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Molecular & cellular oncology最新文献

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JAK3 mutations and HOXA9 expression are important cooperating events in T-cell acute lymphoblastic leukemia. JAK3突变和HOXA9表达是t细胞急性淋巴细胞白血病的重要协同事件。
Molecular & cellular oncology Pub Date : 2018-04-04 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1458014
Charles E de Bock, Jan Cools
{"title":"JAK3 mutations and HOXA9 expression are important cooperating events in T-cell acute lymphoblastic leukemia.","authors":"Charles E de Bock, Jan Cools","doi":"10.1080/23723556.2018.1458014","DOIUrl":"10.1080/23723556.2018.1458014","url":null,"abstract":"<p><p>Sequencing data from large cohorts of T-cell acute lymphoblastic leukemia patients identified a significant association between the presence of <i>JAK3</i> mutations and ectopic <i>HOXA9</i> expression. Mouse models using a constitutive or novel inducible retroviral expression vector to express the <i>JAK3(M511I)</i> mutant and <i>HOXA9</i> led to the development of an aggressive leukemia in vivo, with shorter latency than <i>JAK3(M511I)</i> or <i>HOXA9</i> alone. This was primarily due to the co-binding of STAT5 and HOXA9 to the same genomic loci leading to increased oncogenic JAK-STAT signaling.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1458014"},"PeriodicalIF":0.0,"publicationDate":"2018-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d5/da/kmco-05-03-1458014.PMC6149783.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519911","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 novel mechanism for the prevention of transcription replication conflicts. 一种防止转录复制冲突的新机制。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-03-28 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1451233
Berta Canal, Alba Duch, Francesc Posas, Eulàlia de Nadal
{"title":"A novel mechanism for the prevention of transcription replication conflicts.","authors":"Berta Canal,&nbsp;Alba Duch,&nbsp;Francesc Posas,&nbsp;Eulàlia de Nadal","doi":"10.1080/23723556.2018.1451233","DOIUrl":"https://doi.org/10.1080/23723556.2018.1451233","url":null,"abstract":"<p><p>Transcription and replication complexes can coincide in space and time. Such coincidences may result in collisions that trigger genomic instability. The phosphorylation of Mrc1 by different signaling kinases is part of a general mechanism that serves to delay replication in response to different stresses that trigger a massive transcriptional response in S phase. This mechanism prevents Transcription-Replication Conflicts and maintains genomic integrity in response to unscheduled massive transcription during S phase.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1451233"},"PeriodicalIF":2.1,"publicationDate":"2018-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1451233","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519910","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
A haunted beast: Targeting STAT5BN642H in T-Cell Neoplasia. 一个闹鬼的野兽:靶向STAT5BN642H在t细胞肿瘤中的作用。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-03-28 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1435181
Ha Thi Thanh Pham, Markus Hengstschläger, Richard Moriggl
{"title":"A haunted beast: Targeting STAT5B<sub>N642H</sub> in T-Cell Neoplasia.","authors":"Ha Thi Thanh Pham,&nbsp;Markus Hengstschläger,&nbsp;Richard Moriggl","doi":"10.1080/23723556.2018.1435181","DOIUrl":"https://doi.org/10.1080/23723556.2018.1435181","url":null,"abstract":"<p><p>The somatic hot spot mutation STAT5B<sub>N642H</sub> was found in many T cell leukemia/lymphoma patients. We generated and analyzed a transgenic mouse model with hematopoietic STAT5B<sub>N642H</sub> expression that caused aggressive T-cell leukemia/lymphomas. Herein, we discuss the scientific merit of our model and its relevance for pre-clinical studies.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1435181"},"PeriodicalIF":2.1,"publicationDate":"2018-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1435181","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36200338","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
EXD2: A new regulator of mitochondrial translation and potential target for cancer therapy. EXD2:线粒体翻译的新调控因子和癌症治疗的潜在靶点。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-03-27 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1445943
Travis H Stracker
{"title":"EXD2: A new regulator of mitochondrial translation and potential target for cancer therapy.","authors":"Travis H Stracker","doi":"10.1080/23723556.2018.1445943","DOIUrl":"https://doi.org/10.1080/23723556.2018.1445943","url":null,"abstract":"<p><p>In recent work we identified Exonuclease 3'-5' domain-containing protein 2 (EXD2) as an RNase required for efficient mitochondrial translation. Here I describe in brief the cellular phenotypes caused by EXD2 deficiency and make the case that EXD2 inhibitors could be valuable agents for cancer therapy.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1445943"},"PeriodicalIF":2.1,"publicationDate":"2018-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1445943","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519906","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
Targeting endosomal pH for cancer chemotherapy. 靶向内体pH用于癌症化疗。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-03-13 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1435184
Fabrice Lucien, Roxane R Lavoie, Claire M Dubois
{"title":"Targeting endosomal pH for cancer chemotherapy.","authors":"Fabrice Lucien,&nbsp;Roxane R Lavoie,&nbsp;Claire M Dubois","doi":"10.1080/23723556.2018.1435184","DOIUrl":"https://doi.org/10.1080/23723556.2018.1435184","url":null,"abstract":"<p><p>Altered pH homeostasis in cancer cells has been linked with essentially all classical hallmarks of cancer, including chemoresistance. We recently identified a conceptually novel mechanism for how dysregulated pH in hypoxic cells causes chemoresistance which is based on the aberrant cellular distribution of the endosomal pH regulator, the sodium/hydrogen exchanger 6 (NHE6).</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1435184"},"PeriodicalIF":2.1,"publicationDate":"2018-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1435184","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36521986","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: 8
