NAR cancer最新文献_第3页

Human NTHL1 expression and subcellular distribution determines cisplatin sensitivity in human lung epithelial and non-small cell lung cancer cells. 人类 NTHL1 的表达和亚细胞分布决定了人类肺上皮细胞和非小细胞肺癌细胞对顺铂的敏感性。

IF 3.4

NAR cancer Pub Date : 2024-02-21 eCollection Date: 2024-03-01 DOI: 10.1093/narcan/zcae006

Anirban Kar, Natalya P Degtyareva, Paul W Doetsch

{"title":"Human NTHL1 expression and subcellular distribution determines cisplatin sensitivity in human lung epithelial and non-small cell lung cancer cells.","authors":"Anirban Kar, Natalya P Degtyareva, Paul W Doetsch","doi":"10.1093/narcan/zcae006","DOIUrl":"10.1093/narcan/zcae006","url":null,"abstract":"Base excision repair is critical for maintaining genomic stability and for preventing malignant transformation. NTHL1 is a bifunctional DNA glycosylase/AP lyase that initiates repair of oxidatively damaged pyrimidines. Our recent work established that transient over-expression of NTHL1 leads to acquisition of several hallmarks of cancer in non-tumorigenic immortalized cells likely through interaction with nucleotide excision repair protein XPG. Here, we investigate how NTHL1 expression levels impact cellular sensitivity to cisplatin in non-tumorigenic immortalized cells and five non-small cell lung carcinomas cell lines. The cell line with lowest expression of NTHL1 (H522) shows the highest resistance to cisplatin indicating that decrease in NTHL1 levels may modulate resistance to crosslinking agents in NSCLC tumors. In a complementation study, overexpression of NTHL1 in H522 cell line sensitized it to cisplatin. Using NTHL1 N-terminal deletion mutants defective in nuclear localization we show that cisplatin treatment can alter NTHL1 subcellular localization possibly leading to altered protein-protein interactions and affecting cisplatin sensitivity. Experiments presented in this study reveal a previously unknown link between NTHL1 expression levels and cisplatin sensitivity of NSCLC tumor cells. These findings provide an opportunity to understand how altered NTHL1 expression levels and subcellular distribution can impact cisplatin sensitivity in NSCLC tumor cells.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 1","pages":"zcae006"},"PeriodicalIF":3.4,"publicationDate":"2024-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10880605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139935120","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

Rewiring of RNA methylation by the oncometabolite fumarate in renal cell carcinoma. 肾细胞癌中副代谢物富马酸盐对 RNA 甲基化的重排。

IF 3.4

NAR cancer Pub Date : 2024-02-07 eCollection Date: 2024-03-01 DOI: 10.1093/narcan/zcae004

Christina M Fitzsimmons, Mariana D Mandler, Judith C Lunger, Dalen Chan, Siddhardha S Maligireddy, Alexandra C Schmiechen, Supuni Thalalla Gamage, Courtney Link, Lisa M Jenkins, King Chan, Thorkell Andresson, Daniel R Crooks, Jordan L Meier, W Marston Linehan, Pedro J Batista

{"title":"Rewiring of RNA methylation by the oncometabolite fumarate in renal cell carcinoma.","authors":"Christina M Fitzsimmons, Mariana D Mandler, Judith C Lunger, Dalen Chan, Siddhardha S Maligireddy, Alexandra C Schmiechen, Supuni Thalalla Gamage, Courtney Link, Lisa M Jenkins, King Chan, Thorkell Andresson, Daniel R Crooks, Jordan L Meier, W Marston Linehan, Pedro J Batista","doi":"10.1093/narcan/zcae004","DOIUrl":"10.1093/narcan/zcae004","url":null,"abstract":"Metabolic reprogramming is a hallmark of cancer that facilitates changes in many adaptive biological processes. Mutations in the tricarboxylic acid cycle enzyme fumarate hydratase (FH) lead to fumarate accumulation and cause hereditary leiomyomatosis and renal cell cancer (HLRCC). HLRCC is a rare, inherited disease characterized by the development of non-cancerous smooth muscle tumors of the uterus and skin, and an increased risk of an aggressive form of kidney cancer. Fumarate has been shown to inhibit 2-oxoglutarate-dependent dioxygenases (2OGDDs) involved in the hydroxylation of HIF1α, as well as in DNA and histone demethylation. However, the link between fumarate accumulation and changes in RNA post-transcriptional modifications has not been defined. Here, we determine the consequences of fumarate accumulation on the activity of different members of the 2OGDD family targeting RNA modifications. By evaluating multiple RNA modifications in patient-derived HLRCC cell lines, we show that mutation of FH selectively affects the levels of N6-methyladenosine (m6A), while the levels of 5-formylcytosine (f5C) in mitochondrial tRNA are unaffected. This supports the hypothesis of a differential impact of fumarate accumulation on distinct RNA demethylases. The observation that metabolites modulate specific subsets of RNA-modifying enzymes offers new insights into the intersection between metabolism and the epitranscriptome.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 1","pages":"zcae004"},"PeriodicalIF":3.4,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10849186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139704355","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 large-scale study of peptide features defining immunogenicity of cancer neo-epitopes. 对确定癌症新表位免疫原性的多肽特征进行大规模研究。

