首先,由于卵巢癌症的异质性和回顾性研究的固有偏见,需要更严格的前瞻性试验来验证作者的结论。第二,这些基因调节核糖体应激从而影响癌症药物敏感性的机制仍有待确定。1,2总之,张等人的研究1代表了DNA修复和癌症化疗领域的一个重要里程碑,并可能刺激更多的工作,通过靶向DNA修复途径来寻找新的治疗方法。王金瑞:书写——原稿(等);写作——复习;编辑(相等)。Daniel D.Billadeau:写作——原始草稿(相等);写作——复习;编辑(相等)。应政:书写——原稿(等);写作——复习;编辑(相等)。Da Jia:融资收购(平等);书写——原始草稿(相等);写作——复习;编辑(相等)。所有作者都已阅读并批准了最终手稿。作者声明没有利益冲突。本研究未涉及人类参与者和/或动物或知情同意书。因此,道德许可不适用于本条。
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引用次数: 0
Overexpression of DAPK1 and Beclin1 under oxygen and glucose deprivation conditions promotes excessive autophagy and apoptosis in A549 cells DAPK1和Beclin1在缺氧和缺糖条件下的过表达促进A549细胞的过度自噬和凋亡
Pub Date : 2023-04-26 DOI: 10.1002/mog2.30
Linlin Wu, Wenxue Sun, Dehua Liao, Yujin Guo, Qingying Si, Dadi Xie, Pei Jiang

In this study, we aimed to determine the specific roles of death-associated protein kinase 1 (DAPK1) and Beclin1 in non-small cell lung cancer (NSCLC) under oxygen and glucose deprivation (OGD). We found that OGD caused most cells to shrink, aggregate, and produce many vacuoles in the cytoplasm. Transmission electron microscopy revealed the presence of autophagic vesicles in the OGD group but not in the Control group. Moreover, the cell counting kit-8 assay showed that cell proliferation was reduced in the OGD group. Quantitative reverse transcription-polymerase chain reaction, western blot, and cell function assays showed that DAPK1 overexpression under OGD promoted apoptosis and autophagy in A549 cells. The coimmunoprecipitation assay confirmed the interaction between DAPK1 and Beclin1 protein. Moreover, knockdown of Beclin1 inhibited autophagy, but its overexpression promoted apoptosis in A549 cells. In vivo tumorigenesis experiment revealed that overexpression of DAPK1 promoted A549 cell apoptosis. Collectively, overexpression of DAPK1 and Beclin1 under OGD promoted excessive autophagy and apoptosis in A549 cells. Our study may provide a novel therapeutic target and theoretical basis for NSCLC treatment.

在本研究中,我们旨在确定死亡相关蛋白激酶1(DAPK1)和Beclin1在缺氧和缺糖(OGD)条件下非小细胞肺癌癌症(NSCLC)中的具体作用。我们发现OGD导致大多数细胞收缩、聚集,并在细胞质中产生许多液泡。透射电子显微镜显示OGD组存在自噬小泡,但对照组没有。此外,细胞计数试剂盒-8测定显示,OGD组的细胞增殖减少。定量逆转录聚合酶链式反应、蛋白质印迹和细胞功能测定表明,DAPK1在OGD下过表达促进了A549细胞的凋亡和自噬。共免疫沉淀分析证实DAPK1和Beclin1蛋白之间的相互作用。此外,敲低Beclin1抑制自噬,但其过表达促进A549细胞凋亡。体内肿瘤发生实验显示DAPK1过表达促进A549细胞凋亡。总之,DAPK1和Beclin1在OGD下的过度表达促进了A549细胞的过度自噬和凋亡。我们的研究可能为NSCLC的治疗提供新的治疗靶点和理论依据。
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引用次数: 0
NKT cells contribute to alleviating lung metastasis in adenoid cystic carcinoma NKT细胞有助于减轻腺样囊性癌的肺转移
Pub Date : 2023-04-15 DOI: 10.1002/mog2.29
Ge-xuan Feng, Meng-jiao Zhou, Lin Cao, Ting-yao Ma, Xue-lian Wang, Ran Gao, Xiao-hong Chen, Lu Kong