Cisd2 haploinsufficiency: A driving force for hepatocellular carcinoma. Cisd2单倍体不全:肝细胞癌的驱动力。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-03-13 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1441627
Zhao-Qing Shen, Yi-Long Huang, Ting-Fen Tsai
{"title":"<i>Cisd2</i> haploinsufficiency: A driving force for hepatocellular carcinoma.","authors":"Zhao-Qing Shen,&nbsp;Yi-Long Huang,&nbsp;Ting-Fen Tsai","doi":"10.1080/23723556.2018.1441627","DOIUrl":"https://doi.org/10.1080/23723556.2018.1441627","url":null,"abstract":"<p><p>Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and is the major risk factor leading to hepatocellular carcinoma (HCC). <i>Cisd2</i> haploinsufficiency in mice causes NAFLD by disrupting Ca<sup>2+</sup> homeostasis, indicating that CISD2 is a molecular target for the treatment of NAFLD and the prevention of HCC.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1441627"},"PeriodicalIF":2.1,"publicationDate":"2018-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1441627","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519900","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
Single cell RNA-seq highlights a role for a partial EMT in head and neck cancer. 单细胞RNA-seq强调了部分EMT在头颈癌中的作用。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-03-07 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2018.1448244
Sidharth V Puram, Anuraag S Parikh, Itay Tirosh
{"title":"Single cell RNA-seq highlights a role for a partial EMT in head and neck cancer.","authors":"Sidharth V Puram,&nbsp;Anuraag S Parikh,&nbsp;Itay Tirosh","doi":"10.1080/23723556.2018.1448244","DOIUrl":"https://doi.org/10.1080/23723556.2018.1448244","url":null,"abstract":"<p><p>Studies in single cell transcriptomics have significantly expanded our understanding of tumor biology, including recent analyses in head and neck squamous cell carcinoma. Here, we focus on the role of a partial epithelial-to-mesenchymal (EMT) program in these tumors, with discussion of its dynamics, regulation, and implications for diagnostic and therapeutic approaches.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1448244"},"PeriodicalIF":2.1,"publicationDate":"2018-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1448244","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36519908","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: 58
Moving nuclear receptor Nur77 to damaged mitochondria for clearance by mitophagy. 将核受体Nur77移动到受损的线粒体，通过线粒体自噬进行清除。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-03-05 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2017.1327005
Mengjie Hu, Gulimiran Alitongbieke, Ying Su, Hu Zhou, Xiao-Kun Zhang
{"title":"Moving nuclear receptor Nur77 to damaged mitochondria for clearance by mitophagy.","authors":"Mengjie Hu,&nbsp;Gulimiran Alitongbieke,&nbsp;Ying Su,&nbsp;Hu Zhou,&nbsp;Xiao-Kun Zhang","doi":"10.1080/23723556.2017.1327005","DOIUrl":"https://doi.org/10.1080/23723556.2017.1327005","url":null,"abstract":"<p><p>Selective clearance of damaged mitochondria can reverse pathological status in chronic inflammatory diseases. We recently identified a critical role of nuclear receptor Nur77 and celastrol in priming inflamed mitochondria for autophagy through its mitochondrial targeting and interaction with tumor necrosis factor receptor-associated factor 2 (TRAF2) and the autophagic adaptor p62/SQSTM1.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1327005"},"PeriodicalIF":2.1,"publicationDate":"2018-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2017.1327005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36521977","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
Cellular differentiation: Potential insight into butyrate paradox? 细胞分化:对丁酸盐悖论的潜在洞察?
IF 2.1
Molecular & cellular oncology Pub Date : 2018-02-27 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2016.1212685
Stacy H Ryu, Gerard E Kaiko, Thaddeus S Stappenbeck
{"title":"Cellular differentiation: Potential insight into butyrate paradox?","authors":"Stacy H Ryu,&nbsp;Gerard E Kaiko,&nbsp;Thaddeus S Stappenbeck","doi":"10.1080/23723556.2016.1212685","DOIUrl":"https://doi.org/10.1080/23723556.2016.1212685","url":null,"abstract":"<p><p>We recently demonstrated that cellular responses to butyrate depend on the differentiation status of the colonic epithelium. Here, we apply the implications of these findings to cancer biology and discuss discrepancies in the effects of butyrate on cancer progression.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1212685"},"PeriodicalIF":2.1,"publicationDate":"2018-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2016.1212685","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36522045","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
Tumor-suppressive or tumor-supportive: For p53, that is the question. 肿瘤抑制还是肿瘤支持:对于p53来说，这是一个问题。
IF 2.1
Molecular & cellular oncology Pub Date : 2018-02-27 eCollection Date: 2018-01-01 DOI: 10.1080/23723556.2017.1408537
Muhammad Riaz Khan, Mian Wu, Guangzhi Liu
{"title":"Tumor-suppressive or tumor-supportive: For p53, that is the question.","authors":"Muhammad Riaz Khan,&nbsp;Mian Wu,&nbsp;Guangzhi Liu","doi":"10.1080/23723556.2017.1408537","DOIUrl":"https://doi.org/10.1080/23723556.2017.1408537","url":null,"abstract":"<p><p>We have recently reported a TP53 (known as p53) regulated long noncoding RNA named TRINGS (Tp53-regulated inhibitor of necrosis under glucose starvation). With the aid of TRINGS, p53 was shown to prevent cancer cells against necroptosis under glucose starvation. Our findings suggest that p53 may act as an oncogenic player in metabolic reprogramming.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1408537"},"PeriodicalIF":2.1,"publicationDate":"2018-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2017.1408537","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36521980","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
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