首页 > 最新文献

Molecular and Cellular Oncology最新文献

英文 中文
Cell demise inhibited: Unexpected liaisons between mitochondria and IκΒα. 抑制细胞死亡:线粒体与 IκΒα 之间意想不到的联系。
IF 2.6 Q3 ONCOLOGY Pub Date : 2022-01-11 eCollection Date: 2021-01-01 DOI: 10.4161/23723556.2014.995020
Evangelos Pazarentzos

IκΒα (the protein product of NFKBIA gene) has widely been considered a pro- apoptotic factor due to its ability to inhibit the anti-apoptotic transcription factor NFκB. Our findings indicate that IκΒα also exerts a strong anti-apoptotic activity at the outer mitochondria membrane (OMM). This function we uncovered is distinct from its ability to sequester and inhibit NFκB. IκΒα instead binds to voltage dependent anion channel 1 (VDAC1) and Hexokinase 2 (HK2), stabilizes this complex and prevents mitochondria outer membrane permeabilisation (MOMP) and apoptosis.

IκΒα(NFKBIA 基因的蛋白产物)由于能够抑制抗凋亡转录因子 NFκB 而被广泛认为是一种促凋亡因子。我们的研究结果表明,IκΒα 在线粒体外膜(OMM)上也具有很强的抗凋亡活性。我们发现的这一功能不同于它封存和抑制 NFκB 的能力。IκΒα 与电压依赖性阴离子通道 1(VDAC1)和六激酶 2(HK2)结合,稳定这一复合物并防止线粒体外膜渗透(MOMP)和细胞凋亡。
{"title":"Cell demise inhibited: Unexpected liaisons between mitochondria and IκΒα.","authors":"Evangelos Pazarentzos","doi":"10.4161/23723556.2014.995020","DOIUrl":"10.4161/23723556.2014.995020","url":null,"abstract":"<p><p>IκΒα (the protein product of <i>NFKBIA</i> gene) has widely been considered a pro- apoptotic factor due to its ability to inhibit the anti-apoptotic transcription factor NFκB. Our findings indicate that IκΒα also exerts a strong anti-apoptotic activity at the outer mitochondria membrane (OMM). This function we uncovered is distinct from its ability to sequester and inhibit NFκB. IκΒα instead binds to voltage dependent anion channel 1 (VDAC1) and Hexokinase 2 (HK2), stabilizes this complex and prevents mitochondria outer membrane permeabilisation (MOMP) and apoptosis.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2022-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8997252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70555083","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
APOBEC3 as a driver of genetic intratumor heterogeneity. APOBEC3作为肿瘤内遗传异质性的驱动因素
IF 2.1 Q4 Biochemistry, Genetics and Molecular Biology Pub Date : 2022-01-03 eCollection Date: 2023-01-01 DOI: 10.1080/23723556.2021.2014734
Subramanian Venkatesan, Mihaela Angelova, Jirina Bartkova, Samuel F Bakhoum, Jiri Bartek, Nnennaya Kanu, Charles Swanton

Our recent study revealed that APOBEC3B is upregulated during the preinvasive stages of non-small cell lung cancer and breast cancer. In addition to its role in mediating single nucleotide variants, we propose that APOBEC3 promotes copy number intratumor heterogeneity prior to invasion, providing a substrate for cancer evolution.

我们最近的研究表明,APOBEC3B在非小细胞肺癌和乳腺癌的侵袭前阶段上调。除了介导单核苷酸变异外,我们提出APOBEC3在侵袭前促进肿瘤内拷贝数的异质性,为癌症进化提供了一个底物。
{"title":"APOBEC3 as a driver of genetic intratumor heterogeneity.","authors":"Subramanian Venkatesan, Mihaela Angelova, Jirina Bartkova, Samuel F Bakhoum, Jiri Bartek, Nnennaya Kanu, Charles Swanton","doi":"10.1080/23723556.2021.2014734","DOIUrl":"10.1080/23723556.2021.2014734","url":null,"abstract":"<p><p>Our recent study revealed that APOBEC3B is upregulated during the preinvasive stages of non-small cell lung cancer and breast cancer. In addition to its role in mediating single nucleotide variants, we propose that APOBEC3 promotes copy number intratumor heterogeneity prior to invasion, providing a substrate for cancer evolution.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2022-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10730158/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47306257","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
Establishment, authenticity, and characterization of cervical cancer cell lines. 子宫颈癌细胞系的建立、真实性和特性。
IF 2.1 Q4 Biochemistry, Genetics and Molecular Biology Pub Date : 2022-01-01 DOI: 10.1080/23723556.2022.2078628
Ma de Lourdes Zuñiga Martinez, Carlos Miguel López Mendoza, Jared Tenorio Salazar, Alejandro Manuel García Carrancá, Marco Antonio Cerbón Cervantes, Luz Eugenia Alcántara-Quintana

