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Leveraging genomics, transcriptomics and epigenomics to understand chemoimmunotherapy resistance in chronic lymphocytic leukemia. 利用基因组学、转录组学和表观基因组学了解慢性淋巴细胞白血病的化疗免疫治疗耐药性。
Pub Date : 2024-02-28 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2023.98
Shin Yeu Ong, Lili Wang

Patients with chronic lymphocytic leukemia (CLL) have differing clinical outcomes. Recent advances integrating multi-omic data have uncovered molecular subtypes in CLL with different prognostic implications and may allow better prediction of therapy response. While finite-duration chemoimmunotherapy (CIT) has enabled deep responses and prolonged duration of responses in the past, the advent of novel targeted therapy for the treatment of CLL has dramatically changed the therapeutic landscape. In this review, we discuss the latest genomic, transcriptomic, and epigenetic alterations regarded as major drivers of resistance to CIT in CLL. Further advances in genomic medicine will allow for better prediction of response to therapy and provide the basis for rational selection of therapy for long-term remissions with minimal toxicity.

慢性淋巴细胞白血病(CLL)患者的临床预后各不相同。整合多组学数据的最新进展发现了具有不同预后影响的慢性淋巴细胞白血病分子亚型,从而可以更好地预测治疗反应。过去,有限时间化疗免疫疗法(CIT)能够产生深度反应并延长反应持续时间,而治疗 CLL 的新型靶向疗法的出现则极大地改变了治疗格局。在这篇综述中,我们将讨论被视为CLL对CIT产生耐药性的主要驱动因素的最新基因组、转录组和表观遗传学改变。基因组医学的进一步发展将能更好地预测对治疗的反应,并为合理选择治疗方法提供依据,以实现毒性最小的长期缓解。
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引用次数: 0
Reactive oxygen species and its role in pathogenesis and resistance to therapy in acute myeloid leukemia. 活性氧及其在急性髓性白血病发病机制和抗药性中的作用。
Pub Date : 2024-02-22 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2023.125
Jamshid Sorouri Khorashad, Sian Rizzo, Alex Tonks

Relapse following a short clinical response to therapy is the major challenge for the management of acute myeloid leukemia (AML) patients. Leukemic stem cells (LSC), as the source of relapse, have been investigated for their metabolic preferences and their alterations at the time of relapse. As LSC rely on oxidative phosphorylation (OXPHOS) for energy requirement, reactive oxygen species (ROS), as by-products of OXPHOS, have been investigated for their role in the effectiveness of the standard AML therapy. Increased levels of non-mitochondrial ROS, generated by nicotinamide adenine dinucleotide phosphate oxidase, in a subgroup of AML patients add to the complexity of studying ROS. Although there are various studies presenting the contribution of ROS to AML pathogenesis, resistance, and its inhibition or activation as a target, a model that can clearly explain its role in AML has not been conceptualized. This is due to the heterogeneity of AML, the dynamics of ROS production, which is influenced by factors such as the type of treatment, cell differentiation state, mitochondrial activity, and also the heterogeneous generation of non-mitochondrial ROS and limited available data on their interaction with the microenvironment. This review summarizes these challenges and the recent progress in this field.

急性髓性白血病(AML)患者在短期临床治疗反应后复发是治疗面临的主要挑战。白血病干细胞(LSC)是复发的来源,人们一直在研究它们的代谢偏好及其在复发时的变化。由于白血病干细胞依赖氧化磷酸化(OXPHOS)来获取能量,活性氧(ROS)作为 OXPHOS 的副产物,已被用于研究其在急性髓细胞性白血病标准疗法有效性中的作用。在一部分急性髓细胞性白血病患者中,由烟酰胺腺嘌呤二核苷酸磷酸氧化酶产生的非线粒体 ROS 水平升高,增加了研究 ROS 的复杂性。尽管有各种研究介绍了 ROS 对急性髓细胞性白血病发病机制的贡献、抗药性及其作为靶点的抑制或激活,但尚未形成一个能清楚解释其在急性髓细胞性白血病中作用的模型。这是由于急性髓细胞性白血病的异质性、ROS产生的动态性(受治疗类型、细胞分化状态、线粒体活性等因素的影响)、非线粒体ROS产生的异质性以及它们与微环境相互作用的现有数据有限。本综述总结了这些挑战以及该领域的最新进展。
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引用次数: 0
Glycogen synthase kinase 3β: the nexus of chemoresistance, invasive capacity, and cancer stemness in pancreatic cancer. 糖原合成酶激酶 3β:胰腺癌化疗抗药性、侵袭能力和癌症干细胞的纽带。
Pub Date : 2024-01-31 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2023.84
Masahiro Uehara, Takahiro Domoto, Satoshi Takenaka, Osamu Takeuchi, Takeo Shimasaki, Tomoharu Miyashita, Toshinari Minamoto