Salivary adenoid cystic carcinoma (SACC) with a unique MYB-NFIB fusion has been considered an “immune-cold” tumor, but the mechanisms behind this remain unclear. In this study, we analyzed the immune status of 29 SACC patients and found that most lung metastases exhibited an immunoinflammatory state, in contrast to the primary SACC tissues. Single-cell sequencing data showed that anergic T-cell types were low in primary inflammatory tissues, while inflammatory metastatic lung tissues had elevated levels of anergic CD8+ natural killer T (NKT)-like cells and low levels of memory T cells. Primary exclusive tissues had high levels of myeloid-derived suppressor cells (MDSCs) and low levels of activated CD8+ NKT-like cells. These data support the fact that metastatic SACC cells might induce a stronger immune response in the lung. Additionally, an in vivo experiment showed that a minimally invasive SACC cell line with higher expression of human leukocyte antigens -B and -C induced NKT cell activation in mice and effectively attenuated the incidence of lung metastases caused by a highly invasive SACC cell line. This suggests that NKT therapy may be active in treating SACC lung metastasis. Conclusively, this study sheds light on the immune microenvironment of SACC and highlights the potential of NKT-based therapy.

具有独特MYB-NFIB融合的唾液腺样囊性癌(SACC)被认为是一种“免疫性感冒”肿瘤,但其背后的机制尚不清楚。在这项研究中,我们分析了29名SACC患者的免疫状态,发现与原发性SACC组织相比,大多数肺转移瘤表现出免疫炎症状态。单细胞测序数据显示,原发性炎症组织中无能T细胞类型较低,而炎症转移性肺组织中无能CD8+自然杀伤T(NKT)样细胞水平升高,记忆T细胞水平较低。原发性排斥组织具有高水平的髓源性抑制细胞(MDSCs)和低水平的活化的CD8+NKT样细胞。这些数据支持这样一个事实,即转移性SACC细胞可能在肺部诱导更强的免疫反应。此外,一项体内实验表明,具有较高人类白细胞抗原-B和-C表达的微创SACC细胞系诱导小鼠NKT细胞活化,并有效降低了由高侵袭性SACC细胞株引起的肺转移的发生率。这表明NKT治疗可能对SACC肺转移有积极作用。总之,本研究揭示了SACC的免疫微环境,并强调了基于NKT的治疗的潜力。
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引用次数: 0
Identification of pyroptosis-related clusters for prediction of overall survival and characterization of tumor microenvironment infiltration in laryngeal squamous cell carcinoma 用于预测喉鳞状细胞癌总生存率的焦下垂相关簇的鉴定和肿瘤微环境浸润的表征
Pub Date : 2023-03-22 DOI: 10.1002/mog2.26
Wei Du, Xueming Xia, Jiayun Yu, Bin Shao

Laryngeal squamous cell carcinoma (LSCC) accounts for one-third of head and neck squamous carcinoma (HNSCC). Although improvements have been made in treatments, the prognosis of patients with LSCC is unsatisfactory. Pyroptosis creates an environment that inhibits tumor growth in various cancers, but pyroptosis regulation in the tumor immune microenvironment in LSCC remains little known. The Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases were used to collect clinical traits and gene expression data of LSCC patients. We present a systematic overview of the immune microenvironment of LSCC based on genetics and transcriptional profiles of pyroptosis-related genes (PRGs) and divide 220 LSCC into three distinct PRGclusters. Based on the three survival-related PRGs identified in Lasso-penalized Cox regression, samples from the training and validation cohorts were divided into two discrete geneClusters. We construct a prognostic model based on Risk score, quantify pyroptosis level and link it with patient outcome. Furthermore, we verified the expression level of one prognostic gene Basic Leucine Zipper ATF-Like Transcription Factor at the tissue level in the validation experiment. These findings reveal the crucial role of pyroptosis and can assist in predicting patient prognosis, guiding optimal treatment choices, and developing new immunotherapies for LSCC.