IF 3.4

NAR cancer Pub Date : 2024-01-29 eCollection Date: 2024-03-01 DOI: 10.1093/narcan/zcae002

Yat-Tsai Richie Wan, Zeynep Koşaloğlu-Yalçın, Bjoern Peters, Morten Nielsen

{"title":"A large-scale study of peptide features defining immunogenicity of cancer neo-epitopes.","authors":"Yat-Tsai Richie Wan, Zeynep Koşaloğlu-Yalçın, Bjoern Peters, Morten Nielsen","doi":"10.1093/narcan/zcae002","DOIUrl":"10.1093/narcan/zcae002","url":null,"abstract":"Accurate prediction of immunogenicity for neo-epitopes arising from a cancer associated mutation is a crucial step in many bioinformatics pipelines that predict outcome of checkpoint blockade treatments or that aim to design personalised cancer immunotherapies and vaccines. In this study, we performed a comprehensive analysis of peptide features relevant for prediction of immunogenicity using the Cancer Epitope Database and Analysis Resource (CEDAR), a curated database of cancer epitopes with experimentally validated immunogenicity annotations from peer-reviewed publications. The developed model, ICERFIRE (ICore-based Ensemble Random Forest for neo-epitope Immunogenicity pREdiction), extracts the predicted ICORE from the full neo-epitope as input, i.e. the nested peptide with the highest predicted major histocompatibility complex (MHC) binding potential combined with its predicted likelihood of antigen presentation (%Rank). Key additional features integrated into the model include assessment of the BLOSUM mutation score of the neo-epitope, and antigen expression levels of the wild-type counterpart which is often reflecting a neo-epitope's abundance. We demonstrate improved and robust performance of ICERFIRE over existing immunogenicity and epitope prediction models, both in cross-validation and on external validation datasets.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 1","pages":"zcae002"},"PeriodicalIF":3.4,"publicationDate":"2024-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10823584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139577133","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 ORFIUS complex regulates ORC2 localization at replication origins. ORFIUS 复合物调节 ORC2 在复制起源的定位。

IF 3.4

NAR cancer Pub Date : 2024-01-29 eCollection Date: 2024-03-01 DOI: 10.1093/narcan/zcae003

Zelei Yang, Saie Mogre, Ruiyang He, Emma L Berdan, Shannan J Ho Sui, Sarah J Hill

{"title":"The ORFIUS complex regulates ORC2 localization at replication origins.","authors":"Zelei Yang, Saie Mogre, Ruiyang He, Emma L Berdan, Shannan J Ho Sui, Sarah J Hill","doi":"10.1093/narcan/zcae003","DOIUrl":"10.1093/narcan/zcae003","url":null,"abstract":"High-grade serous ovarian cancer (HGSC) is a lethal malignancy with elevated replication stress (RS) levels and defective RS and RS-associated DNA damage responses. Here we demonstrate that the bromodomain-containing protein BRD1 is a RS suppressing protein that forms a replication origin regulatory complex with the histone acetyltransferase HBO1, the BRCA1 tumor suppressor, and BARD1, ORigin FIring Under Stress (ORFIUS). BRD1 and HBO1 promote eventual origin firing by supporting localization of the origin licensing protein ORC2 at origins. In the absence of BRD1 and/or HBO1, both origin firing and nuclei with ORC2 foci are reduced. BRCA1 regulates BRD1, HBO1, and ORC2 localization at replication origins. In the absence of BRCA1, both origin firing and nuclei with BRD1, HBO1, and ORC2 foci are increased. In normal and non-HGSC ovarian cancer cells, the ORFIUS complex responds to ATR and CDC7 origin regulatory signaling and disengages from origins during RS. In BRCA1-mutant and sporadic HGSC cells, BRD1, HBO1, and ORC2 remain associated with replication origins, and unresponsive to RS, DNA damage, or origin regulatory kinase inhibition. ORFIUS complex dysregulation may promote HGSC cell survival by allowing for upregulated origin firing and cell cycle progression despite accumulating DNA damage, and may be a RS target.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 1","pages":"zcae003"},"PeriodicalIF":3.4,"publicationDate":"2024-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10823580/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139577136","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

