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Cancer Cell

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https://www.readbyqxmd.com/read/27916615/characterization-of-rare-dormant-and-therapy-resistant-cells-in-acute-lymphoblastic-leukemia
#1
Sarah Ebinger, Erbey Ziya Özdemir, Christoph Ziegenhain, Sebastian Tiedt, Catarina Castro Alves, Michaela Grunert, Michael Dworzak, Christoph Lutz, Virginia A Turati, Tariq Enver, Hans-Peter Horny, Karl Sotlar, Swati Parekh, Karsten Spiekermann, Wolfgang Hiddemann, Aloys Schepers, Bernhard Polzer, Stefan Kirsch, Martin Hoffmann, Bettina Knapp, Jan Hasenauer, Heike Pfeifer, Renate Panzer-Grümayer, Wolfgang Enard, Olivier Gires, Irmela Jeremias
Tumor relapse is associated with dismal prognosis, but responsible biological principles remain incompletely understood. To isolate and characterize relapse-inducing cells, we used genetic engineering and proliferation-sensitive dyes in patient-derived xenografts of acute lymphoblastic leukemia (ALL). We identified a rare subpopulation that resembled relapse-inducing cells with combined properties of long-term dormancy, treatment resistance, and stemness. Single-cell and bulk expression profiling revealed their similarity to primary ALL cells isolated from pediatric and adult patients at minimal residual disease (MRD)...
November 18, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27889185/nup98-fusion-proteins-interact-with-the-nsl-and-mll1-complexes-to-drive-leukemogenesis
#2
Haiming Xu, Daria G Valerio, Meghan E Eisold, Amit Sinha, Richard P Koche, Wenhuo Hu, Chun-Wei Chen, S Haihua Chu, Gerard L Brien, Christopher Y Park, James J Hsieh, Patricia Ernst, Scott A Armstrong
The nucleoporin 98 gene (NUP98) is fused to a variety of partner genes in multiple hematopoietic malignancies. Here, we demonstrate that NUP98 fusion proteins, including NUP98-HOXA9 (NHA9), NUP98-HOXD13 (NHD13), NUP98-NSD1, NUP98-PHF23, and NUP98-TOP1 physically interact with mixed lineage leukemia 1 (MLL1) and the non-specific lethal (NSL) histone-modifying complexes. Chromatin immunoprecipitation sequencing illustrates that NHA9 and MLL1 co-localize on chromatin and are found associated with Hox gene promoter regions...
November 15, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27889186/circadian-homeostasis-of-liver-metabolism-suppresses-hepatocarcinogenesis
#3
Nicole M Kettner, Horatio Voicu, Milton J Finegold, Cristian Coarfa, Arun Sreekumar, Nagireddy Putluri, Chinenye A Katchy, Choogon Lee, David D Moore, Loning Fu
Chronic jet lag induces spontaneous hepatocellular carcinoma (HCC) in wild-type mice following a mechanism very similar to that observed in obese humans. The process initiates with non-alcoholic fatty liver disease (NAFLD) that progresses to steatohepatitis and fibrosis before HCC detection. This pathophysiological pathway is driven by jet-lag-induced genome-wide gene deregulation and global liver metabolic dysfunction, with nuclear receptor-controlled cholesterol/bile acid and xenobiotic metabolism among the top deregulated pathways...
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27866850/deubiquitination-and-stabilization-of-pd-l1-by-csn5
#4
Seung-Oe Lim, Chia-Wei Li, Weiya Xia, Jong-Ho Cha, Li-Chuan Chan, Yun Wu, Shih-Shin Chang, Wan-Chi Lin, Jung-Mao Hsu, Yi-Hsin Hsu, Taewan Kim, Wei-Chao Chang, Jennifer L Hsu, Hirohito Yamaguchi, Qingqing Ding, Yan Wang, Yi Yang, Chung-Hsuan Chen, Aysegul A Sahin, Dihua Yu, Gabriel N Hortobagyi, Mien-Chie Hung
Pro-inflammatory cytokines produced in the tumor microenvironment lead to eradication of anti-tumor immunity and enhanced tumor cell survival. In the current study, we identified tumor necrosis factor alpha (TNF-α) as a major factor triggering cancer cell immunosuppression against T cell surveillance via stabilization of programmed cell death-ligand 1 (PD-L1). We demonstrated that COP9 signalosome 5 (CSN5), induced by NF-κB p65, is required for TNF-α-mediated PD-L1 stabilization in cancer cells. CSN5 inhibits the ubiquitination and degradation of PD-L1...
