NAR Cancer最新文献_第4页

Current proteomics methods applicable to dissecting the DNA damage response. 适用于剖析 DNA 损伤反应的当前蛋白质组学方法。

NAR Cancer Pub Date : 2023-05-19 eCollection Date: 2023-06-01 DOI: 10.1093/narcan/zcad020

Monita Muralidharan, Nevan J Krogan, Mehdi Bouhaddou, Minkyu Kim

引用次数: 0

GSK-3484862 targets DNMT1 for degradation in cells. GSK-3484862靶向DNMT1用于细胞中的降解。

NAR Cancer Pub Date : 2023-05-17 eCollection Date: 2023-06-01 DOI: 10.1093/narcan/zcad022

Qin Chen, Bigang Liu, Yang Zeng, Jee Won Hwang, Nan Dai, Ivan R Corrêa, Marcos R Estecio, Xing Zhang, Margarida A Santos, Taiping Chen, Xiaodong Cheng

{"title":"GSK-3484862 targets DNMT1 for degradation in cells.","authors":"Qin Chen, Bigang Liu, Yang Zeng, Jee Won Hwang, Nan Dai, Ivan R Corrêa, Marcos R Estecio, Xing Zhang, Margarida A Santos, Taiping Chen, Xiaodong Cheng","doi":"10.1093/narcan/zcad022","DOIUrl":"10.1093/narcan/zcad022","url":null,"abstract":"Maintenance of genomic methylation patterns at DNA replication forks by DNMT1 is the key to faithful mitotic inheritance. DNMT1 is often overexpressed in cancer cells and the DNA hypomethylating agents azacytidine and decitabine are currently used in the treatment of hematologic malignancies. However, the toxicity of these cytidine analogs and their ineffectiveness in treating solid tumors have limited wider clinical use. GSK-3484862 is a newly-developed, dicyanopyridine containing, non-nucleoside DNMT1-selective inhibitor with low cellular toxicity. Here, we show that GSK-3484862 targets DNMT1 for protein degradation in both cancer cell lines and murine embryonic stem cells (mESCs). DNMT1 depletion was rapid, taking effect within hours following GSK-3484862 treatment, leading to global hypomethylation. Inhibitor-induced DNMT1 degradation was proteasome-dependent, with no discernible loss of DNMT1 mRNA. In mESCs, GSK-3484862-induced Dnmt1 degradation requires the Dnmt1 accessory factor Uhrf1 and its E3 ubiquitin ligase activity. We also show that Dnmt1 depletion and DNA hypomethylation induced by the compound are reversible after its removal. Together, these results indicate that this DNMT1-selective degrader/inhibitor will be a valuable tool for dissecting coordinated events linking DNA methylation to gene expression and identifying downstream effectors that ultimately regulate cellular response to altered DNA methylation patterns in a tissue/cell-specific manner.","PeriodicalId":18879,"journal":{"name":"NAR Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/bd/6b/zcad022.PMC10189803.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9864768","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

Molecular mechanisms protecting centromeres from self-sabotage and implications for cancer therapy. 保护着丝粒免受自我破坏的分子机制及其对癌症治疗的意义。

NAR Cancer Pub Date : 2023-05-09 eCollection Date: 2023-06-01 DOI: 10.1093/narcan/zcad019