Cell lines have been considered excellent research models in many areas of biomedicine and, specifically, in the study of carcinogenesis. However, they cease to be effective models if their behavior changes. Although studies on the cross-contamination of cell lines originating from different tissues have been performed, little is known about cell lines derived from cervical neoplasia. We know that high-risk HPV (HR-HPV) is associated with the development of this type of cancer. This link between HPV infection and cancer was first established over 35 years ago when HPV16 DNA was found to be present in a large proportion of cervical cancer biopsies. The present review paper aims to report the status of the establishment, authenticity, and characterization of cervical cancer (CC) cell lines. This is a systematic review of articles on the establishment, authenticity, and characterization of CC cell lines, published from 1960 to date in the databases and in cell repository databases. 52 cell lines were identified in the literature. Only 25 cell lines were derived from cervical neoplasia, of which only 45.8% have a reported identity test (genomic fingerprint). Despite the increase in the establishment of cell lines of cervical neoplasia and the standards for the regulation of these study models, the criteria for their characterization continue to be diverse.

细胞系在生物医学的许多领域,特别是在癌变研究中被认为是极好的研究模型。然而,如果他们的行为改变了,他们就不再是有效的榜样。虽然对来自不同组织的细胞系的交叉污染进行了研究,但对来自宫颈肿瘤的细胞系知之甚少。我们知道高危HPV (HR-HPV)与这类癌症的发展有关。HPV感染和癌症之间的联系是在35年前首次确立的,当时在大部分宫颈癌活检中发现了HPV16 DNA。本文综述了宫颈癌细胞系的建立、真实性和特性的研究现状。这是一篇关于CC细胞系的建立、真实性和特性的文章的系统综述,从1960年至今发表在数据库和细胞库数据库中。在文献中鉴定了52个细胞系。只有25个细胞系来源于宫颈肿瘤,其中只有45.8%有报道的身份测试(基因组指纹)。尽管宫颈肿瘤细胞系的建立和这些研究模型的调节标准有所增加,但其表征标准仍然多样化。
{"title":"Establishment, authenticity, and characterization of cervical cancer cell lines.","authors":"Ma de Lourdes Zuñiga Martinez,&nbsp;Carlos Miguel López Mendoza,&nbsp;Jared Tenorio Salazar,&nbsp;Alejandro Manuel García Carrancá,&nbsp;Marco Antonio Cerbón Cervantes,&nbsp;Luz Eugenia Alcántara-Quintana","doi":"10.1080/23723556.2022.2078628","DOIUrl":"https://doi.org/10.1080/23723556.2022.2078628","url":null,"abstract":"<p><p>Cell lines have been considered excellent research models in many areas of biomedicine and, specifically, in the study of carcinogenesis. However, they cease to be effective models if their behavior changes. Although studies on the cross-contamination of cell lines originating from different tissues have been performed, little is known about cell lines derived from cervical neoplasia. We know that high-risk HPV (HR-HPV) is associated with the development of this type of cancer. This link between HPV infection and cancer was first established over 35 years ago when HPV16 DNA was found to be present in a large proportion of cervical cancer biopsies. The present review paper aims to report the status of the establishment, authenticity, and characterization of cervical cancer (CC) cell lines. This is a systematic review of articles on the establishment, authenticity, and characterization of CC cell lines, published from 1960 to date in the databases and in cell repository databases. 52 cell lines were identified in the literature. Only 25 cell lines were derived from cervical neoplasia, of which only 45.8% have a reported identity test (genomic fingerprint). Despite the increase in the establishment of cell lines of cervical neoplasia and the standards for the regulation of these study models, the criteria for their characterization continue to be diverse.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9176225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10432933","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
A mitochondrial response to oxidative stress mediated by unscheduled RNA-DNA hybrids (R-loops). 线粒体对氧化应激的反应由非程序性RNA-DNA杂交体(R-loops)介导
IF 2.1 Q4 Biochemistry, Genetics and Molecular Biology Pub Date : 2021-12-14 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.2007028
Xavier Renaudin, Ashok R Venkitaraman

How oxidative stress promotes aging-related human diseases like cancer and neurodegeneration remains unclear. Here, we discuss the origins and implications of an oxidative-stress response recently reported to destabilize the mitochondrial (mt) genome via unscheduled RNA/DNA hybrid (R-loop) accumulation, by impairing the recruitment of RNAseH1 to the regulatory regions of mtDNA.