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27866851/inhibition-of-the-glycolytic-activator-pfkfb3-in-endothelium-induces-tumor-vessel-normalization-impairs-metastasis-and-improves-chemotherapy
#5
Anna Rita Cantelmo, Lena-Christin Conradi, Aleksandra Brajic, Jermaine Goveia, Joanna Kalucka, Andreas Pircher, Pallavi Chaturvedi, Johanna Hol, Bernard Thienpont, Laure-Anne Teuwen, Sandra Schoors, Bram Boeckx, Joris Vriens, Anna Kuchnio, Koen Veys, Bert Cruys, Lise Finotto, Lucas Treps, Tor Espen Stav-Noraas, Francesco Bifari, Peter Stapor, Ilaria Decimo, Kim Kampen, Katrien De Bock, Guttorm Haraldsen, Luc Schoonjans, Ton Rabelink, Guy Eelen, Bart Ghesquière, Jalees Rehman, Diether Lambrechts, Asrar B Malik, Mieke Dewerchin, Peter Carmeliet
Abnormal tumor vessels promote metastasis and impair chemotherapy. Hence, tumor vessel normalization (TVN) is emerging as an anti-cancer treatment. Here, we show that tumor endothelial cells (ECs) have a hyper-glycolytic metabolism, shunting intermediates to nucleotide synthesis. EC haplo-deficiency or blockade of the glycolytic activator PFKFB3 did not affect tumor growth, but reduced cancer cell invasion, intravasation, and metastasis by normalizing tumor vessels, which improved vessel maturation and perfusion...
November 8, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27908736/cd98-mediated-adhesive-signaling-enables-the-establishment-and-propagation-of-acute-myelogenous-leukemia
#6
Jeevisha Bajaj, Takaaki Konuma, Nikki K Lytle, Hyog Young Kwon, Jailal N Ablack, Joseph M Cantor, David Rizzieri, Charles Chuah, Vivian G Oehler, Elizabeth H Broome, Edward D Ball, Edward H van der Horst, Mark H Ginsberg, Tannishtha Reya
Acute myelogenous leukemia (AML) is an aggressive disease associated with drug resistance and relapse. To improve therapeutic strategies, it is critical to better understand the mechanisms that underlie AML progression. Here we show that the integrin binding glycoprotein CD98 plays a central role in AML. CD98 promotes AML propagation and lethality by driving engagement of leukemia cells with their microenvironment and maintaining leukemic stem cells. Further, delivery of a humanized anti-CD98 antibody blocks growth of patient-derived AML, highlighting the importance of this pathway in human disease...
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27908735/unr-csde1-drives-a-post-transcriptional-program-to-promote-melanoma-invasion-and-metastasis
#7
Laurence Wurth, Panagiotis Papasaikas, David Olmeda, Nadine Bley, Guadalupe T Calvo, Santiago Guerrero, Daniela Cerezo-Wallis, Javier Martinez-Useros, María García-Fernández, Stefan Hüttelmaier, Maria S Soengas, Fátima Gebauer
RNA binding proteins (RBPs) modulate cancer progression through poorly understood mechanisms. Here we show that the RBP UNR/CSDE1 is overexpressed in melanoma tumors and promotes invasion and metastasis. iCLIP sequencing, RNA sequencing, and ribosome profiling combined with in silico studies unveiled sets of pro-metastatic factors coordinately regulated by UNR as part of RNA regulons. In addition to RNA steady-state levels, UNR was found to control many of its targets at the level of translation elongation/termination...
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846394/restoring-p53-function-in-human-melanoma-cells-by-inhibiting-mdm2-and-cyclin-b1-cdk1-phosphorylated-nuclear-iaspp
#8
Min Lu, Hilde Breyssens, Victoria Salter, Shan Zhong, Ying Hu, Caroline Baer, Indrika Ratnayaka, Alex Sullivan, Nicholas R Brown, Jane Endicott, Stefan Knapp, Benedikt M Kessler, Mark R Middleton, Christian Siebold, E Yvonne Jones, Elena V Sviderskaya, Jonathan Cebon, Thomas John, Otavia L Caballero, Colin R Goding, Xin Lu
No abstract text is available yet for this article.