Rim Nassar, Lily Thompson, Elise Fouquerel

{"title":"Molecular mechanisms protecting centromeres from self-sabotage and implications for cancer therapy.","authors":"Rim Nassar, Lily Thompson, Elise Fouquerel","doi":"10.1093/narcan/zcad019","DOIUrl":"10.1093/narcan/zcad019","url":null,"abstract":"Centromeres play a crucial role in DNA segregation by mediating the cohesion and separation of sister chromatids during cell division. Centromere dysfunction, breakage or compromised centromeric integrity can generate aneuploidies and chromosomal instability, which are cellular features associated with cancer initiation and progression. Maintaining centromere integrity is thus essential for genome stability. However, the centromere itself is prone to DNA breaks, likely due to its intrinsically fragile nature. Centromeres are complex genomic loci that are composed of highly repetitive DNA sequences and secondary structures and require the recruitment and homeostasis of a centromere-associated protein network. The molecular mechanisms engaged to preserve centromere inherent structure and respond to centromeric damage are not fully understood and remain a subject of ongoing research. In this article, we provide a review of the currently known factors that contribute to centromeric dysfunction and the molecular mechanisms that mitigate the impact of centromere damage on genome stability. Finally, we discuss the potential therapeutic strategies that could arise from a deeper understanding of the mechanisms preserving centromere integrity.","PeriodicalId":18879,"journal":{"name":"NAR Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/20/a5/zcad019.PMC10167631.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9509927","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: 3

Therapeutic disruption of RAD52-ssDNA complexation via novel drug-like inhibitors. 通过新型药物抑制剂对 RAD52-ssDNA 复合物进行治疗性破坏。

NAR Cancer Pub Date : 2023-05-01 eCollection Date: 2023-06-01 DOI: 10.1093/narcan/zcad018

Divya S Bhat, Eva Malacaria, Ludovica Di Biagi, Mortezaali Razzaghi, Masayoshi Honda, Kathryn F Hobbs, Sarah R Hengel, Pietro Pichierri, M Ashley Spies, Maria Spies

{"title":"Therapeutic disruption of RAD52-ssDNA complexation via novel drug-like inhibitors.","authors":"Divya S Bhat, Eva Malacaria, Ludovica Di Biagi, Mortezaali Razzaghi, Masayoshi Honda, Kathryn F Hobbs, Sarah R Hengel, Pietro Pichierri, M Ashley Spies, Maria Spies","doi":"10.1093/narcan/zcad018","DOIUrl":"10.1093/narcan/zcad018","url":null,"abstract":"RAD52 protein is a coveted target for anticancer drug discovery. Similar to poly-ADP-ribose polymerase (PARP) inhibitors, pharmacological inhibition of RAD52 is synthetically lethal with defects in genome caretakers BRCA1 and BRCA2 (∼25% of breast and ovarian cancers). Emerging structure activity relationships for RAD52 are complex, making it challenging to transform previously identified disruptors of the RAD52-ssDNA interaction into drug-like leads using traditional medicinal chemistry approaches. Using pharmacophoric informatics on the RAD52 complexation by epigallocatechin (EGC), and the Enamine in silico REAL database, we identified six distinct chemical scaffolds that occupy the same physical space on RAD52 as EGC. All six were RAD52 inhibitors (IC50 ∼23-1200 μM) with two of the compounds (Z56 and Z99) selectively killing BRCA-mutant cells and inhibiting cellular activities of RAD52 at micromolar inhibitor concentrations. While Z56 had no effect on the ssDNA-binding protein RPA and was toxic to BRCA-mutant cells only, Z99 inhibited both proteins and displayed toxicity towards BRCA-complemented cells. Optimization of the Z99 scaffold resulted in a set of more powerful and selective inhibitors (IC50 ∼1.3-8 μM), which were only toxic to BRCA-mutant cells. RAD52 complexation by Z56, Z99 and its more specific derivatives provide a roadmap for next generation of cancer therapeutics.","PeriodicalId":18879,"journal":{"name":"NAR Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/1c/4d/zcad018.PMC10150327.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9797966","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

Deletion of the mRNA stability factor ELAVL1 (HuR) in pancreatic cancer cells disrupts the tumor microenvironment integrity. 胰腺癌症细胞中mRNA稳定因子ELAVL1（HuR）的缺失破坏了肿瘤微环境的完整性。

NAR Cancer Pub Date : 2023-04-19 eCollection Date: 2023-06-01 DOI: 10.1093/narcan/zcad016

Grace A McCarthy, Roberto Di Niro, Jennifer M Finan, Aditi Jain, Yifei Guo, Cory R Wyatt, Alexander R Guimaraes, Trent A Waugh, Dove Keith, Terry K Morgan, Rosalie C Sears, Jonathan R Brody

