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Cancer Cell

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https://www.readbyqxmd.com/read/28810149/o2-%C3%A2-and-h2o2-mediated-disruption-of-fe-metabolism-causes-the-differential-susceptibility-of-nsclc-and-gbm-cancer-cells-to-pharmacological-ascorbate
#1
Joshua D Schoenfeld, Zita A Sibenaller, Kranti A Mapuskar, Brett A Wagner, Kimberly L Cramer-Morales, Muhammad Furqan, Sonia Sandhu, Thomas L Carlisle, Mark C Smith, Taher Abu Hejleh, Daniel J Berg, Jun Zhang, John Keech, Kalpaj R Parekh, Sudershan Bhatia, Varun Monga, Kellie L Bodeker, Logan Ahmann, Sandy Vollstedt, Heather Brown, Erin P Shanahan Kauffman, Mary E Schall, Ray J Hohl, Gerald H Clamon, Jeremy D Greenlee, Matthew A Howard, Michael K Schultz, Brian J Smith, Dennis P Riley, Frederick E Domann, Joseph J Cullen, Garry R Buettner, John M Buatti, Douglas R Spitz, Bryan G Allen
No abstract text is available yet for this article.
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28810148/choose-and-use-your-chemical-probe-wisely-to-explore-cancer-biology
#2
Julian Blagg, Paul Workman
No abstract text is available yet for this article.
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28810147/macrophage-polarization-contributes-to-glioblastoma-eradication-by-combination-immunovirotherapy-and-immune-checkpoint-blockade
#3
Dipongkor Saha, Robert L Martuza, Samuel D Rabkin
Glioblastoma is an immunosuppressive, fatal brain cancer that contains glioblastoma stem-like cells (GSCs). Oncolytic herpes simplex virus (oHSV) selectively replicates in cancer cells while inducing anti-tumor immunity. oHSV G47Δ expressing murine IL-12 (G47Δ-mIL12), antibodies to immune checkpoints (CTLA-4, PD-1, PD-L1), or dual combinations modestly extended survival of a mouse glioma model. However, the triple combination of anti-CTLA-4, anti-PD-1, and G47Δ-mIL12 cured most mice in two glioma models...
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28810146/swarm-intelligence-enhanced-detection-of-non-small-cell-lung-cancer-using-tumor-educated-platelets
#4
Myron G Best, Nik Sol, Sjors G J G In 't Veld, Adrienne Vancura, Mirte Muller, Anna-Larissa N Niemeijer, Aniko V Fejes, Lee-Ann Tjon Kon Fat, Anna E Huis In 't Veld, Cyra Leurs, Tessa Y Le Large, Laura L Meijer, Irsan E Kooi, François Rustenburg, Pepijn Schellen, Heleen Verschueren, Edward Post, Laurine E Wedekind, Jillian Bracht, Michelle Esenkbrink, Leon Wils, Francesca Favaro, Jilian D Schoonhoven, Jihane Tannous, Hanne Meijers-Heijboer, Geert Kazemier, Elisa Giovannetti, Jaap C Reijneveld, Sander Idema, Joep Killestein, Michal Heger, Saskia C de Jager, Rolf T Urbanus, Imo E Hoefer, Gerard Pasterkamp, Christine Mannhalter, Jose Gomez-Arroyo, Harm-Jan Bogaard, David P Noske, W Peter Vandertop, Daan van den Broek, Bauke Ylstra, R Jonas A Nilsson, Pieter Wesseling, Niki Karachaliou, Rafael Rosell, Elizabeth Lee-Lewandrowski, Kent B Lewandrowski, Bakhos A Tannous, Adrianus J de Langen, Egbert F Smit, Michel M van den Heuvel, Thomas Wurdinger
Blood-based liquid biopsies, including tumor-educated blood platelets (TEPs), have emerged as promising biomarker sources for non-invasive detection of cancer. Here we demonstrate that particle-swarm optimization (PSO)-enhanced algorithms enable efficient selection of RNA biomarker panels from platelet RNA-sequencing libraries (n = 779). This resulted in accurate TEP-based detection of early- and late-stage non-small-cell lung cancer (n = 518 late-stage validation cohort, accuracy, 88%; AUC, 0.94; 95% CI, 0...
