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Genomic instability cancer

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https://www.readbyqxmd.com/read/28231327/functionally-focused-algorithmic-analysis-of-high-resolution-microarray-cgh-genomic-landscapes-demonstrates-comparable-genomic-copy-number-aberrations-in-msi-and-mss-sporadic-colorectal-cancer
#1
Hamad Ali, Milad S Bitar, Ashraf Al Madhoun, Makia Marafie, Fahd Al-Mulla
Array-based comparative genomic hybridization (aCGH) emerged as a powerful technology for studying copy number variations at higher resolution in many cancers including colorectal cancer. However, the lack of standardized systematic protocols including bioinformatic algorithms to obtain and analyze genomic data resulted in significant variation in the reported copy number aberration (CNA) data. Here, we present genomic aCGH data obtained using highly stringent and functionally relevant statistical algorithms from 116 well-defined microsatellites instable (MSI) and microsatellite stable (MSS) colorectal cancers...
2017: PloS One
https://www.readbyqxmd.com/read/28213433/chromosomal-instability-as-a-driver-of-tumor-heterogeneity-and-evolution
#2
Samuel F Bakhoum, Dan Avi Landau
Large-scale, massively parallel sequencing of human cancer samples has revealed tremendous genetic heterogeneity within individual tumors. Indeed, tumors are composed of an admixture of diverse subpopulations-subclones-that vary in space and time. Here, we discuss a principal driver of clonal diversification in cancer known as chromosomal instability (CIN), which complements other modes of genetic diversification creating the multilayered genomic instability often seen in human cancer. Cancer cells have evolved to fine-tune chromosome missegregation rates to balance the acquisition of heterogeneity while preserving favorable genotypes, a dependence that can be exploited for a therapeutic benefit...
February 17, 2017: Cold Spring Harbor Perspectives in Medicine
https://www.readbyqxmd.com/read/28212810/chromosomal-instability-analysis-and-regional-tumor-heterogeneity-in-colon-cancer
#3
Vincenza Barresi, Sergio Castorina, Nicolò Musso, Carmela Capizzi, Tonia Luca, Giovanna Privitera, Daniele Filippo Condorelli
Chromosomal instability (CIN) is classically defined as an increase in the rate at which numerical or structural chromosomal aberrations are acquired in a cancer cell. The number of somatic copy number abnormalities (CNAs) revealed by high resolution genomic array can be considered as a surrogate marker for CIN, but several points, related to sample processing and data analysis, need to be standardized. In this work we analyzed 51 CRC samples and matched normal mucosae by whole genome SNP arrays and compared different bioinformatics tools in order to identify broad (>25% of a chromosomal arm) and focal somatic copy number abnormalities (BCNAs and FCNAs respectively)...
January 2017: Cancer Genetics
https://www.readbyqxmd.com/read/28202506/recurrent-patterns-of-dna-copy-number-alterations-in-tumors-reflect-metabolic-selection-pressures
#4
Nicholas A Graham, Aspram Minasyan, Anastasia Lomova, Ashley Cass, Nikolas G Balanis, Michael Friedman, Shawna Chan, Sophie Zhao, Adrian Delgado, James Go, Lillie Beck, Christian Hurtz, Carina Ng, Rong Qiao, Johanna Ten Hoeve, Nicolaos Palaskas, Hong Wu, Markus Müschen, Asha S Multani, Elisa Port, Steven M Larson, Nikolaus Schultz, Daniel Braas, Heather R Christofk, Ingo K Mellinghoff, Thomas G Graeber
Copy number alteration (CNA) profiling of human tumors has revealed recurrent patterns of DNA amplifications and deletions across diverse cancer types. These patterns are suggestive of conserved selection pressures during tumor evolution but cannot be fully explained by known oncogenes and tumor suppressor genes. Using a pan-cancer analysis of CNA data from patient tumors and experimental systems, here we show that principal component analysis-defined CNA signatures are predictive of glycolytic phenotypes, including (18)F-fluorodeoxy-glucose (FDG) avidity of patient tumors, and increased proliferation...