{"title":"Deletion of the mRNA stability factor ELAVL1 (HuR) in pancreatic cancer cells disrupts the tumor microenvironment integrity.","authors":"Grace A McCarthy, Roberto Di Niro, Jennifer M Finan, Aditi Jain, Yifei Guo, Cory R Wyatt, Alexander R Guimaraes, Trent A Waugh, Dove Keith, Terry K Morgan, Rosalie C Sears, Jonathan R Brody","doi":"10.1093/narcan/zcad016","DOIUrl":"10.1093/narcan/zcad016","url":null,"abstract":"Stromal cells promote extensive fibrosis in pancreatic ductal adenocarcinoma (PDAC), which is associated with poor prognosis and therapeutic resistance. We report here for the first time that loss of the RNA-binding protein human antigen R (HuR, ELAVL1) in PDAC cells leads to reprogramming of the tumor microenvironment. In multiple in vivo models, CRISPR deletion of ELAVL1 in PDAC cells resulted in a decrease of collagen deposition, accompanied by a decrease of stromal markers (i.e. podoplanin, α-smooth muscle actin, desmin). RNA-sequencing data showed that HuR plays a role in cell-cell communication. Accordingly, cytokine arrays identified that HuR regulates the secretion of signaling molecules involved in stromal activation and extracellular matrix organization [i.e. platelet-derived growth factor AA (PDGFAA) and pentraxin 3]. Ribonucleoprotein immunoprecipitation analysis and transcription inhibition studies validated PDGFA mRNA as a novel HuR target. These data suggest that tumor-intrinsic HuR supports extrinsic activation of the stroma to produce collagen and desmoplasia through regulating signaling molecules (e.g. PDGFAA). HuR-deficient PDAC in vivo tumors with an altered tumor microenvironment are more sensitive to the standard of care gemcitabine, as compared to HuR-proficient tumors. Taken together, we identified a novel role of tumor-intrinsic HuR in its ability to modify the surrounding tumor microenvironment and regulate PDGFAA.","PeriodicalId":18879,"journal":{"name":"NAR Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a9/5c/zcad016.PMC10113877.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9387874","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

Molecular origins of mutational spectra produced by the environmental carcinogen N-nitrosodimethylamine and S_N1 chemotherapeutic agents. 环境致癌物质 N-亚硝基二甲胺和 SN1 化疗药物产生突变谱的分子起源。

NAR Cancer Pub Date : 2023-03-27 eCollection Date: 2023-06-01 DOI: 10.1093/narcan/zcad015

Amanda L Armijo, Pennapa Thongararm, Bogdan I Fedeles, Judy Yau, Jennifer E Kay, Joshua J Corrigan, Marisa Chancharoen, Supawadee Chawanthayatham, Leona D Samson, Sebastian E Carrasco, Bevin P Engelward, James G Fox, Robert G Croy, John M Essigmann

{"title":"Molecular origins of mutational spectra produced by the environmental carcinogen N-nitrosodimethylamine and SN1 chemotherapeutic agents.","authors":"Amanda L Armijo, Pennapa Thongararm, Bogdan I Fedeles, Judy Yau, Jennifer E Kay, Joshua J Corrigan, Marisa Chancharoen, Supawadee Chawanthayatham, Leona D Samson, Sebastian E Carrasco, Bevin P Engelward, James G Fox, Robert G Croy, John M Essigmann","doi":"10.1093/narcan/zcad015","DOIUrl":"10.1093/narcan/zcad015","url":null,"abstract":"DNA-methylating environmental carcinogens such as N-nitrosodimethylamine (NDMA) and certain alkylators used in chemotherapy form O 6-methylguanine (m6G) as a functionally critical intermediate. NDMA is a multi-organ carcinogen found in contaminated water, polluted air, preserved foods, tobacco products, and many pharmaceuticals. Only ten weeks after exposure to NDMA, neonatally-treated mice experienced elevated mutation frequencies in liver, lung and kidney of ∼35-fold, 4-fold and 2-fold, respectively. High-resolution mutational spectra (HRMS) of liver and lung revealed distinctive patterns dominated by GC→AT mutations in 5'-Pu-G-3' contexts, very similar to human COSMIC mutational signature SBS11. Commonly associated with alkylation damage, SBS11 appears in cancers treated with the DNA alkylator temozolomide (TMZ). When cells derived from the mice were treated with TMZ, N-methyl-N-nitrosourea, and streptozotocin (two other therapeutic methylating agents), all displayed NDMA-like HRMS, indicating mechanistically convergent mutational processes. The role of m6G in shaping the mutational spectrum of NDMA was probed by removing MGMT, the main cellular defense against m6G. MGMT-deficient mice displayed a strikingly enhanced mutant frequency, but identical HRMS, indicating that the mutational properties of these alkylators is likely owed to sequence-specific DNA binding. In sum, the HRMS of m6G-forming agents constitute an early-onset biomarker of exposure to DNA methylating carcinogens and drugs.","PeriodicalId":18879,"journal":{"name":"NAR Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10041537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9743909","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