摘要氧化应激如何促进与衰老相关的人类疾病,如癌症和神经退行性变,目前尚不清楚。在这里,我们讨论了最近报道的氧化应激反应的起源和意义,该反应通过非计划的RNA/DNA杂交(R-loop)积累,通过削弱RNAseH1向线粒体DNA调控区的募集,破坏线粒体(mt)基因组的稳定。
{"title":"A mitochondrial response to oxidative stress mediated by unscheduled RNA-DNA hybrids (R-loops).","authors":"Xavier Renaudin, Ashok R Venkitaraman","doi":"10.1080/23723556.2021.2007028","DOIUrl":"10.1080/23723556.2021.2007028","url":null,"abstract":"<p><p>How oxidative stress promotes aging-related human diseases like cancer and neurodegeneration remains unclear. Here, we discuss the origins and implications of an oxidative-stress response recently reported to destabilize the mitochondrial (mt) genome via unscheduled RNA/DNA hybrid (R-loop) accumulation, by impairing the recruitment of RNAseH1 to the regulatory regions of mtDNA.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8997250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41787791","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
Enhancer recruitment of a RUNX1, HDAC1 and TLE3 co-repressor complex by mis-expressed FOXC1 blocks differentiation in acute myeloid leukemia. 错误表达的FOXC1对RUNX1、HDAC1和TLE3共阻遏物复合物的增强子募集阻断急性髓系白血病的分化
IF 2.1 Q4 Biochemistry, Genetics and Molecular Biology Pub Date : 2021-11-19 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.2003161
Fabrizio Simeoni, Tim Cp Somervaille

Tissue-inappropriate expression of FOXC1 (Forkhead Box C1) in acute myeloid leukemia confers a monocyte/macrophage lineage differentiation block. We discovered that FOXC1 interacts with RUNX1 (Runt-Related Transcription Factor 1) to stabilize a RUNX1, HDAC1 (Histone Deacetylase 1) and TLE3 (Transducin-like enhancer protein 3) repressor complex at enhancers controlling myeloid differentiation genes.

摘要FOXC1(叉头盒C1)在急性髓系白血病中的组织不恰当表达导致单核细胞/巨噬细胞谱系分化阻滞。我们发现FOXC1与RUNX1(Runt相关转录因子1)相互作用,在控制骨髓分化基因的增强子处稳定RUNX1、HDAC1(组蛋白脱乙酰酶1)和TLE3(转导样增强子蛋白3)阻遏物复合物。
{"title":"Enhancer recruitment of a RUNX1, HDAC1 and TLE3 co-repressor complex by mis-expressed FOXC1 blocks differentiation in acute myeloid leukemia.","authors":"Fabrizio Simeoni, Tim Cp Somervaille","doi":"10.1080/23723556.2021.2003161","DOIUrl":"10.1080/23723556.2021.2003161","url":null,"abstract":"<p><p>Tissue-inappropriate expression of <i>FOXC1</i> (Forkhead Box C1) in acute myeloid leukemia confers a monocyte/macrophage lineage differentiation block. We discovered that FOXC1 interacts with RUNX1 (Runt-Related Transcription Factor 1) to stabilize a RUNX1, HDAC1 (Histone Deacetylase 1) and TLE3 (Transducin-like enhancer protein 3) repressor complex at enhancers controlling myeloid differentiation genes.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8997249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41889564","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
Genome-wide CRISPR screening reveals novel therapeutic targets in RIT1-driven lung cancer. 全基因组CRISPR筛选揭示了RIT1-驱动的癌症的新治疗靶点。
IF 2.1 Q4 Biochemistry, Genetics and Molecular Biology Pub Date : 2021-11-16 DOI: 10.1080/23723556.2021.2000318
Amanda K Riley, Alice H Berger

In recent work, we performed CRISPR/Cas9 screening in RIT1 (Ras-like in all tissues)-mutant cancer cells. We found that RIT1-mutant cells are vulnerable to loss of mitotic regulators, and mutant RIT1 synergizes with YAP1 (yes-associated protein 1) in oncogenesis. These findings can be leveraged to identify targeted therapies for RIT1-mutant cancer.