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846393/decoding-the-dna-methylome-of-mantle-cell-lymphoma-in-the-light-of-the-entire-b-cell-lineage
#9
Ana C Queirós, Renée Beekman, Roser Vilarrasa-Blasi, Martí Duran-Ferrer, Guillem Clot, Angelika Merkel, Emanuele Raineri, Nuria Russiñol, Giancarlo Castellano, Sílvia Beà, Alba Navarro, Marta Kulis, Núria Verdaguer-Dot, Pedro Jares, Anna Enjuanes, María José Calasanz, Anke Bergmann, Inga Vater, Itziar Salaverría, Harmen J G van de Werken, Wyndham H Wilson, Avik Datta, Paul Flicek, Romina Royo, Joost Martens, Eva Giné, Armando Lopez-Guillermo, Hendrik G Stunnenberg, Wolfram Klapper, Christiane Pott, Simon Heath, Ivo G Gut, Reiner Siebert, Elías Campo, José I Martín-Subero
We analyzed the in silico purified DNA methylation signatures of 82 mantle cell lymphomas (MCL) in comparison with cell subpopulations spanning the entire B cell lineage. We identified two MCL subgroups, respectively carrying epigenetic imprints of germinal-center-inexperienced and germinal-center-experienced B cells, and we found that DNA methylation profiles during lymphomagenesis are largely influenced by the methylation dynamics in normal B cells. An integrative epigenomic approach revealed 10,504 differentially methylated regions in regulatory elements marked by H3K27ac in MCL primary cases, including a distant enhancer showing de novo looping to the MCL oncogene SOX11...
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846392/a-druggable-tcf4-and-brd4-dependent-transcriptional-network-sustains-malignancy-in-blastic-plasmacytoid-dendritic-cell-neoplasm
#10
Michele Ceribelli, Zhiying Esther Hou, Priscilla N Kelly, Da Wei Huang, George Wright, Karthik Ganapathi, Moses O Evbuomwan, Stefania Pittaluga, Arthur L Shaffer, Guido Marcucci, Stephen J Forman, Wenming Xiao, Rajarshi Guha, Xiaohu Zhang, Marc Ferrer, Laurence Chaperot, Joel Plumas, Elaine S Jaffe, Craig J Thomas, Boris Reizis, Louis M Staudt
Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is an aggressive and largely incurable hematologic malignancy originating from plasmacytoid dendritic cells (pDCs). Using RNAi screening, we identified the E-box transcription factor TCF4 as a master regulator of the BPDCN oncogenic program. TCF4 served as a faithful diagnostic marker of BPDCN, and its downregulation caused the loss of the BPDCN-specific gene expression program and apoptosis. High-throughput drug screening revealed that bromodomain and extra-terminal domain inhibitors (BETis) induced BPDCN apoptosis, which was attributable to disruption of a BPDCN-specific transcriptional network controlled by TCF4-dependent super-enhancers...
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846391/instructive-role-of-mll-fusion-proteins-revealed-by-a-model-of-t-4-11-pro-b-acute-lymphoblastic-leukemia
#11
Shan Lin, Roger T Luo, Anetta Ptasinska, Jon Kerry, Salam A Assi, Mark Wunderlich, Toshihiko Imamura, Joseph J Kaberlein, Ahmad Rayes, Mark J Althoff, John Anastasi, Maureen M O'Brien, Amom Ruhikanta Meetei, Thomas A Milne, Constanze Bonifer, James C Mulloy, Michael J Thirman
The t(4;11)(q21;q23) fuses mixed-lineage leukemia (MLL) to AF4, the most common MLL-fusion partner. Here we show that MLL fused to murine Af4, highly conserved with human AF4, produces high-titer retrovirus permitting efficient transduction of human CD34(+) cells, thereby generating a model of t(4;11) pro-B acute lymphoblastic leukemia (ALL) that fully recapitulates the immunophenotypic and molecular aspects of the disease. MLL-Af4 induces a B ALL distinct from MLL-AF9 through differential genomic target binding of the fusion proteins leading to specific gene expression patterns...