The hereditary N363K POLE exonuclease mutant extends PPAP tumor spectrum to glioblastomas by causing DNA damage and aneuploidy in addition to increased mismatch mutagenicity. 遗传性 N363K POLE 外切酶突变体除了增加错配诱变性外，还造成 DNA 损伤和非整倍体，从而将 PPAP 的肿瘤谱扩展到胶质母细胞瘤。

NAR Cancer Pub Date : 2023-03-11 eCollection Date: 2023-06-01 DOI: 10.1093/narcan/zcad011

Guillaume Labrousse, Pierre Vande Perre, Genis Parra, Marion Jaffrelot, Laura Leroy, Frederic Chibon, Frederic Escudie, Janick Selves, Jean-Sebastien Hoffmann, Rosine Guimbaud, Malik Lutzmann

{"title":"The hereditary N363K POLE exonuclease mutant extends PPAP tumor spectrum to glioblastomas by causing DNA damage and aneuploidy in addition to increased mismatch mutagenicity.","authors":"Guillaume Labrousse, Pierre Vande Perre, Genis Parra, Marion Jaffrelot, Laura Leroy, Frederic Chibon, Frederic Escudie, Janick Selves, Jean-Sebastien Hoffmann, Rosine Guimbaud, Malik Lutzmann","doi":"10.1093/narcan/zcad011","DOIUrl":"10.1093/narcan/zcad011","url":null,"abstract":"The exonuclease domain of DNA polymerases epsilon's catalytic subunit (POLE) removes misincorporated nucleotides, called proofreading. POLE-exonuclease mutations cause colorectal- and endometrial cancers with an extreme burden of single nucleotide substitutions. We recently reported that particularly the hereditary POLE exonuclease mutation N363K predisposes in addition to aggressive giant cell glioblastomas. We knocked-in this mutation homozygously into human cell lines and compared its properties to knock-ins of the likewise hereditary POLE L424V mutation and to a complete proofreading-inactivating mutation (exo-null). We found that N363K cells have higher mutation rates as both L424V- or exo-null mutant cells. In contrast to L424V cells, N363K cells expose a growth defect, replication stress and DNA damage. In non-transformed cells, these burdens lead to aneuploidy but macroscopically normal nuclei. In contrast, transformed N363K cells phenocopy the enlarged and disorganized nuclei of giant cell glioblastomas. Taken together, our data characterize a POLE exonuclease domain mutant that not only causes single nucleotide hypermutation, but in addition DNA damage and chromosome instability, leading to an extended tumor spectrum. Our results expand the understanding of the polymerase exonuclease domain and suggest that an assessment of both the mutational potential and the genetic instability might refine classification and treatment of POLE-mutated tumors.","PeriodicalId":18879,"journal":{"name":"NAR Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fd/95/zcad011.PMC10006997.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9168828","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

ICI efficacy information portal: a knowledgebase for responder prediction to immune checkpoint inhibitors. ICI 疗效信息门户：免疫检查点抑制剂应答者预测知识库。