The treatment of pancreatic cancer remains a significant clinical challenge due to the limited number of patients eligible for curative (R0) surgery, failures in the clinical development of targeted and immune therapies, and the pervasive acquisition of chemotherapeutic resistance. Refractory pancreatic cancer is typified by high invasiveness and resistance to therapy, with both attributes related to tumor cell stemness. These malignant characteristics mutually enhance each other, leading to rapid cancer progression. Over the past two decades, numerous studies have produced evidence of the pivotal role of glycogen synthase kinase (GSK)3β in the progression of over 25 different cancer types, including pancreatic cancer. In this review, we synthesize the current knowledge on the pathological roles of aberrant GSK3β in supporting tumor cell proliferation and invasion, as well as its contribution to gemcitabine resistance in pancreatic cancer. Importantly, we discuss the central role of GSK3β as a molecular hub that mechanistically connects chemoresistance, tumor cell invasion, and stemness in pancreatic cancer. We also discuss the involvement of GSK3β in the formation of desmoplastic tumor stroma and in promoting anti-cancer immune evasion, both of which constitute major obstacles to successful cancer treatment. Overall, GSK3β has characteristics of a promising therapeutic target to overcome chemoresistance in pancreatic cancer.

由于符合治愈性(R0)手术条件的患者人数有限、靶向疗法和免疫疗法的临床开发失败以及化疗耐药性的普遍存在,胰腺癌的治疗仍然是一项重大的临床挑战。难治性胰腺癌具有高侵袭性和耐药性,这两种特性都与肿瘤细胞的干性有关。这些恶性特征相互促进,导致癌症迅速发展。在过去二十年中,大量研究证明糖原合酶激酶(GSK)3β在包括胰腺癌在内的超过 25 种不同癌症类型的进展过程中起着关键作用。在这篇综述中,我们总结了目前关于异常 GSK3β 在支持肿瘤细胞增殖和侵袭中的病理作用及其对胰腺癌吉西他滨耐药性的贡献的知识。重要的是,我们讨论了 GSK3β 作为分子枢纽的核心作用,它从机理上将胰腺癌的化疗耐药性、肿瘤细胞侵袭和干性联系在一起。我们还讨论了 GSK3β 参与脱鳞肿瘤基质的形成和促进抗癌免疫逃避的情况,这两者都是成功治疗癌症的主要障碍。总之,GSK3β具有克服胰腺癌化疗耐药性的治疗靶点的特征。
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引用次数: 0
Ritonavir reverses resistance to docetaxel and cabazitaxel in prostate cancer cells with acquired resistance to docetaxel. 利托那韦能逆转前列腺癌细胞对多西他赛和卡巴他赛的耐药性。
Pub Date : 2024-01-31 eCollection Date: 2024-01-01 DOI: 10.20517/cdr.2023.136
Eric van der Putten, Katja Wosikowski, Jos H Beijnen, Gábor Imre, Colin R Freund