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846390/erk-activation-globally-downregulates-mirnas-through-phosphorylating-exportin-5
#12
Hui-Lung Sun, Ri Cui, JianKang Zhou, Kun-Yu Teng, Yung-Hsuan Hsiao, Kotaro Nakanishi, Matteo Fassan, Zhenghua Luo, Guqin Shi, Esmerina Tili, Huban Kutay, Francesca Lovat, Caterina Vicentini, Han-Li Huang, Shih-Wei Wang, Taewan Kim, Nicola Zanesi, Young-Jun Jeon, Tae Jin Lee, Jih-Hwa Guh, Mien-Chie Hung, Kalpana Ghoshal, Che-Ming Teng, Yong Peng, Carlo M Croce
MicroRNAs (miRNA) are mostly downregulated in cancer. However, the mechanism underlying this phenomenon and the precise consequence in tumorigenesis remain obscure. Here we show that ERK suppresses pre-miRNA export from the nucleus through phosphorylation of exportin-5 (XPO5) at T345/S416/S497. After phosphorylation by ERK, conformation of XPO5 is altered by prolyl isomerase Pin1, resulting in reduction of pre-miRNA loading. In liver cancer, the ERK-mediated XPO5 suppression reduces miR-122, increases microtubule dynamics, and results in tumor development and drug resistance...
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846389/characteristics-and-significance-of-the-pre-metastatic-niche
#13
REVIEW
Yang Liu, Xuetao Cao
Primary tumors create a favorable microenvironment, namely, pre-metastatic niche, in secondary organs and tissue sites for subsequent metastases. The pre-metastatic niche can be primed and established through a complex interplay among primary tumor-derived factors, tumor-mobilized bone marrow-derived cells, and local stromal components. We review here our current understanding of the key components and underlying mechanisms for pre-metastatic niche formation. We propose six characteristics that define the pre-metastatic niche, which enable tumor cell colonization and promote metastasis, including immunosuppression, inflammation, angiogenesis/vascular permeability, lymphangiogenesis, organotropism, and reprogramming...
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846388/unraveling-the-dna-methylome-in-mantle-cell-lymphoma-new-insights-into-the-cellular-origin
#14
Larry Mansouri, Richard Rosenquist
Our understanding of the DNA methylome and its impact on cancer evolution and disease progression is rapidly evolving. In this issue of Cancer Cell, Queirós et al. provide a detailed characterization of the DNA methylome in mantle cell lymphoma and reveal novel molecular subtypes, potentially with different cellular origins.
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846387/sticking-it-to-the-niche-cd98-mediates-critical-adhesive-signals-in-aml
#15
Andreas Reinisch, Ravindra Majeti
In this issue of Cancer Cell, Bajaj and colleagues report that CD98, a heterodimeric protein highly expressed in acute myeloid leukemia (AML) and largely dispensable for basal hematopoiesis, plays an important role in facilitating leukemia stem cell adhesion to bone marrow vasculature and is a potential therapeutic target in AML.
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846386/an-alternative-sugar-fuels-aml
#16
Rob A Cairns, Tak W Mak
Although altered glucose metabolism is a well-studied feature of malignant cells, little is known about the direct metabolism of fructose. In this issue of Cancer Cell, Chen et al. report that AML cells consume fructose and use it to maintain viability, especially when glucose is scarce.
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846385/an-unexpected-chink-in-the-transcriptional-armor-of-plasmacytoid-dendritic-neoplasms
#17
Maria Kleppe, Ross L Levine
In this issue of Cancer Cell, Ceribelli et al. use functional genomic and chemical screening to reveal the existence of a TCF4/BRD4-dependent oncogenic regulatory network in blastic plasmacytoid dendritic cell neoplasm (BPDCN) and demonstrate that BPDCN cells are highly sensitive to therapeutic targeting of this novel dependency.
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846384/one-step-forward-in-the-challenging-arena-of-mll-af4-leukemia
#18
Nancy J Zeleznik-Le
MLL-AF4 leukemia is the predominant infant acute leukemia and has a poor prognosis. No current experimental models accurately reflect the human disease. Lin et al., in this issue of Cancer Cell, describe their model that recapitulates multiple key aspects of this aggressive disease, facilitating future mechanistic and preclinical studies.
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846383/unrelenting-translation-unrestrains-melanoma-migration
#19
Ashani T Weeraratna, Myriam Gorospe
The cytoplasmic RNA-binding protein UNR influences key developmental processes by controlling mRNA turnover and translation initiation. In this issue of Cancer Cell, Wurth et al. report that UNR is highly expressed in melanoma and enhances invasion and metastasis at least partly by inducing translation elongation of VIM and RAC1 mRNAs.
November 14, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27846382/cholesterol-an-achilles-heel-for-glioblastoma
#20
Zhenyi An, William A Weiss
In this issue of Cancer Cell, Villa et al. report that survival of glioblastoma cells is dependent on uptake of cholesterol. A synthetic agonist of the Liver X receptor depleted cholesterol in GBM cells, slowing growth of GBM xenografts.
November 14, 2016: Cancer Cell
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