在最近的工作中,我们在RIT1(所有组织中的Ras-like)突变癌症细胞中进行了CRISPR/Cas9筛选。我们发现RIT1突变细胞容易失去有丝分裂调节因子,并且突变RIT1在致癌过程中与YAP1(yes相关蛋白1)协同作用。这些发现可用于确定RIT1-毛特癌症的靶向治疗。
{"title":"Genome-wide CRISPR screening reveals novel therapeutic targets in RIT1-driven lung cancer.","authors":"Amanda K Riley,&nbsp;Alice H Berger","doi":"10.1080/23723556.2021.2000318","DOIUrl":"https://doi.org/10.1080/23723556.2021.2000318","url":null,"abstract":"<p><p>In recent work, we performed CRISPR/Cas9 screening in <i>RIT1 (Ras-like in all tissues)-</i>mutant cancer cells. We found that <i>RIT1</i>-mutant cells are vulnerable to loss of mitotic regulators, and mutant RIT1 synergizes with YAP1 (yes-associated protein 1) in oncogenesis. These findings can be leveraged to identify targeted therapies for <i>RIT1</i>-mutant cancer.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8997261/pdf/KMCO_8_2000318.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41145264","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
Epigenetic condensates regulate chromatin activity and tumorigenesis. 表观遗传凝聚体调节染色质活性和肿瘤发生。
IF 2.1 Q4 Biochemistry, Genetics and Molecular Biology Pub Date : 2021-11-09 eCollection Date: 2021-01-01 DOI: 10.1080/23723556.2021.1997040
Bi Shi, Wei Li, Hao Jiang

Alterations of epigenetic modulators are extensively associated with cancer, but their key molecular activities in cancer regulation are often unclear. We discovered that lysine demethylase 6A (KDM6A, also known as UTX) suppresses cancer by forming liquid-like condensates with lysine methyltransferase 2D (KMT2D, also known as MLL4) and regulating chromatin activity at multiple levels.