Aim: Docetaxel is a microtubule-stabilizing drug used for the treatment of several cancers, including prostate cancer. Resistance to docetaxel can either occur through intrinsic resistance or develop under therapeutic pressure, i.e., acquired resistance. A possible explanation for the occurrence of acquired resistance to docetaxel is increased drug efflux via P-glycoprotein (P-gp) drug transporters. Methods: We have generated docetaxel-resistant cell lines DU-145DOC10 and 22Rv1DOC8 by exposing parental cell lines DU-145DOC and 22Rv1 to increasing levels of docetaxel. Gene expression levels between DU-145DOC10 and 22Rv1DOC8 were compared with those of their respective originator cell lines. Both parental and resistant cell lines were treated with the taxane drugs docetaxel and cabazitaxel in combination with the P-gp/CYP3A4 inhibitor ritonavir and the P-gp inhibitor elacridar. Results: In the docetaxel-resistant cell lines DU-145DOC10 and 22Rv1DOC8, the ABCB1 (P-gp) gene was highly up-regulated. Expression of the P-gp protein was also significantly increased in the docetaxel-resistant cell lines in a Western blotting assay. The addition of ritonavir to docetaxel resulted in a return of the sensitivity to docetaxel in the DU-145DOC10 and 22Rv1DOC8 to a level similar to the sensitivity in the originator cells. We found that these docetaxel-resistant cell lines could also be re-sensitized to cabazitaxel in a similar manner. In a Caco-2 P-gp transporter assay, functional inhibition of P-gp-mediated transport of docetaxel with ritonavir was demonstrated. Conclusion: Our results demonstrate that ritonavir restores sensitivity to both docetaxel and cabazitaxel in docetaxel-resistant cell lines, most likely by inhibiting P-gp-mediated drug efflux.

目的:多西他赛是一种微管稳定药物,用于治疗包括前列腺癌在内的多种癌症。对多西他赛的耐药性可以通过内在耐药性产生,也可以在治疗压力下产生,即获得性耐药性。对多西他赛产生获得性耐药性的一个可能解释是,通过 P 糖蛋白(P-gp)药物转运体的药物外流增加。方法:我们将亲本细胞株 DU-145DOC 和 22Rv1 暴露于不断增加的多西他赛水平,生成了多西他赛耐药细胞株 DU-145DOC10 和 22Rv1DOC8。将 DU-145DOC10 和 22Rv1DOC8 的基因表达水平与其各自的原代细胞系的基因表达水平进行了比较。亲代细胞系和耐药细胞系都接受了多西他赛和卡巴齐他赛与 P-gp/CYP3A4 抑制剂利托那韦和 P-gp 抑制剂艾拉克瑞达联合治疗。研究结果在多西他赛耐药细胞系 DU-145DOC10 和 22Rv1DOC8 中,ABCB1(P-gp)基因高度上调。在 Western 印迹检测中,多西他赛耐药细胞系的 P-gp 蛋白表达也明显增加。在多西他赛中加入利托那韦后,DU-145DOC10和22Rv1DOC8对多西他赛的敏感性恢复到与原代细胞相似的水平。我们发现,这些对多西他赛耐药的细胞系也能以类似的方式重新对卡巴他赛敏感。在 Caco-2 P-gp 转运试验中,利托那韦对 P-gp 介导的多西他赛转运起到了功能性抑制作用。结论我们的研究结果表明,利托那韦很可能通过抑制 P-gp 介导的药物外流,恢复了多西他赛耐药细胞株对多西他赛和卡巴他赛的敏感性。
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引用次数: 0
Supramolecular host-guest nanosystems for overcoming cancer drug resistance. 用于克服癌症抗药性的超分子主客体纳米系统。
IF 4.6 Q1 ONCOLOGY Pub Date : 2023-11-22 eCollection Date: 2023-01-01 DOI: 10.20517/cdr.2023.77
Sha Wu, Miaomiao Yan, Minghao Liang, Wenzhi Yang, Jingyu Chen, Jiong Zhou

Cancer drug resistance has become one of the main challenges for the failure of chemotherapy, greatly limiting the selection and use of anticancer drugs and dashing the hopes of cancer patients. The emergence of supramolecular host-guest nanosystems has brought the field of supramolecular chemistry into the nanoworld, providing a potential solution to this challenge. Compared with conventional chemotherapeutic platforms, supramolecular host-guest nanosystems can reverse cancer drug resistance by increasing drug uptake, reducing drug efflux, activating drugs, and inhibiting DNA repair. Herein, we summarize the research progress of supramolecular host-guest nanosystems for overcoming cancer drug resistance and discuss the future research direction in this field. It is hoped that this review will provide more positive references for overcoming cancer drug resistance and promoting the development of supramolecular host-guest nanosystems.

