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癌症治疗的药物研发 | Molecular Oncology 特刊荐读

日期: 来源:Wiley威立收集编辑:

Molecular Oncology 是一本开放获取期刊,由欧洲生物化学学会联合会(FEBS)出版。期刊出版范围涉及基础、转化和临床肿瘤研究领域,关注肿瘤诊断、预防和预后方面的创新观念。期刊发表文章类型包括研究型文章、综述、Commentaries 及 Policy Papers。期刊执行透明的同行评议政策,投稿均由专职学术编辑团队处理。期刊利润均回馈科学研究。


期刊主页:

https://febs.onlinelibrary.wiley.com/toc/18780261


近期,Molecular Oncology 先后发表了两个和癌症相关的特刊专题:“衰老与癌症” 以及 “癌症治疗的药物研发”,本文将为您介绍“癌症治疗的药物研发”这个专题,欢迎点击阅读。


了解“衰老与癌症”主题特刊,请点击:

衰老与癌症 | Molecular Oncology 特刊荐读


特刊主题

Drug discovery for cancer therapy


特刊主页:

https://febs.onlinelibrary.wiley.com/toc/18780261/2022/16/21


扫描以下二维码浏览全部特刊内容


特刊介绍

Research over the last century has dramatically improved cancer prognosis. Molecular Oncology published a Thematic Issue on Drug Discovery for cancer therapy discussing the latest developments in discovering new biological therapies in a series of Review articles. Kirsten McAulay and colleagues highlighted important considerations when opting for fragment-based drug discovery (FBDD) such as candidate diversity and desirable lead properties for rapid drug development. Jordan Wilson and Joanna Loizou presented a multitude of approaches for the use of CRISPR-based genetic screens to elucidate novel gene-gene interactions that can be disrupted pharmacologically for the purpose of cancer treatment, focusing on DNA repair inhibitors. Rudd and Helleday reviewed inhibitors that target enzymes in dNTP metabolism, with a focus on the enzymes MTH1, MTHFD2 and SAMHD1. Lord et al. complemented the previous article by outlining mechanisms that may lead to resistance to DNA repair inhibitors (such as PARP, ATR, PolΘ or WRN) and describe mutations which would render patients unresponsive.


Laura Bousset and Jesus Gil summarised the current understanding of how senolytic drugs could complement anticancer therapies and how monitoring senescence in cancer patients can serve as a proxy for assessing the efficacy of the ‘one-two punch approach’. Giulio Donati and Bruno Amati condensed efforts from the field to limit c-Myc activity by targeting c-Myc interaction with MAX or modulating c-Myc transcription via BRD inhibitors. Fátima Al-Shahrour et al provided an overview of bioinformatics tools that can be used to infer the mechanism of action of a drug, stratify patients for personalized cancer medicine, or follow the evolutionary trajectories of cancer cells in a given tumor.



Fragment-based drug discovery—the importance of high-quality molecule libraries

Marta Bon, Alan Bilsland, Justin Bower, Kirsten McAulay



Fragment-based drug discovery (FBDD) uses collections (libraries) of smaller, less complex molecules (fragments) than drug-like molecules used in high-throughput screening. Herein, we highlight the advantages of FBDD, which has already resulted in several marketed drugs. Finding quality FBDD hits depends on good library design. Here, Marta Bon et al. describe their views on chemical and computational aspects of library design and discuss emerging technologies.


原文链接:

https://febs.onlinelibrary.wiley.com/doi/10.1002/1878-0261.13277





Exploring the genetic space of the DNA damage response for cancer therapy through CRISPR-based screens

Jordan Wilson, Joanna I. Loizou



The combination of CRISPR gene editing and drug treatments in a pooled screening format allows for the discovery of novel gene-drug interactions. These interactions can potentially provide biomarkers for drug sensitivity and resistance in a clinical setting.


原文链接:

https://febs.onlinelibrary.wiley.com/doi/10.1002/1878-0261.13272





Targeting the DNA damage response and repair in cancer through nucleotide metabolism

Marta BonThomas Helleday, Sean G. Rudd, Alan Bilsland, Justin Bower, Kirsten McAulay



The exploitation of the DNA damage response and DNA repair proficiency of cancer cells is an important anticancer strategy. The replication and repair of the DNA molecule are dependent upon the supply of deoxynucleoside triphosphate (dNTP) building blocks, which are produced and maintained by nucleotide metabolic pathways. Here, Thomas Helleda and Sean Rudd discuss how targeting these pathways can be a promising anticancer strategy.


原文链接:

https://febs.onlinelibrary.wiley.com/doi/10.1002/1878-0261.13227





Resistance to DNA repair inhibitors in cancer

Joseph S. Baxter, Diana Zatreanu, Stephen J. Pettitt, Christopher J. Lord



Drug resistance is a common phenomenon that impairs the overall effectiveness of cancer treatments including DNA repair inhibitors. How PARP inhibitor resistance emerges is partially understood. Here, Christopher Lord and colleagues discuss how resistance to inhibitors of ATR kinase, WRN helicase or the DNA polymerase/helicase Polθ could emerge and how DNA repair inhibitor resistance could be targeted.


原文链接:

https://febs.onlinelibrary.wiley.com/doi/10.1002/1878-0261.13224





MYC and therapy resistance in cancer: risks and opportunities

Giulio Donati, Bruno Amati



Therapy resistance is a major limitation in clinical oncology. The MYC oncogene not only drives cancer progression, but also favors resistance to classical chemotherapy and targeted therapies. Giulio Donati and Bruno Amati summarize the clinical evidence and molecular mechanisms linking MYC and therapy resistance, and discusses possible innovative strategies to target the specific vulnerabilities of MYC-driven cancer.


原文链接:

https://febs.onlinelibrary.wiley.com/doi/10.1002/1878-0261.13319





Targeting senescence as an anticancer therapy

Laura Bousset, Jesús Gil



Conventional cancer therapies induce senescence. While senescence contributes to therapy outcome, accumulation of senescent cells can promote cancer progression, metastasis and therapy resistance. One-two punch approaches aim to combine cancer therapies with senolytics to remove senescent tumour cells. Here, Laura Bousset, Jesús Gilreview senescence in the context of cancer and discuss future challenges of senotherapies for cancer treatment.


原文链接:

https://febs.onlinelibrary.wiley.com/doi/10.1002/1878-0261.13312





Bioinformatics roadmap for therapy selection in cancer genomics

María José Jiménez-Santos, Santiago García-Martín, Coral Fustero-Torre, Tomás Di Domenico, Gonzalo Gómez-López, Fátima Al-Shahrour



Intertumour heterogeneity and intratumour heterogeneity have been revealed as key causes of treatment failure and relapse. This review aims to provide a bioinformatics roadmap and general guidelines to propose anticancer data-driven treatment strategies for bulk and single-cell omics data in order to target tumour heterogeneity. Moreover, Fátima Al-Shahrour and colleagues discuss how these workflows could be integrated into the clinical practice.


原文链接:

https://febs.onlinelibrary.wiley.com/doi/10.1002/1878-0261.13286





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