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28810145/integrative-analysis-identifies-four-molecular-and-clinical-subsets-in-uveal-melanoma
#5
A Gordon Robertson, Juliann Shih, Christina Yau, Ewan A Gibb, Junna Oba, Karen L Mungall, Julian M Hess, Vladislav Uzunangelov, Vonn Walter, Ludmila Danilova, Tara M Lichtenberg, Melanie Kucherlapati, Patrick K Kimes, Ming Tang, Alexander Penson, Ozgun Babur, Rehan Akbani, Christopher A Bristow, Katherine A Hoadley, Lisa Iype, Matthew T Chang, Andrew D Cherniack, Christopher Benz, Gordon B Mills, Roel G W Verhaak, Klaus G Griewank, Ina Felau, Jean C Zenklusen, Jeffrey E Gershenwald, Lynn Schoenfield, Alexander J Lazar, Mohamed H Abdel-Rahman, Sergio Roman-Roman, Marc-Henri Stern, Colleen M Cebulla, Michelle D Williams, Martine J Jager, Sarah E Coupland, Bita Esmaeli, Cyriac Kandoth, Scott E Woodman
Comprehensive multiplatform analysis of 80 uveal melanomas (UM) identifies four molecularly distinct, clinically relevant subtypes: two associated with poor-prognosis monosomy 3 (M3) and two with better-prognosis disomy 3 (D3). We show that BAP1 loss follows M3 occurrence and correlates with a global DNA methylation state that is distinct from D3-UM. Poor-prognosis M3-UM divide into subsets with divergent genomic aberrations, transcriptional features, and clinical outcomes. We report change-of-function SRSF2 mutations...
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28810144/integrated-genomic-characterization-of-pancreatic-ductal-adenocarcinoma
#6
(no author information available yet)
We performed integrated genomic, transcriptomic, and proteomic profiling of 150 pancreatic ductal adenocarcinoma (PDAC) specimens, including samples with characteristic low neoplastic cellularity. Deep whole-exome sequencing revealed recurrent somatic mutations in KRAS, TP53, CDKN2A, SMAD4, RNF43, ARID1A, TGFβR2, GNAS, RREB1, and PBRM1. KRAS wild-type tumors harbored alterations in other oncogenic drivers, including GNAS, BRAF, CTNNB1, and additional RAS pathway genes. A subset of tumors harbored multiple KRAS mutations, with some showing evidence of biallelic mutations...
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28810143/genomic-evolution-of-breast-cancer-metastasis-and-relapse
#7
Lucy R Yates, Stian Knappskog, David Wedge, James H R Farmery, Santiago Gonzalez, Inigo Martincorena, Ludmil B Alexandrov, Peter Van Loo, Hans Kristian Haugland, Peer Kaare Lilleng, Gunes Gundem, Moritz Gerstung, Elli Pappaemmanuil, Patrycja Gazinska, Shriram G Bhosle, David Jones, Keiran Raine, Laura Mudie, Calli Latimer, Elinor Sawyer, Christine Desmedt, Christos Sotiriou, Michael R Stratton, Anieta M Sieuwerts, Andy G Lynch, John W Martens, Andrea L Richardson, Andrew Tutt, Per Eystein Lønning, Peter J Campbell
Patterns of genomic evolution between primary and metastatic breast cancer have not been studied in large numbers, despite patients with metastatic breast cancer having dismal survival. We sequenced whole genomes or a panel of 365 genes on 299 samples from 170 patients with locally relapsed or metastatic breast cancer. Several lines of analysis indicate that clones seeding metastasis or relapse disseminate late from primary tumors, but continue to acquire mutations, mostly accessing the same mutational processes active in the primary tumor...
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28810142/control-of-metastasis-by-nk-cells
#8
REVIEW
Alejandro López-Soto, Segundo Gonzalez, Mark J Smyth, Lorenzo Galluzzi
The metastatic spread of malignant cells to distant anatomical locations is a prominent cause of cancer-related death. Metastasis is governed by cancer-cell-intrinsic mechanisms that enable neoplastic cells to invade the local microenvironment, reach the circulation, and colonize distant sites, including the so-called epithelial-to-mesenchymal transition. Moreover, metastasis is regulated by microenvironmental and systemic processes, such as immunosurveillance. Here, we outline the cancer-cell-intrinsic and -extrinsic factors that regulate metastasis, discuss the key role of natural killer (NK) cells in the control of metastatic dissemination, and present potential therapeutic approaches to prevent or target metastatic disease by harnessing NK cells...
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28810141/a-viro-immunotherapy-triple-play-for-the-treatment-of-glioblastoma
#9
John C Bell, Carolina S Ilkow
In this issue of Cancer Cell, Saha et al. systematically test and optimize combination therapy strategies in a challenging model of glioblastoma. Durable complete responses were seen only when an oncolytic virus expressing IL12 was coupled with anti-CTLA-4 and anti-PD-1 therapeutics.
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28810140/new-views-into-the-genetic-landscape-of-metastatic-breast-cancer
#10
Xiaoyu Zhao, Scott Powers
Whether metastasis-specific genetic alterations exist remains controversial. The study by Yates et al. in this issue of Cancer Cell provides evidence that metastases emerge late during primary breast cancer progression and that additional driver mutations are often acquired, posing both challenges and opportunities for precision treatment of metastatic breast cancer.
