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Molecular & cellular oncology最新文献

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ARID1A mutation and genomic stability. ARID1A突变与基因组稳定性。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-02-23 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2019.1690923
Timothy Nacarelli, Bo Zhao, Xue Hao, Rugang Zhang
{"title":"<i>ARID1A</i> mutation and genomic stability.","authors":"Timothy Nacarelli,&nbsp;Bo Zhao,&nbsp;Xue Hao,&nbsp;Rugang Zhang","doi":"10.1080/23723556.2019.1690923","DOIUrl":"https://doi.org/10.1080/23723556.2019.1690923","url":null,"abstract":"<p><p>We have recently discovered that AT-rich interactive domain-containing protein 1A (ARID1A) protects telomere cohesion through regulation of the cohesin subunit stromal antigen 1 (STAG1). ARID1A inactivation results in mitotic defects and negatively selects gross chromosomal aberrations, resulting in preservation of genomic stability in <i>ARID1A</i>-mutated cancers. These findings explain the long-standing paradox between mitotic defects caused by ARID1A inactivation and the lack of genomic instability in <i>ARID1A</i>-mutated cancers.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1690923"},"PeriodicalIF":2.1,"publicationDate":"2020-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2019.1690923","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37919888","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: 1
Protective role of p53 in doxorubicin-induced cardiomyopathy as a mitochondrial disease. p53在阿霉素诱导的心肌病作为线粒体疾病中的保护作用。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-02-23 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2020.1724598
Masahiro Nishi, Ping-Yuan Wang, Paul M Hwang
{"title":"Protective role of p53 in doxorubicin-induced cardiomyopathy as a mitochondrial disease.","authors":"Masahiro Nishi,&nbsp;Ping-Yuan Wang,&nbsp;Paul M Hwang","doi":"10.1080/23723556.2020.1724598","DOIUrl":"https://doi.org/10.1080/23723556.2020.1724598","url":null,"abstract":"<p><p>Doxorubicin is widely used against cancer but carries the risk of a progressive cardiomyopathy associated with mitochondrial loss. Using genetic models, our recent study demonstrates that mitochondrial genomic DNA regulation by tumor protein p53 (TP53, best known as p53) prevents the cardiotoxicity of low dose doxorubicin which does not activate the p53-dependent cell death pathway.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1724598"},"PeriodicalIF":2.1,"publicationDate":"2020-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1724598","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37922227","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: 2
Deep learning: shaping the medicine of tomorrow. 深度学习:塑造未来的医学。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-02-19 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2020.1723462
Konstantinos Vougas, Spyridon Almpanis, Vassilis Gorgoulis
{"title":"Deep learning: shaping the medicine of tomorrow.","authors":"Konstantinos Vougas,&nbsp;Spyridon Almpanis,&nbsp;Vassilis Gorgoulis","doi":"10.1080/23723556.2020.1723462","DOIUrl":"https://doi.org/10.1080/23723556.2020.1723462","url":null,"abstract":"<p><p>Predicting response to therapy is a major challenge in medicine. Machine learning algorithms are promising tools for assisting this aim. Amongst them, Deep Neural Networks are emerging as the most capable of interrogating across multiple data types. Their further development will lead to sophisticated knowledge extraction, shaping the medicine of tomorrow.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1723462"},"PeriodicalIF":2.1,"publicationDate":"2020-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1723462","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37922226","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: 2
The metabolic reprogramming and vulnerability of SF3B1 mutations. SF3B1突变的代谢重编程和易感性。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-02-16 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2019.1697619
W Brian Dalton
{"title":"The metabolic reprogramming and vulnerability of <i>SF3B1</i> mutations.","authors":"W Brian Dalton","doi":"10.1080/23723556.2019.1697619","DOIUrl":"https://doi.org/10.1080/23723556.2019.1697619","url":null,"abstract":"<p><p>Mutations in the splicing factor 3b subunit 1 (<i>SF3B1</i>) gene create a neomorphic protein that disrupts RNA splicing, but the downstream consequences of this missplicing are unclear. Our recent study of isogenic human cells demonstrated that <i>SF3B1</i> <sup>MUT</sup> induces reprogramming of energy metabolism and a targetable vulnerability to deprivation of the nonessential amino acid serine.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1697619"},"PeriodicalIF":2.1,"publicationDate":"2020-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2019.1697619","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37919889","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: 4
Mapping the breakome reveals tight regulation on oncogenic super-enhancers. 绘制破缺基因揭示了对致癌超级增强因子的严格调控。
IF 2.1
Molecular & cellular oncology Pub Date : 2020-02-11 eCollection Date: 2020-01-01 DOI: 10.1080/23723556.2019.1698933
Sara Oster, Rami I Aqeilan
{"title":"Mapping the breakome reveals tight regulation on oncogenic super-enhancers.","authors":"Sara Oster,&nbsp;Rami I Aqeilan","doi":"10.1080/23723556.2019.1698933","DOIUrl":"https://doi.org/10.1080/23723556.2019.1698933","url":null,"abstract":"<p><p>DNA double-strand breaks (DSBs) could be deleterious and lead to age-related diseases, such as cancer. Recent evidence, however, associates DSBs with vital cellular processes. As discussed here, genome-wide mapping of DSBs revealed an unforeseen coupling mechanism between transcription and DNA repair at super-enhancers, as means of hypertranscription of oncogenic drivers.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1698933"},"PeriodicalIF":2.1,"publicationDate":"2020-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2019.1698933","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37921789","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