Correction to 'Translation reprogramming by eIF3 linked to glioblastoma resistance'. eIF3 的翻译重编程与胶质母细胞瘤的抗药性有关 "的更正。

IF 3.4

NAR cancer Pub Date : 2024-01-15 eCollection Date: 2024-03-01 DOI: 10.1093/narcan/zcae001

引用次数: 0

Single-cell genomics analysis reveals complex genetic interactions in an in vivo model of acquired BRAF inhibitor resistance. 单细胞基因组学分析揭示了获得性 BRAF 抑制剂耐药性体内模型中复杂的基因相互作用。

IF 3.4

NAR cancer Pub Date : 2024-01-11 eCollection Date: 2024-03-01 DOI: 10.1093/narcan/zcad061

Jacob L Schillo, Charlotte R Feddersen, Rebekah M Peplinski, Lexy S Powell, Afshin Varzavand, Christopher S Stipp, Jesse D Riordan, Adam J Dupuy

{"title":"Single-cell genomics analysis reveals complex genetic interactions in an in vivo model of acquired BRAF inhibitor resistance.","authors":"Jacob L Schillo, Charlotte R Feddersen, Rebekah M Peplinski, Lexy S Powell, Afshin Varzavand, Christopher S Stipp, Jesse D Riordan, Adam J Dupuy","doi":"10.1093/narcan/zcad061","DOIUrl":"10.1093/narcan/zcad061","url":null,"abstract":"The evolution of therapeutic resistance is a major obstacle to the success of targeted oncology drugs. While both inter- and intratumoral heterogeneity limit our ability to detect resistant subpopulations that pre-exist or emerge during treatment, our ability to analyze tumors with single-cell resolution is limited. Here, we utilized a cell-based transposon mutagenesis method to identify mechanisms of BRAF inhibitor resistance in a model of cutaneous melanoma. This screen identified overexpression of NEDD4L and VGLL3 as significant drivers of BRAF inhibitor resistance in vivo. In addition, we describe a novel single-cell genomics profiling method to genotype thousands of individual cells within tumors driven by transposon mutagenesis. This approach revealed a surprising genetic diversity among xenograft tumors and identified recurrent co-occurring mutations that emerge within distinct tumor subclones. Taken together, these observations reveal an unappreciated genetic complexity that drives BRAF inhibitor resistance.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 1","pages":"zcad061"},"PeriodicalIF":3.4,"publicationDate":"2024-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10782916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139428199","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

Preclinical exploration of the DNA damage response pathway using the interactive neuroblastoma cell line explorer CLEAN. 利用交互式神经母细胞瘤细胞系探索器 CLEAN 对 DNA 损伤反应途径进行临床前探索。

IF 3.4

NAR cancer Pub Date : 2024-01-11 eCollection Date: 2024-03-01 DOI: 10.1093/narcan/zcad062

Jonatan L Gabre, Peter Merseburger, Arne Claeys, Joachim Siaw, Sarah-Lee Bekaert, Frank Speleman, Bengt Hallberg, Ruth H Palmer, Jimmy Van den Eynden

{"title":"Preclinical exploration of the DNA damage response pathway using the interactive neuroblastoma cell line explorer CLEAN.","authors":"Jonatan L Gabre, Peter Merseburger, Arne Claeys, Joachim Siaw, Sarah-Lee Bekaert, Frank Speleman, Bengt Hallberg, Ruth H Palmer, Jimmy Van den Eynden","doi":"10.1093/narcan/zcad062","DOIUrl":"10.1093/narcan/zcad062","url":null,"abstract":"Neuroblastoma (NB) is the most common cancer in infancy with an urgent need for more efficient targeted therapies. The development of novel (combinatorial) treatment strategies relies on extensive explorations of signaling perturbations in neuroblastoma cell lines, using RNA-Seq or other high throughput technologies (e.g. phosphoproteomics). This typically requires dedicated bioinformatics support, which is not always available. Additionally, while data from published studies are highly valuable and raw data (e.g. fastq files) are nowadays released in public repositories, data processing is time-consuming and again difficult without bioinformatics support. To facilitate NB research, more user-friendly and immediately accessible platforms are needed to explore newly generated as well as existing high throughput data. To make this possible, we developed an interactive data centralization and visualization web application, called CLEAN (the Cell Line Explorer web Application of Neuroblastoma data; https://ccgg.ugent.be/shiny/clean/). By focusing on the regulation of the DNA damage response, a therapeutic target of major interest in neuroblastoma, we demonstrate how CLEAN can be used to gain novel mechanistic insights and identify putative drug targets in neuroblastoma.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 1","pages":"zcad062"},"PeriodicalIF":3.4,"publicationDate":"2024-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10782898/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139428198","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