NAR Cancer Pub Date : 2023-03-03 eCollection Date: 2023-03-01 DOI: 10.1093/narcan/zcad012

Jiamin Chen, Daniel Rebibo, Jianquan Cao, Simon Yat-Man Mok, Neel Patel, Po-Cheng Tseng, Zhenghao Zhang, Kevin Y Yip

{"title":"ICI efficacy information portal: a knowledgebase for responder prediction to immune checkpoint inhibitors.","authors":"Jiamin Chen, Daniel Rebibo, Jianquan Cao, Simon Yat-Man Mok, Neel Patel, Po-Cheng Tseng, Zhenghao Zhang, Kevin Y Yip","doi":"10.1093/narcan/zcad012","DOIUrl":"10.1093/narcan/zcad012","url":null,"abstract":"Immune checkpoint inhibitors (ICIs) have led to durable responses in cancer patients, yet their efficacy varies significantly across cancer types and patients. To stratify patients based on their potential clinical benefits, there have been substantial research efforts in identifying biomarkers and computational models that can predict the efficacy of ICIs, and it has become difficult to keep track of all of them. It is also difficult to compare findings of different studies since they involve different cancer types, ICIs, and various other details. To make it easy to access the latest information about ICI efficacy, we have developed a knowledgebase and a corresponding web-based portal (https://iciefficacy.org/). Our knowledgebase systematically records information about latest publications related to ICI efficacy, predictors proposed, and datasets used to test them. All information recorded is checked carefully by a manual curation process. The web-based portal provides functions to browse, search, filter, and sort the information. Digests of method details are provided based on the original descriptions in the publications. Evaluation results of the effectiveness of the predictors reported in the publications are summarized for quick overviews. Overall, our resource provides centralized access to the burst of information produced by the vibrant research on ICI efficacy.","PeriodicalId":18879,"journal":{"name":"NAR Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9984987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9612060","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

Recent advancements in the structural biology of human telomerase and their implications for improved design of cancer therapeutics. 人类端粒酶结构生物学的最新进展及其对癌症治疗方法改进设计的意义。

NAR Cancer Pub Date : 2023-03-03 eCollection Date: 2023-03-01 DOI: 10.1093/narcan/zcad010

Griffin A Welfer, Bret D Freudenthal

{"title":"Recent advancements in the structural biology of human telomerase and their implications for improved design of cancer therapeutics.","authors":"Griffin A Welfer, Bret D Freudenthal","doi":"10.1093/narcan/zcad010","DOIUrl":"10.1093/narcan/zcad010","url":null,"abstract":"Telomerase is a specialized reverse transcriptase that synthesizes telomeric repeats at the ends of linear chromosomes. Telomerase is transiently expressed in germ and stem cells, but nearly all somatic cells silence it after differentiating. However, the vast majority of cancer cells reactivate and constitutively express telomerase to maintain replicative immortality. Because of this, telomerase has remained a promising broad-spectrum chemotherapeutic target for over 30 years. However, various challenges associated with obtaining high-resolution structural data for telomerase have limited the development of rationally designed structure-based therapeutics. Various techniques and model systems have been utilized to advance our understanding of the structural biology of telomerase. In particular, multiple high-resolution cryogenic electron microscopy (cryo-EM) structures published within the past few years have revealed new components of the telomerase complex with near atomic resolution structural models. Additionally, these structures have provided details for how telomerase is recruited to telomeres and its mechanism of telomere synthesis. With these new pieces of evidence, and the promising outlook for future refinements to our current models, the possibility of telomerase specific chemotherapeutics is becoming more tangible than ever. This review summarizes these recent advancements and outlines outstanding questions in the field.","PeriodicalId":18879,"journal":{"name":"NAR Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9984990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9112498","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

R-loops, type I topoisomerases and cancer. R环、I型拓扑异构酶与癌症

NAR Cancer Pub Date : 2023-03-03 eCollection Date: 2023-03-01 DOI: 10.1093/narcan/zcad013

Sourav Saha, Yves Pommier

引用次数: 0