癌症耐药性已成为化疗失败的主要挑战之一,极大地限制了抗癌药物的选择和使用,使癌症患者的希望破灭。超分子主客体纳米系统的出现将超分子化学领域带入了纳米世界,为解决这一难题提供了可能。与传统的化疗平台相比,超分子主客体纳米系统可以通过增加药物吸收、减少药物外流、激活药物和抑制DNA修复来逆转癌症耐药性。在此,我们总结了超分子主客体纳米系统克服癌症耐药性的研究进展,并探讨了该领域未来的研究方向。希望本综述能为克服癌症耐药性、促进超分子主客体纳米系统的发展提供更多积极的参考。
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引用次数: 0
Unveiling T cell evasion mechanisms to immune checkpoint inhibitors in acute myeloid leukemia. 揭示急性髓系白血病免疫检查点抑制剂的T细胞逃避机制。
Pub Date : 2023-09-26 eCollection Date: 2023-01-01 DOI: 10.20517/cdr.2023.39
Lindsay Gurska, Kira Gritsman

Acute myeloid leukemia (AML) is a heterogeneous and aggressive hematologic malignancy that is associated with a high relapse rate and poor prognosis. Despite advances in immunotherapies in solid tumors and other hematologic malignancies, AML has been particularly difficult to treat with immunotherapies, as their efficacy is limited by the ability of leukemic cells to evade T cell recognition. In this review, we discuss the common mechanisms of T cell evasion in AML: (1) increased expression of immune checkpoint molecules; (2) downregulation of antigen presentation molecules; (3) induction of T cell exhaustion; and (4) creation of an immunosuppressive environment through the increased frequency of regulatory T cells. We also review the clinical investigation of immune checkpoint inhibitors (ICIs) in AML. We discuss the limitations of ICIs, particularly in the context of T cell evasion mechanisms in AML, and we describe emerging strategies to overcome T cell evasion, including combination therapies. Finally, we provide an outlook on the future directions of immunotherapy research in AML, highlighting the need for a more comprehensive understanding of the complex interplay between AML cells and the immune system.

急性髓细胞白血病(AML)是一种异质性和侵袭性血液系统恶性肿瘤,复发率高,预后差。尽管在实体瘤和其他血液系统恶性肿瘤的免疫疗法方面取得了进展,但AML特别难以用免疫疗法治疗,因为其疗效受到白血病细胞逃避T细胞识别能力的限制。在这篇综述中,我们讨论了AML中T细胞逃避的常见机制:(1)免疫检查点分子表达增加;(2) 抗原呈递分子的下调;(3) 诱导T细胞耗竭;以及(4)通过增加调节性T细胞的频率来创造免疫抑制环境。我们还回顾了免疫检查点抑制剂(ICIs)在AML中的临床研究。我们讨论了ICIs的局限性,特别是在AML中T细胞逃避机制的背景下,并描述了克服T细胞逃避的新策略,包括联合疗法。最后,我们展望了AML免疫治疗研究的未来方向,强调需要更全面地了解AML细胞和免疫系统之间的复杂相互作用。
{"title":"Unveiling T cell evasion mechanisms to immune checkpoint inhibitors in acute myeloid leukemia.","authors":"Lindsay Gurska, Kira Gritsman","doi":"10.20517/cdr.2023.39","DOIUrl":"10.20517/cdr.2023.39","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is a heterogeneous and aggressive hematologic malignancy that is associated with a high relapse rate and poor prognosis. Despite advances in immunotherapies in solid tumors and other hematologic malignancies, AML has been particularly difficult to treat with immunotherapies, as their efficacy is limited by the ability of leukemic cells to evade T cell recognition. In this review, we discuss the common mechanisms of T cell evasion in AML: (1) increased expression of immune checkpoint molecules; (2) downregulation of antigen presentation molecules; (3) induction of T cell exhaustion; and (4) creation of an immunosuppressive environment through the increased frequency of regulatory T cells. We also review the clinical investigation of immune checkpoint inhibitors (ICIs) in AML. We discuss the limitations of ICIs, particularly in the context of T cell evasion mechanisms in AML, and we describe emerging strategies to overcome T cell evasion, including combination therapies. Finally, we provide an outlook on the future directions of immunotherapy research in AML, highlighting the need for a more comprehensive understanding of the complex interplay between AML cells and the immune system.</p>","PeriodicalId":70759,"journal":{"name":"癌症耐药(英文)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10571054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41241496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A review of strategies to overcome immune resistance in the treatment of advanced prostate cancer. 克服免疫抵抗治疗晚期前列腺癌症的策略综述。
IF 4.6 Q1 ONCOLOGY Pub Date : 2023-09-25 eCollection Date: 2023-01-01 DOI: 10.20517/cdr.2023.48
Kenneth Sooi, Robert Walsh, Nesaretnam Kumarakulasinghe, Alvin Wong, Natalie Ngoi