喉鳞状细胞癌(LSCC)占头颈部鳞状细胞癌的三分之一。尽管治疗有所改善,但LSCC患者的预后并不令人满意。Pyroptosis在各种癌症中创造了一种抑制肿瘤生长的环境,但LSCC中肿瘤免疫微环境中的Pyroptosi调节仍鲜为人知。利用基因表达综合数据库(GEO)和癌症基因组图谱(TCGA)数据库收集LSCC患者的临床特征和基因表达数据。基于pyroptosis相关基因(PRG)的遗传学和转录谱,我们对LSCC的免疫微环境进行了系统综述,并将220个LSCC分为三个不同的PRG簇。基于Lasso惩罚Cox回归中确定的三个与生存相关的PRG,将来自训练和验证队列的样本分为两个离散的基因簇。我们构建了一个基于风险评分的预后模型,量化焦下垂水平,并将其与患者结果联系起来。此外,我们在验证实验中验证了一种预后基因碱性亮氨酸拉链ATF样转录因子在组织水平上的表达水平。这些发现揭示了pyroptosis的关键作用,有助于预测患者预后,指导最佳治疗选择,并开发新的LSCC免疫疗法。
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引用次数: 0
Precision gas therapy by ultrasound-triggered for anticancer therapeutics 超声触发的精确气体疗法用于抗癌治疗
Pub Date : 2023-03-20 DOI: 10.1002/mog2.27
Fangxue Du, Ruiqian Guo, Ziyan Feng, Ziyao Wang, Xi Xiang, Bihui Zhu, Raul D. Rodriguez, Li Qiu

In recent years, ultrasound, as an external stimuli that can activate different types of naonocatalysts for therapy, has attracted extensive attention. One characteristic that makes ultrasound a particularly attractive trigger stimulus for nanomedicine is that it can be applied to the deep regions of the body noninvasively in a focused way. Different biological effects can be achieved by integrating ultrasound with nanocatalysts, and nanodroplets. Gas therapy, as a green antitumor treatment, has attracted substantial attention. The development of nanotechnology and nanomedicine has made gas therapy more precious by controlled release under internal, and outside factors and targeted delivery. In this article, an overview of ultrasound-based gas therapy on antitumor therapy has been provided. First, we explored the mechanism of ultrasound-triggered gas release. Second, we list the common gas release pathways and their mechanism in response to ultrasound activity. Third, exemplary instances of gas-generating facilities under ultrasound controllable are explored, with an emphasis on their originality and guiding principles. The impact of the gas-generating platform as a tumor therapy has also been considered. Finally, the difficulties and future prospects for this effective therapeutic approach are examined.

近年来,超声作为一种可以激活不同类型脑催化剂进行治疗的外部刺激物,引起了人们的广泛关注。使超声波成为纳米医学特别有吸引力的触发刺激的一个特征是,它可以以集中的方式无创地应用于身体深层。通过将超声波与纳米催化剂和纳米液滴结合,可以实现不同的生物效果。气体疗法作为一种绿色的抗肿瘤治疗方法,引起了人们的广泛关注。纳米技术和纳米医学的发展使气体疗法在内外因素的控制下释放和靶向递送变得更加珍贵。本文综述了基于超声的气体疗法在抗肿瘤治疗中的应用。首先,我们探讨了超声波触发气体释放的机制。其次,我们列出了常见的气体释放途径及其对超声活动的反应机制。第三,探讨了超声可控气体发生装置的实例,重点介绍了它们的独创性和指导原则。还考虑了气体产生平台作为肿瘤治疗的影响。最后,对这种有效治疗方法的困难和未来前景进行了探讨。
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引用次数: 0
Fatty acids in cancer: Metabolic functions and potential treatment 癌症中的脂肪酸:代谢功能和潜在治疗
Pub Date : 2023-03-10 DOI: 10.1002/mog2.25
Ao Du, Zhen Wang, Tengda Huang, Shuai Xue, Chuang Jiang, Guoteng Qiu, Kefei Yuan

Lipid metabolic reprogramming is one of the important metabolic characteristics of cancer cells. As major components of lipids, fatty acids provide energy and material basis for cancer cell survival. Abnormal fatty acid metabolism has been found in many cancers. Fatty acid uptake, transport, and synthesis are closely related to the pathogenesis of cancer. Meanwhile, fatty acid changes in the membrane structure of cancer cells and signal transduction mediated by signaling lipids are also helping cancer cells survive in the changing microenvironment. Some of these enzymes and metabolites involved in fatty acid metabolism are emerging as unique cancer biomarkers. Multiple studies have shown that disordered fatty acids can regulate tumor cell proliferation, metastasis, and drug resistance. Therefore, targeting fatty acid metabolism has become a promising treatment strategy. Here, we mainly present metabolic alterations of fatty acids, the basic components of lipids, in cancer. We discuss the cancer treatment based on fatty acid and fatty acid metabolism. These may provide a basis for a better understanding of lipid metabolic reprogramming in cancer, and also provide new ideas for cancer biomarker search, drug development, and combination therapy.