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28810139/cliques-and-schisms-of-cancer-genes
#11
Peter J Campbell
With a few exceptions, cancers typically carry more than one driver mutation, sometimes five, ten, or more, and these driver mutations do not necessarily assort randomly. In this issue of Cancer Cell, Mina et al. systematically characterize patterns of co-mutation and mutual exclusivity in 6,456 cancers across 23 tumor types.
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28781121/repression-of-stress-induced-line-1-expression-protects-cancer-cell-subpopulations-from-lethal-drug-exposure
#12
Gulfem Dilek Guler, Charles Albert Tindell, Robert Pitti, Catherine Wilson, Katrina Nichols, Tommy KaiWai Cheung, Hyo-Jin Kim, Matthew Wongchenko, Yibing Yan, Benjamin Haley, Trinna Cuellar, Joshua Webster, Navneet Alag, Ganapati Hegde, Erica Jackson, Tracy Leah Nance, Paul Garrett Giresi, Kuan-Bei Chen, Jinfeng Liu, Suchit Jhunjhunwala, Jeff Settleman, Jean-Philippe Stephan, David Arnott, Marie Classon
Maintenance of phenotypic heterogeneity within cell populations is an evolutionarily conserved mechanism that underlies population survival upon stressful exposures. We show that the genomes of a cancer cell subpopulation that survives treatment with otherwise lethal drugs, the drug-tolerant persisters (DTPs), exhibit a repressed chromatin state characterized by increased methylation of histone H3 lysines 9 and 27 (H3K9 and H3K27). We also show that survival of DTPs is, in part, maintained by regulators of H3K9me3-mediated heterochromatin formation and that the observed increase in H3K9me3 in DTPs is most prominent over long interspersed repeat element 1 (LINE-1)...
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28756993/conditional-selection-of-genomic-alterations-dictates-cancer-evolution-and-oncogenic-dependencies
#13
Marco Mina, Franck Raynaud, Daniele Tavernari, Elena Battistello, Stephanie Sungalee, Sadegh Saghafinia, Titouan Laessle, Francisco Sanchez-Vega, Nikolaus Schultz, Elisa Oricchio, Giovanni Ciriello
Cancer evolves through the emergence and selection of molecular alterations. Cancer genome profiling has revealed that specific events are more or less likely to be co-selected, suggesting that the selection of one event depends on the others. However, the nature of these evolutionary dependencies and their impact remain unclear. Here, we designed SELECT, an algorithmic approach to systematically identify evolutionary dependencies from alteration patterns. By analyzing 6,456 genomes from multiple tumor types, we constructed a map of oncogenic dependencies associated with cellular pathways, transcriptional readouts, and therapeutic response...
August 14, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28697345/choose-and-use-your-chemical-probe-wisely-to-explore-cancer-biology
#14
REVIEW
Julian Blagg, Paul Workman
Small-molecule chemical probes or tools have become progressively more important in recent years as valuable reagents to investigate fundamental biological mechanisms and processes causing disease, including cancer. Chemical probes have also achieved greater prominence alongside complementary biological reagents for target validation in drug discovery. However, there is evidence of widespread continuing misuse and promulgation of poor-quality and insufficiently selective chemical probes, perpetuating a worrisome and misleading pollution of the scientific literature...
July 10, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28697344/muc1-and-hif-1alpha-signaling-crosstalk-induces-anabolic-glucose-metabolism-to-impart-gemcitabine-resistance-to-pancreatic-cancer
#15
Surendra K Shukla, Vinee Purohit, Kamiya Mehla, Venugopal Gunda, Nina V Chaika, Enza Vernucci, Ryan J King, Jaime Abrego, Gennifer D Goode, Aneesha Dasgupta, Alysha L Illies, Teklab Gebregiworgis, Bingbing Dai, Jithesh J Augustine, Divya Murthy, Kuldeep S Attri, Oksana Mashadova, Paul M Grandgenett, Robert Powers, Quan P Ly, Audrey J Lazenby, Jean L Grem, Fang Yu, José M Matés, John M Asara, Jung-Whan Kim, Jordan H Hankins, Colin Weekes, Michael A Hollingsworth, Natalie J Serkova, Aaron R Sasson, Jason B Fleming, Jennifer M Oliveto, Costas A Lyssiotis, Lewis C Cantley, Lyudmyla Berim, Pankaj K Singh
Poor response to cancer therapy due to resistance remains a clinical challenge. The present study establishes a widely prevalent mechanism of resistance to gemcitabine in pancreatic cancer, whereby increased glycolytic flux leads to glucose addiction in cancer cells and a corresponding increase in pyrimidine biosynthesis to enhance the intrinsic levels of deoxycytidine triphosphate (dCTP). Increased levels of dCTP diminish the effective levels of gemcitabine through molecular competition. We also demonstrate that MUC1-regulated stabilization of hypoxia inducible factor-1α (HIF-1α) mediates such metabolic reprogramming...