Immunotherapy has become integral in cancer therapeutics over the past two decades and is now part of standard-of-care treatment in multiple cancer types. While various biomarkers and pathway alterations such as dMMR, CDK12, and AR-V7 have been identified in advanced prostate cancer to predict immunotherapy responsiveness, the vast majority of prostate cancer remain intrinsically immune-resistant, as evidenced by low response rates to anti-PD(L)1 monotherapy. Since regulatory approval of the vaccine therapy sipuleucel-T in the biomarker-unselected population, there has not been much success with immunotherapy treatment in advanced prostate cancer. Researchers have looked at various strategies to overcome immune resistance, including the identification of more biomarkers and the combination of immunotherapy with existing effective prostate cancer treatments. On the horizon, novel drugs using bispecific T-cell engager (BiTE) and chimeric antigen receptors (CAR) technology are being explored and have shown promising early efficacy in this disease. Here we discuss the features of the tumour microenvironment that predispose to immune resistance and rational strategies to enhance antitumour responsiveness in advanced prostate cancer.

在过去的二十年里,免疫治疗已经成为癌症治疗的一部分,并且现在是多种癌症类型的标准护理治疗的组成部分。虽然已经在晚期前列腺癌症中鉴定了多种生物标志物和途径改变,如dMMR、CDK12和AR-V7,以预测免疫疗法的反应性,但绝大多数癌症仍然具有内在的免疫耐受性,抗PD(L)1单药疗法的低反应率证明了这一点。自从监管部门批准在生物标志物选择人群中使用sipuleucel-T疫苗疗法以来,晚期前列腺癌症的免疫疗法治疗并没有取得多大成功。研究人员研究了克服免疫抵抗的各种策略,包括识别更多的生物标志物,以及将免疫疗法与现有的有效前列腺癌症治疗相结合。展望未来,使用双特异性T细胞接合剂(BiTE)和嵌合抗原受体(CAR)技术的新药正在探索中,并在该疾病中显示出有希望的早期疗效。在这里,我们讨论了肿瘤微环境的特点,易于免疫抵抗和提高晚期前列腺癌症抗肿瘤反应性的合理策略。
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引用次数: 0
Emerging resistance vs. losing response to immune check point inhibitors in renal cell carcinoma: two differing phenomena. 肾细胞癌对免疫检查点抑制剂产生耐药性与失去反应:两种不同的现象。
Pub Date : 2023-09-20 eCollection Date: 2023-01-01 DOI: 10.20517/cdr.2023.47
Arya Mariam Roy, Saby George