Insidious communication amongst cancer cells. 癌细胞之间阴险的交流。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-19 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2017.1356898
Jeffrey J Rodvold, Maurizio Zanetti
{"title":"Insidious communication amongst cancer cells.","authors":"Jeffrey J Rodvold,&nbsp;Maurizio Zanetti","doi":"10.1080/23723556.2017.1356898","DOIUrl":"https://doi.org/10.1080/23723556.2017.1356898","url":null,"abstract":"<p><p>The tumor microenvironment is home to various types of cognate and non-cognate cell interactions. Here we comment on a newly discovered form of intercellular communication, which is based on endoplasmic reticulum stress signaling. Through this mechanism transmitter cancer cells impart receiver cancer cells with resistance to secondary metabolic, pharmacologic and genotoxic stress, providing survival advantage. The implications of this finding are briefly discussed.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1356898"},"PeriodicalIF":2.1,"publicationDate":"2018-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2017.1356898","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36521978","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
ADHFE1 is a MYC-linked oncogene that induces metabolic reprogramming and cellular de-differentiation in breast cancer. ADHFE1是一种与myc相关的癌基因，在乳腺癌中诱导代谢重编程和细胞去分化。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-19 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1432260
Prachi Mishra, Wei Tang, Stefan Ambs
{"title":"ADHFE1 is a MYC-linked oncogene that induces metabolic reprogramming and cellular de-differentiation in breast cancer.","authors":"Prachi Mishra,&nbsp;Wei Tang,&nbsp;Stefan Ambs","doi":"10.1080/23723556.2018.1432260","DOIUrl":"https://doi.org/10.1080/23723556.2018.1432260","url":null,"abstract":"<p><p>The oncometabolite, <i>D</i>-2-hydroxyglutarate, accumulates in various cancers because of acquired mutations in isocitrate dehydrogenase 1 & 2. Here, we describe a new mechanism for <i>D</i>-2-hydroxyglutarate accumulation in breast cancer. It involves c-Myc signaling and alcohol dehydrogenase, iron-containing protein 1 (ADHFE1) and leads to metabolic reprogramming, de-differentiation, and increased mammary tumorigenesis.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1432260"},"PeriodicalIF":2.1,"publicationDate":"2018-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1432260","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36521984","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: 11
Targeting the KEAP1/NRF2 pathway to manipulate the expression of oncogenic and oncosuppressive miRNAs in human leukemia. 靶向KEAP1/NRF2通路调控人白血病中致癌和抑癌mirna的表达
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-19 eCollection Date: 2018-01-01 DOI: 10.4161/23723556.2014.988484
Kristian M Bowles, Stuart A Rushworth
{"title":"Targeting the KEAP1/NRF2 pathway to manipulate the expression of oncogenic and oncosuppressive miRNAs in human leukemia.","authors":"Kristian M Bowles,&nbsp;Stuart A Rushworth","doi":"10.4161/23723556.2014.988484","DOIUrl":"https://doi.org/10.4161/23723556.2014.988484","url":null,"abstract":"<p><p>The Kelch-like ECH-associated protein 1 (KEAP1)/nuclear factor E2-related factor 2 (NRF2L2, best known as NRF2) pathway plays a pivotal cytoprotective role in the regulation of cellular responses to oxidative stress. We report that NRF2 modulates the expression of microRNA-125B and microRNA-29B in acute myeloid leukemia. The regulation of microRNA in leukemia can now be added to the growing list of prosurvival functions of NRF2.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e988484"},"PeriodicalIF":2.1,"publicationDate":"2018-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/23723556.2014.988484","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36522039","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
Cell fate in colon cancer stem cells: To GLI or not to GLI? 结肠癌干细胞的细胞命运:致GLI还是不致GLI?
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-19 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1445940
Joseph L Regan
{"title":"Cell fate in colon cancer stem cells: To GLI or not to GLI?","authors":"Joseph L Regan","doi":"10.1080/23723556.2018.1445940","DOIUrl":"https://doi.org/10.1080/23723556.2018.1445940","url":null,"abstract":"<p><p>Colon cancer is a heterogeneous tumor driven by subpopulations of cancer stem cells (CSCs). We recently used patient-derived organoids (PDOs) to demonstrate that CSC survival is regulated by autocrine non-canonical Hedgehog signaling, which acts as a positive regulator of Wnt signaling to block CSC differentiation.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1445940"},"PeriodicalIF":2.1,"publicationDate":"2018-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1445940","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519904","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: 2
The Cohesion complex maintains genome stability by preventing end joining of distant DNA ends in S phase. 内聚复合体通过阻止远端DNA末端在S期的末端连接来维持基因组的稳定性。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-04-19 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2016.1154123
Camille Gelot, Josée Guirouilh-Barbat, Bernard S Lopez
{"title":"The Cohesion complex maintains genome stability by preventing end joining of distant DNA ends in S phase.","authors":"Camille Gelot,&nbsp;Josée Guirouilh-Barbat,&nbsp;Bernard S Lopez","doi":"10.1080/23723556.2016.1154123","DOIUrl":"https://doi.org/10.1080/23723556.2016.1154123","url":null,"abstract":"<p><p>Genome instability is a hallmark of cancer cells. The joining of distant DNA double-strand ends (DSEs) ineluctably leads to genome rearrangements. We found that the cohesion complex maintains genome stability by repressing the joining of distant DSEs specifically in the S phase, i.e., the main phase producing one-ended DSEs.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1154123"},"PeriodicalIF":2.1,"publicationDate":"2018-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2016.1154123","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36522044","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: 1
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