TSCRE: a comprehensive database for tumor-specific cis-regulatory elements. TSCRE：肿瘤特异性顺式调节元件综合数据库。

IF 3.4

NAR cancer Pub Date : 2024-01-11 eCollection Date: 2024-03-01 DOI: 10.1093/narcan/zcad063

Guanjie Peng, Bingyuan Liu, Mohan Zheng, Luowanyue Zhang, Huiqin Li, Mengni Liu, Yuan Liang, Tianjian Chen, Xiaotong Luo, Xianping Shi, Jian Ren, Yueyuan Zheng

{"title":"TSCRE: a comprehensive database for tumor-specific cis-regulatory elements.","authors":"Guanjie Peng, Bingyuan Liu, Mohan Zheng, Luowanyue Zhang, Huiqin Li, Mengni Liu, Yuan Liang, Tianjian Chen, Xiaotong Luo, Xianping Shi, Jian Ren, Yueyuan Zheng","doi":"10.1093/narcan/zcad063","DOIUrl":"10.1093/narcan/zcad063","url":null,"abstract":"Cis-regulatory elements (CREs) and super cis-regulatory elements (SCREs) are non-coding DNA regions which influence the transcription of nearby genes and play critical roles in development. Dysregulated CRE and SCRE activities have been reported to alter the expression of oncogenes and tumor suppressors, thereby regulating cancer hallmarks. To address the strong need for a comprehensive catalogue of dysregulated CREs and SCREs in human cancers, we present TSCRE (http://tscre.zsqylab.com/), an open resource providing tumor-specific and cell type-specific CREs and SCREs derived from the re-analysis of publicly available histone modification profiles. Currently, TSCRE contains 1 864 941 dysregulated CREs and 68 253 dysregulated SCREs identified from 1366 human patient samples spanning 17 different cancer types and 9 histone marks. Over 95% of these elements have been validated in public resources. TSCRE offers comprehensive annotations for each element, including associated genes, expression patterns, clinical prognosis, somatic mutations, transcript factor binding sites, cancer-type specificity, and drug response. Additionally, TSCRE integrates pathway and transcript factor enrichment analyses for each study, enabling in-depth functional and mechanistic investigations. Furthermore, TSCRE provides an interactive interface for users to explore any CRE and SCRE of interest. We believe TSCRE will be a highly valuable platform for the community to discover candidate cancer biomarkers.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 1","pages":"zcad063"},"PeriodicalIF":3.4,"publicationDate":"2024-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10782923/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139428200","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

Codelivery of TGFβ and Cox2 siRNA inhibits HCC by promoting T-cell penetration into the tumor and improves response to Immune Checkpoint Inhibitors. TGFβ和Cox2 siRNA联合递送可通过促进T细胞穿透肿瘤抑制HCC，并改善对免疫检查点抑制剂的反应。

IF 3.4

NAR cancer Pub Date : 2024-01-09 eCollection Date: 2024-03-01 DOI: 10.1093/narcan/zcad059

Wookhyun Kim, Zhou Ye, Vera Simonenko, Aashirwad Shahi, Asra Malikzay, Steven Z Long, John J Xu, Alan Lu, Jau-Hau Horng, Chang-Ru Wu, Pei-Jer Chen, Patrick Y Lu, David M Evans