脂质代谢重编程是癌症细胞的重要代谢特征之一。脂肪酸作为脂质的主要成分,为癌症细胞的生存提供能量和物质基础。在许多癌症中都发现了脂肪酸代谢异常。脂肪酸的摄取、转运和合成与癌症的发病机制密切相关。同时,癌症细胞膜结构的脂肪酸变化和信号脂质介导的信号传导也有助于癌症细胞在不断变化的微环境中生存。这些参与脂肪酸代谢的酶和代谢产物中的一些正在作为独特的癌症生物标志物出现。多项研究表明,紊乱的脂肪酸可以调节肿瘤细胞的增殖、转移和耐药性。因此,靶向脂肪酸代谢已成为一种很有前途的治疗策略。在这里,我们主要介绍癌症中脂肪酸的代谢变化,脂肪酸是脂质的基本成分。我们讨论了基于脂肪酸和脂肪酸代谢的癌症治疗。这些可能为更好地理解癌症的脂质代谢重编程提供基础,也为癌症生物标志物搜索、药物开发和联合治疗提供新的思路。
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引用次数: 0
Morus alba derived Kuwanon-A combined with 5-fluorouracil reduce tumor progression via synergistic activation of GADD153 in gastric cancer 桑椹衍生的Kuwanon-A联合5-氟尿嘧啶通过协同激活GADD153在癌症中减少肿瘤进展
Pub Date : 2023-02-19 DOI: 10.1002/mog2.24
Jingjing Su, Abhimanyu Thakur, Guangzhao Pan, Jianglong Yan, Isha Gaurav, Sudha Thakur, Zhijun Yang, Alma Cili, Kui Zhang

Despite the application of conventional strategies including chemotherapy, radiotherapy, surgery, or immunotherapy, the mortality of gastric cancer (GC) patients remains high. Often, GC is not diagnosed until it has reached late stage, resulting in a missed surgical window. Therefore, a new therapeutic intervention for GC is necessary. Here, the combined application of Kuwanon-A (KA) and 5-fluorouracil (5-FU) was evaluated for its potential to combat GC for the first time. To determine the anticancer activity of KA (from Morus alba) along with 5-FU against GC, and their mechanism via GADD153, we examained anticancer potential of KA along with 5-FU via in vitro assays with GC cells, namely MKN-45, SGC-7901, HGC-27, and BGC-823, and in vivo assays with mouse xenograft of GC. KA alone could induce G2/M phase arrest and apoptosis in GC cells by activating GADD153 through the PERK/elF2α/ATF4 and IRE1/XBP1 signaling pathways, suggesting a critical role of increased endoplasmic reticulum stress in KA-induced apoptosis of GC cells. Moreover, the combination of KA and 5-FU showed an enhanced synergistic anticancer effect against GC both in vitro and in vivo. Conclusively, the combination of KA and 5-FU can act as an effective anticancer regimen in combating GC.

尽管应用了包括化疗、放疗、手术或免疫疗法在内的常规策略,但癌症(GC)患者的死亡率仍然很高。通常,GC直到晚期才被诊断出来,导致错过了手术窗口。因此,有必要对GC进行一种新的治疗干预。在此,首次评估了库瓦农-A(KA)和5-氟尿嘧啶(5-FU)联合应用对抗GC的潜力。为了确定KA(来自桑叶)和5-FU对GC的抗癌活性,以及它们通过GADD153的机制,我们通过用GC细胞(即MKN-45、SGC-7901、HGC-27和BGC-823)进行体外测定,以及用GC的小鼠异种移植物进行体内测定,来测试KA和5-FU的抗癌潜力。KA单独可通过PERK/elF2α/ATF4和IRE1/XBP1信号通路激活GADD153,诱导GC细胞G2/M期阻滞和凋亡,这表明内质网应激增加在KA诱导的GC细胞凋亡中起着关键作用。此外,KA和5-FU的组合在体外和体内对GC显示出增强的协同抗癌作用。总之,KA和5-FU联合用药可以作为一种有效的对抗GC的抗癌方案。
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引用次数: 1
Insight on the cellular and molecular basis of blood vessel formation: A specific focus on tumor targets and therapy 深入了解血管形成的细胞和分子基础:特别关注肿瘤靶点和治疗
Pub Date : 2023-02-08 DOI: 10.1002/mog2.22
Nimish Mol Stephen, Udayawara Rudresh Deepika, Tehreem Maradagi, Tatsuya Sugawara, Takashi Hirata, Ponesakki Ganesan