The introduction of immune checkpoint inhibitor (ICI) has revolutionized the treatment of metastatic renal cell carcinoma (mRCC) and has dramatically improved the outcomes of patients. The use of monotherapy or combinations of ICIs targeting PD-1/PD-L1 and CTLA-4, as well as the addition of ICIs with tyrosine kinase inhibitors, has significantly enhanced the overall survival of mRCC patients. Despite these promising results, there remains a subset of patients who either do not respond to treatment (primary resistance) or develop resistance to therapy over time (acquired resistance). Understanding the mechanisms underlying the development of resistance to ICI treatment is crucial in the management of mRCC, as they can be used to identify new targets for innovative therapeutic strategies. Currently, there is an unmet need to develop new predictive and prognostic biomarkers that can aid in the development of personalized treatment options for mRCC patients. In this review, we summarize several mechanisms of ICI resistance in RCC, including alterations in tumor microenvironment, upregulation of alternative immune checkpoint pathways, and genetic and epigenetic changes. Additionally, we highlight potential strategies that can be used to overcome resistance, such as combination therapy, targeted therapy, and immune modulation.

免疫检查点抑制剂(ICI)的引入彻底改变了转移性肾细胞癌(mRCC)的治疗,并显著改善了患者的预后。使用靶向PD-1/PD-L1和CTLA-4的ICIs的单一疗法或组合,以及添加ICIs和酪氨酸激酶抑制剂,显著提高了mRCC患者的总体生存率。尽管有这些有希望的结果,但仍有一部分患者对治疗没有反应(原发性耐药性)或随着时间的推移对治疗产生耐药性(获得性耐药性)。了解ICI治疗耐药性发展的机制对于mRCC的管理至关重要,因为它们可以用于确定创新治疗策略的新靶点。目前,开发新的预测和预后生物标志物的需求尚未得到满足,这些生物标志物可以帮助mRCC患者开发个性化的治疗方案。在这篇综述中,我们总结了RCC中ICI耐药性的几种机制,包括肿瘤微环境的改变、替代免疫检查点途径的上调以及遗传和表观遗传学变化。此外,我们强调了可用于克服耐药性的潜在策略,如联合治疗、靶向治疗和免疫调节。
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引用次数: 0
Tumor-intrinsic metabolic reprogramming and how it drives resistance to anti-PD-1/PD-L1 treatment. 肿瘤内在代谢重编程及其如何驱动抗PD-1/PD-L1治疗的耐药性。
Pub Date : 2023-09-04 eCollection Date: 2023-01-01 DOI: 10.20517/cdr.2023.60
Kyra Laubach, Tolga Turan, Rebecca Mathew, Julie Wilsbacher, John Engelhardt, Josue Samayoa

The development of immune checkpoint blockade (ICB) therapies has been instrumental in advancing the field of immunotherapy. Despite the prominence of these treatments, many patients exhibit primary or acquired resistance, rendering them ineffective. For example, anti-programmed cell death protein 1 (anti-PD-1)/anti-programmed cell death ligand 1 (anti-PD-L1) treatments are widely utilized across a range of cancer indications, but the response rate is only 10%-30%. As such, it is necessary for researchers to identify targets and develop drugs that can be used in combination with existing ICB therapies to overcome resistance. The intersection of cancer, metabolism, and the immune system has gained considerable traction in recent years as a way to comprehensively study the mechanisms that drive oncogenesis, immune evasion, and immunotherapy resistance. As a result, new research is continuously emerging in support of targeting metabolic pathways as an adjuvant to ICB to boost patient response and overcome resistance. Due to the plethora of studies in recent years highlighting this notion, this review will integrate the relevant articles that demonstrate how tumor-derived alterations in energy, amino acid, and lipid metabolism dysregulate anti-tumor immune responses and drive resistance to anti-PD-1/PD-L1 therapy.