表观遗传调节剂的改变与癌症广泛相关,但其在癌症调控中的关键分子活动往往不清楚。我们发现赖氨酸去甲基化酶6A (KDM6A,也称为UTX)通过与赖氨酸甲基转移酶2D (KMT2D,也称为MLL4)形成液体状凝聚体并在多个水平上调节染色质活性来抑制癌症。
{"title":"Epigenetic condensates regulate chromatin activity and tumorigenesis.","authors":"Bi Shi,&nbsp;Wei Li,&nbsp;Hao Jiang","doi":"10.1080/23723556.2021.1997040","DOIUrl":"https://doi.org/10.1080/23723556.2021.1997040","url":null,"abstract":"<p><p>Alterations of epigenetic modulators are extensively associated with cancer, but their key molecular activities in cancer regulation are often unclear. We discovered that lysine demethylase 6A (KDM6A, also known as UTX) suppresses cancer by forming liquid-like condensates with lysine methyltransferase 2D (KMT2D, also known as MLL4) and regulating chromatin activity at multiple levels.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6f/d8/KMCO_8_1997040.PMC8632315.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39688332","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 therapeutic window for preventive therapy in NF1-associated optic pathway glioma nf1相关视神经胶质瘤预防性治疗的治疗窗口期
IF 2.1 Q4 Biochemistry, Genetics and Molecular Biology Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.1989262
Yuan Zhu, Wang Zheng, Emmanuelle S. Jecrois, Brianna R. Pierce, Daniel M. Treisman
ABSTRACT Pediatric low-grade gliomas (pLGGs) are almost universally driven by abnormal activation of RAS-mediated MEK-ERK/MAPK signaling pathway. pLGGs predominantly occur in children, suggesting that they originate in an ERK-dependent neural stem/progenitor population(s) transiently present in the developing brain. Our recent preclinical study reveals a cell-lineage-of-origin and develops a chemopreventative therapeutic strategy.
儿童低级别胶质瘤(pLGGs)几乎普遍由ras介导的MEK-ERK/MAPK信号通路异常激活驱动。pLGGs主要发生在儿童中,这表明它们起源于短暂存在于发育中的大脑中的erk依赖性神经干/祖细胞群。我们最近的临床前研究揭示了细胞谱系的起源,并开发了一种化学预防治疗策略。
{"title":"A therapeutic window for preventive therapy in NF1-associated optic pathway glioma","authors":"Yuan Zhu, Wang Zheng, Emmanuelle S. Jecrois, Brianna R. Pierce, Daniel M. Treisman","doi":"10.1080/23723556.2021.1989262","DOIUrl":"https://doi.org/10.1080/23723556.2021.1989262","url":null,"abstract":"ABSTRACT Pediatric low-grade gliomas (pLGGs) are almost universally driven by abnormal activation of RAS-mediated MEK-ERK/MAPK signaling pathway. pLGGs predominantly occur in children, suggesting that they originate in an ERK-dependent neural stem/progenitor population(s) transiently present in the developing brain. Our recent preclinical study reveals a cell-lineage-of-origin and develops a chemopreventative therapeutic strategy.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44070503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Interdisciplinary team science to understand and intercept rare cancers 跨学科团队科学理解和拦截罕见癌症
IF 2.1 Q4 Biochemistry, Genetics and Molecular Biology Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.1997331
S. Fröhling
ABSTRACT For most rare cancers, precision oncology approaches are not established because these entities are poorly understood and their investigation requires the collaboration of many centers. The MASTER precision oncology network demonstrates that clinical whole-genome/exome and RNA sequencing yield molecular mechanism-aware treatments that benefit a substantial proportion of patients with advanced rare cancers and will prepare the ground for future clinical trials.
摘要对于大多数罕见的癌症,由于对这些实体的了解不多,并且它们的研究需要多个中心的合作,因此没有建立精确的肿瘤学方法。MASTER精准肿瘤学网络表明,临床全基因组/外显子组和RNA测序产生了分子机制感知治疗,使相当一部分晚期罕见癌症患者受益,并将为未来的临床试验奠定基础。
{"title":"Interdisciplinary team science to understand and intercept rare cancers","authors":"S. Fröhling","doi":"10.1080/23723556.2021.1997331","DOIUrl":"https://doi.org/10.1080/23723556.2021.1997331","url":null,"abstract":"ABSTRACT For most rare cancers, precision oncology approaches are not established because these entities are poorly understood and their investigation requires the collaboration of many centers. The MASTER precision oncology network demonstrates that clinical whole-genome/exome and RNA sequencing yield molecular mechanism-aware treatments that benefit a substantial proportion of patients with advanced rare cancers and will prepare the ground for future clinical trials.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47283118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The perfect PTEN – transcriptional regulation by PTEN dictates sarcoma identity PTEN的完美转录调控决定了肉瘤的特性
IF 2.1 Q4 Biochemistry, Genetics and Molecular Biology Pub Date : 2021-11-02 DOI: 10.1080/23723556.2021.2002120
C. G. Langdon, M. Hatley
ABSTRACT Fusion-negative rhabdomyosarcoma (FN-RMS) is molecularly heterogeneous with few universal alterations except for Phosphatase and tensin homolog (PTEN) promoter hypermethylation. We demonstrate that losing Pten in FN-RMS engages an aberrant transcriptional program key in tumor maintenance and cell identity. These results highlight the importance between transcriptional state, cell of origin, and genetic perturbation in tumorigenesis.
摘要融合阴性横纹肌肉瘤(FN-RMS)是一种分子异质性肿瘤,除了磷酸酶和张力蛋白同源物(PTEN)启动子超甲基化外,几乎没有普遍的改变。我们证明,在FN-RMS中失去Pten参与了一个异常转录程序,这是肿瘤维持和细胞身份的关键。这些结果强调了转录状态、起源细胞和遗传干扰在肿瘤发生中的重要性。
{"title":"The perfect PTEN – transcriptional regulation by PTEN dictates sarcoma identity","authors":"C. G. Langdon, M. Hatley","doi":"10.1080/23723556.2021.2002120","DOIUrl":"https://doi.org/10.1080/23723556.2021.2002120","url":null,"abstract":"ABSTRACT Fusion-negative rhabdomyosarcoma (FN-RMS) is molecularly heterogeneous with few universal alterations except for Phosphatase and tensin homolog (PTEN) promoter hypermethylation. We demonstrate that losing Pten in FN-RMS engages an aberrant transcriptional program key in tumor maintenance and cell identity. These results highlight the importance between transcriptional state, cell of origin, and genetic perturbation in tumorigenesis.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43439788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
期刊
Molecular and Cellular Oncology
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1