July 10, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28697343/redefining-hormonal-therapy-for-advanced-prostate-cancer-results-from-the-latitude-and-chaarted-studies
#16
Eric J Small
Two papers published recently in the New England Journal of Medicine describe the utility of abiraterone acetate, an androgen biosynthesis inhibitor, in the early treatment of metastatic prostate cancer. In addition to establishing a new standard of care, these two articles pose a number of important questions for future investigation.
July 10, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28697342/tumor-evolution-of-glioma-intrinsic-gene-expression-subtypes-associates-with-immunological-changes-in-the-microenvironment
#17
Qianghu Wang, Baoli Hu, Xin Hu, Hoon Kim, Massimo Squatrito, Lisa Scarpace, Ana C deCarvalho, Sali Lyu, Pengping Li, Yan Li, Floris Barthel, Hee Jin Cho, Yu-Hsi Lin, Nikunj Satani, Emmanuel Martinez-Ledesma, Siyuan Zheng, Edward Chang, Charles-Etienne Gabriel Sauvé, Adriana Olar, Zheng D Lan, Gaetano Finocchiaro, Joanna J Phillips, Mitchel S Berger, Konrad R Gabrusiewicz, Guocan Wang, Eskil Eskilsson, Jian Hu, Tom Mikkelsen, Ronald A DePinho, Florian Muller, Amy B Heimberger, Erik P Sulman, Do-Hyun Nam, Roel G W Verhaak
We leveraged IDH wild-type glioblastomas, derivative neurospheres, and single-cell gene expression profiles to define three tumor-intrinsic transcriptional subtypes designated as proneural, mesenchymal, and classical. Transcriptomic subtype multiplicity correlated with increased intratumoral heterogeneity and presence of tumor microenvironment. In silico cell sorting identified macrophages/microglia, CD4(+) T lymphocytes, and neutrophils in the glioma microenvironment. NF1 deficiency resulted in increased tumor-associated macrophages/microglia infiltration...
July 10, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28697341/muc-king-with-hif-may-rewire-pyrimidine-biosynthesis-and-curb-gemcitabine-resistance-in-pancreatic-cancer
#18
Chi V Dang
In this issue of Cancer Cell, Singh and colleagues report a role for MUC1-induced HIF expression in rewiring ribose synthesis, which drives pyridimine production as a possible resistance mechanism to gemcitabine, adding to complexity and multiple paths to resistance.
July 10, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28697340/stabilization-of-the-c-myc-protein-by-camkii%C3%AE-promotes-t-cell-lymphoma
#19
Ying Gu, Jiawei Zhang, Xiaoxiao Ma, Byung-Wook Kim, Hailong Wang, Jinfan Li, Yi Pan, Yang Xu, Lili Ding, Lu Yang, Chao Guo, Xiwei Wu, Jun Wu, Kirk Wu, Xiaoxian Gan, Gang Li, Ling Li, Stephen J Forman, Wing-Chung Chan, Rongzhen Xu, Wendong Huang
Although high c-Myc protein expression is observed alongside MYC amplification in some cancers, in most cases protein overexpression occurs in the absence of gene amplification, e.g., T cell lymphoma (TCL). Here, Ca(2+)/calmodulin-dependent protein kinase II γ (CAMKIIγ) was shown to stabilize the c-Myc protein by directly phosphorylating it at serine 62 (S62). Furthermore, CAMKIIγ was shown to be essential for tumor maintenance. Inhibition of CAMKIIγ with a specific inhibitor destabilized c-Myc and reduced tumor burden...
July 10, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28697339/oncogenic-activation-of-the-rna-binding-protein-nelfe-and-myc-signaling-in-hepatocellular-carcinoma
#20
Hien Dang, Atsushi Takai, Marshonna Forgues, Yotsowat Pomyen, Haiwei Mou, Wen Xue, Debashish Ray, Kevin C H Ha, Quaid D Morris, Timothy R Hughes, Xin Wei Wang
Global transcriptomic imbalance is a ubiquitous feature associated with cancer, including hepatocellular carcinoma (HCC). Analyses of 1,225 clinical HCC samples revealed that a large numbers of RNA binding proteins (RBPs) are dysregulated and that RBP dysregulation is associated with poor prognosis. We further identified that oncogenic activation of a top candidate RBP, negative elongation factor E (NELFE), via somatic copy-number alterations enhanced MYC signaling and promoted HCC progression. Interestingly, NELFE induces a unique tumor transcriptome by selectively regulating MYC-associated genes...
July 10, 2017: Cancer Cell
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