免疫检查点阻断(ICB)疗法的发展有助于推进免疫治疗领域。尽管这些治疗方法很突出,但许多患者表现出原发性或获得性耐药性,使其无效。例如,抗程序性细胞死亡蛋白1(抗PD-1)/抗程序性电池死亡配体1(抗PD-L1)治疗在一系列癌症适应症中广泛使用,但应答率仅为10%-30%。因此,研究人员有必要确定靶点,并开发出可与现有ICB疗法结合使用的药物,以克服耐药性。近年来,癌症、新陈代谢和免疫系统的交叉已经获得了相当大的吸引力,作为全面研究驱动肿瘤发生、免疫逃避和免疫疗法耐药性的机制的一种方式。因此,新的研究不断出现,支持靶向代谢途径作为ICB的佐剂,以提高患者反应并克服耐药性。由于近年来有大量研究强调了这一概念,这篇综述将整合相关文章,证明肿瘤引起的能量、氨基酸和脂质代谢的改变如何失调抗肿瘤免疫反应,并导致对抗PD-1/PD-L1治疗的耐药性。
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引用次数: 0
Resistance of breast cancer cells to paclitaxel is associated with low expressions of miRNA-186 and miRNA-7. 癌症细胞对紫杉醇的耐药性与miRNA-186和miRNA-7的低表达有关。
Pub Date : 2023-09-01 eCollection Date: 2023-01-01 DOI: 10.20517/cdr.2023.19
Vera Apollonova, Daniil Plevako, Alexandr Garanin, Elena Sidina, Lidia Zabegina, Margarita Knyazeva, Viktoria Smirnova, Anna Artemyeva, Petr Krivorotko, Anastasia Malek

Aim: Neo-adjuvant chemotherapy is a common approach for the complex treatment of breast cancer (BC) and paclitaxel (PTX) is frequently included in the therapeutic regimen. However, the effect of PTX-based treatment is hard to predict precisely based on routinely used markers. As microRNAs are considered a new promising class of biomarkers, the link between miRNA expression and PTX resistance of BC cells needs to be well investigated. This study aimed at the identification of miRNAs associated with responses of BC cells to PTX. Methods: Intrinsic PTX sensitivity and miRNA profiling were assayed in five BC cell lines to identify candidate miRNAs. Selected miRNA (n. 15) expressions were analyzed by real-time-quantitative polymerase chain reaction (RT-qPCR) in BC tissue samples (n. 31) obtained from a diagnostic biopsy. Results were analyzed in the context of the effect of two cycles of PTX and the effect of the completed scheme of neoadjuvant therapy. The study's design facilitated the evaluation of the effect of PTX on cells and the identification of features of the microRNA expression profiles associated exclusively with sensitivity to this drug. Results: miR-186 and miR-7 expression in BC tissues was higher in patients with better outcomes of PTX-based neoadjuvant therapy. Conclusion: High expressions of miR-186 and miR-7 are associated with good response to PTX, whereas their low expressions may be associated with resistance to PTX in BC, indicating the possibility of developing innovative test systems for the prediction of the PTX response, which can be used before the start of neo-adjuvant chemotherapy for BC.

目的:新辅助化疗是癌症(BC)复杂治疗的常用方法,紫杉醇(PTX)经常被纳入治疗方案。然而,基于PTX的治疗效果很难根据常规使用的标志物准确预测。由于微小RNA被认为是一类新的有前景的生物标志物,miRNA表达与BC细胞PTX抗性之间的联系需要深入研究。本研究旨在鉴定与BC细胞对PTX反应相关的miRNA。方法:在5个BC细胞系中测定固有PTX敏感性和miRNA图谱,以鉴定候选miRNA。通过实时定量聚合酶链反应(RT-qPCR)分析从诊断活检获得的BC组织样本(n.31)中选定的miRNA(n.15)表达。在两个周期的PTX效果和完成的新辅助治疗方案的效果的背景下分析结果。该研究的设计有助于评估PTX对细胞的影响,并鉴定仅与该药物敏感性相关的微小RNA表达谱的特征。结果:基于PTX的新辅助治疗效果较好的患者,BC组织中miR-186和miR-7的表达较高。结论:miR-186和miR-7的高表达与BC对PTX的良好反应有关,而它们的低表达可能与BC对PT的耐药性有关,这表明开发用于预测PTX反应的创新测试系统的可能性,该系统可在BC新辅助化疗开始前使用。
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引用次数: 0
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