{"title":"Codelivery of TGFβ and Cox2 siRNA inhibits HCC by promoting T-cell penetration into the tumor and improves response to Immune Checkpoint Inhibitors.","authors":"Wookhyun Kim, Zhou Ye, Vera Simonenko, Aashirwad Shahi, Asra Malikzay, Steven Z Long, John J Xu, Alan Lu, Jau-Hau Horng, Chang-Ru Wu, Pei-Jer Chen, Patrick Y Lu, David M Evans","doi":"10.1093/narcan/zcad059","DOIUrl":"10.1093/narcan/zcad059","url":null,"abstract":"Upregulation of TGFβ and Cox2 in the tumor microenvironment results in blockade of T-cell penetration into the tumor. Without access to tumor antigens, the T-cell response will not benefit from administration of the immune checkpoint antibodies. We created an intravenous polypeptide nanoparticle that can deliver two siRNAs (silencing TGFβ and Cox2). Systemic administration in mice, bearing a syngeneic orthotopic hepatocellular carcinoma (HCC), delivers the siRNAs to various cells in the liver, and significantly reduces the tumor. At 2 mg/kg (BIW) the nanoparticle demonstrated a single agent action and induced tumor growth inhibition to undetectable levels after five doses. Reducing the siRNAs to 1mg/kg BIW demonstrated greater inhibition in the presence of PD-L1 mAbs. After only three doses BIW, we could still recover a smaller tumor and, in tumor sections, showed an increase in penetration of CD4+ and CD8+ T-cells deeper into the remaining tumor that was not evident in animals treated with non-silencing siRNA. The combination of TGFβ and Cox2 siRNA co-administered in a polypeptide nanoparticle can act as a novel therapeutic alone against HCC and may augment the activity of the immune checkpoint antibodies. Silencing TGFβ and Cox2 converts an immune excluded (cold) tumor into a T-cell inflamed (hot) tumor.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 1","pages":"zcad059"},"PeriodicalIF":3.4,"publicationDate":"2024-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10776204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139418788","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

CanVaxKB: a web-based cancer vaccine knowledgebase. CanVaxKB：基于网络的癌症疫苗知识库。

IF 3.4

NAR cancer Pub Date : 2024-01-09 eCollection Date: 2024-03-01 DOI: 10.1093/narcan/zcad060

Eliyas Asfaw, Asiyah Yu Lin, Anthony Huffman, Siqi Li, Madison George, Chloe Darancou, Madison Kalter, Nader Wehbi, Davis Bartels, Elyse Fleck, Nancy Tran, Daniel Faghihnia, Kimberly Berke, Ronak Sutariya, Farah Reyal, Youssef Tammam, Bin Zhao, Edison Ong, Zuoshuang Xiang, Virginia He, Justin Song, Andrey I Seleznev, Jinjing Guo, Yuanyi Pan, Jie Zheng, Yongqun He

{"title":"CanVaxKB: a web-based cancer vaccine knowledgebase.","authors":"Eliyas Asfaw, Asiyah Yu Lin, Anthony Huffman, Siqi Li, Madison George, Chloe Darancou, Madison Kalter, Nader Wehbi, Davis Bartels, Elyse Fleck, Nancy Tran, Daniel Faghihnia, Kimberly Berke, Ronak Sutariya, Farah Reyal, Youssef Tammam, Bin Zhao, Edison Ong, Zuoshuang Xiang, Virginia He, Justin Song, Andrey I Seleznev, Jinjing Guo, Yuanyi Pan, Jie Zheng, Yongqun He","doi":"10.1093/narcan/zcad060","DOIUrl":"10.1093/narcan/zcad060","url":null,"abstract":"Cancer vaccines have been increasingly studied and developed to prevent or treat various types of cancers. To systematically survey and analyze different reported cancer vaccines, we developed CanVaxKB (https://violinet.org/canvaxkb), the first web-based cancer vaccine knowledgebase that compiles over 670 therapeutic or preventive cancer vaccines that have been experimentally verified to be effective at various stages. Vaccine construction and host response data are also included. These cancer vaccines are developed against various cancer types such as melanoma, hematological cancer, and prostate cancer. CanVaxKB has stored 263 genes or proteins that serve as cancer vaccine antigen genes, which we have collectively termed 'canvaxgens'. Top three mostly used canvaxgens are PMEL, MLANA and CTAG1B, often targeting multiple cancer types. A total of 193 canvaxgens are also reported in cancer-related ONGene, Network of Cancer Genes and/or Sanger Cancer Gene Consensus databases. Enriched functional annotations and clusters of canvaxgens were identified and analyzed. User-friendly web interfaces are searchable for querying and comparing cancer vaccines. CanVaxKB cancer vaccines are also semantically represented by the community-based Vaccine Ontology to support data exchange. Overall, CanVaxKB is a timely and vital cancer vaccine source that facilitates efficient collection and analysis, further helping researchers and physicians to better understand cancer mechanisms.","PeriodicalId":94149,"journal":{"name":"NAR cancer","volume":"6 1","pages":"zcad060"},"PeriodicalIF":3.4,"publicationDate":"2024-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10776203/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139418869","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