The cellular and molecular switches that govern angiogenesis are considered therapeutic targets for several diseases like tumors and atherosclerosis. Thus, understanding the detailed molecular mechanisms underlying the formation of the new blood vessel is essential for developing novel therapeutic strategies. The formation of a new blood vessel (angiogenesis) is tightly regulated by balancing pro- and antiangiogenic molecules. Dysregulated angiogenesis contributes to the pathogenicity of several diseases, including tumors associated with uncontrolled vessel growth. Experimental and clinical studies emphasize that angiogenesis is a critical step for the transition of the tumor to a life-threatening malignancy. In recent years, angiogenesis has been targeted as one of the primary therapeutic goals for treating tumors, and rapid progress has been made by modulating its molecular regulators. Hence, the mechanisms of how blood vessel formation occurs could provide molecular insight into future angiogenic therapy. This review summarizes briefly the molecular players of blood vessel formation comprising vasculogenesis and angiogenesis and their role in tumor progression alongside antiangiogenic therapy.

控制血管生成的细胞和分子开关被认为是肿瘤和动脉粥样硬化等几种疾病的治疗靶点。因此,了解新血管形成的详细分子机制对于开发新的治疗策略至关重要。新血管的形成(血管生成)是通过平衡促血管生成和抗血管生成分子来严格调节的。血管生成失调导致了几种疾病的致病性,包括与血管生长失控相关的肿瘤。实验和临床研究强调,血管生成是肿瘤转变为危及生命的恶性肿瘤的关键步骤。近年来,血管生成已成为治疗肿瘤的主要治疗目标之一,并通过调节其分子调节因子取得了快速进展。因此,血管形成的机制可以为未来的血管生成治疗提供分子见解。这篇综述简要总结了血管形成的分子作用,包括血管生成和血管生成,以及它们在肿瘤进展和抗血管生成治疗中的作用。
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引用次数: 0
Oncolytic virotherapy using neural stem cells as a novel treatment option for glioblastoma multiforme 利用神经干细胞进行溶瘤病毒治疗多形性胶质母细胞瘤
Pub Date : 2023-01-31 DOI: 10.1002/mog2.23
Tanvir Ahmed

The most deadly and aggressive form of brain cancer is called a glioblastoma multiforme. Following diagnosis, the median duration of survival is only 14 months. It is imperative to develop cutting-edge therapeutic options because the results of conventional treatments are so poor. Replication-competent oncolytic viruses and replication-deficient viral vectors can be used to treat malignant tumors, an idea that has been around for more than a century. Cancer cells can be eliminated by any class. Oncolytic viruses are created with the specific purpose of locating, attacking, and multiplying in cancerous cells while bypassing normal brain tissue. Because of this, the viruses can kill tumors while protecting healthy brain cells. Getting the oncolytic virus reach tumor locations where it is needed is the biggest challenge. If neural stem cells were used as carrier cells to deliver oncolytic viruses to the right tumor locations, glioblastoma multiforme virotherapy will be significantly more efficient. The most recent advancements in the field of utilizing neural stem cells to deliver oncolytic viruses into glioblastoma tumors are the main focus of this review.

癌症最致命和最具侵袭性的形式被称为多形性胶质母细胞瘤。诊断后,中位生存期仅为14 月。由于传统治疗的效果非常差,因此必须开发尖端的治疗方案。具有复制能力的溶瘤病毒和复制缺陷的病毒载体可以用于治疗恶性肿瘤,这一想法已经存在了一个多世纪。癌症细胞可以被任何种类的细胞消灭。溶瘤病毒的产生具有特定的目的,即绕过正常脑组织,在癌细胞中定位、攻击和繁殖。正因为如此,病毒可以杀死肿瘤,同时保护健康的脑细胞。让溶瘤病毒到达需要它的肿瘤部位是最大的挑战。如果使用神经干细胞作为载体细胞将溶瘤病毒输送到正确的肿瘤位置,多形性胶质母细胞瘤病毒治疗将明显更有效。利用神经干细胞向胶质母细胞瘤中递送溶瘤病毒领域的最新进展是本综述的主要焦点。
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引用次数: 1
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MedComm – Oncology
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