February 15, 2017: Molecular Systems Biology
https://www.readbyqxmd.com/read/28202223/filtration-based-enrichment-of-circulating-tumor-cells-from-all-prostate-cancer-risk-groups
#5
Julius Adebayo Awe, Jeff Saranchuk, Darrel Drachenberg, Sabine Mai
OBJECTIVE: To combine circulating tumor cell (CTC) isolation by filtration and immunohistochemistry to investigate the presence of CTCs in low, intermediate, and high-risk prostate cancer (PCa). CTCs isolated from these risk groups stained positive for both cytokeratin and androgen receptors, but negative for CD45. PATIENTS AND METHODS: Blood samples from 41 biopsy confirmed patients with PCa at different clinical stages such as low, intermediate, and high risk were analyzed...
February 12, 2017: Urologic Oncology
https://www.readbyqxmd.com/read/28199992/fragile-genes-that-are-frequently-altered-in-cancer-players-not-passengers
#6
Jenna R Karras, Morgan S Schrock, Bahadir Batar, Kay Huebner
FHIT, located at FRA3B, is one of the most commonly deleted genes in human cancers, and loss of FHIT protein is one of the earliest events in cancer initiation. However, location of FHIT at a chromosomal fragile site, a locus prone to breakage and gap formation under even mild replication stress, has encouraged claims that FHIT loss is a passenger event in cancers. We summarize accumulated evidence that FHIT protein functions as a genome "caretaker" required to protect the stability of genomes of normal cells of most tissues from agents causing intrinsic and extrinsic DNA damage...
February 16, 2017: Cytogenetic and Genome Research
https://www.readbyqxmd.com/read/28196964/fancd2-binds-human-papillomavirus-genomes-and-associates-with-a-distinct-set-of-dna-repair-proteins-to-regulate-viral-replication
#7
Chelsey C Spriggs, Laimonis A Laimins
The life cycle of human papillomavirus (HPV) is dependent on the differentiation state of its host cell. HPV genomes are maintained as low-copy episomes in basal epithelial cells and amplified to thousands of copies per cell in differentiated layers. Replication of high-risk HPVs requires the activation of the ataxia telangiectasia-mutated (ATM) and ATM and Rad3-related (ATR) DNA repair pathways. The Fanconi anemia (FA) pathway is a part of the DNA damage response and mediates cross talk between the ATM and ATR pathways...
February 14, 2017: MBio
https://www.readbyqxmd.com/read/28196590/singling-out-chromosome-gains-in-tumor-evolution
#8
Ryan M Naylor, Jan M van Deursen
In this issue of Cancer Cell, Sheltzer et al. shed new light on Theodor Boveri's century-old hypothesis by demonstrating that aneuploidy characterized by single-chromosome gains acts to suppress tumorigenesis and that aneuploidy itself is a nidus for genomic instability.
February 13, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28192779/chromosome-imbalances-in-cancer-molecular-cytogenetics-meets-genomics
#9
Elisa Palumbo, Antonella Russo
Genomic instability is a hallmark of cancer, and it is well-known that in several cancers the karyotype is unstable and rapidly evolving. Molecular cytogenetics has contributed to the description and interpretation of cancer karyotypes, in particular through multicolor FISH approaches which can define even complex chromosome rearrangements. The introduction of genome-wide methods has made available a powerful set of tools with higher resolution than cytogenetics, thus appropriate to comprehend the huge variability of cancer cells...
February 14, 2017: Cytogenetic and Genome Research
https://www.readbyqxmd.com/read/28188185/response-to-pd-1-blockade-in-microsatellite-stable-metastatic-colorectal-cancer-harboring-a-pole-mutation
#10
Jun Gong, Chongkai Wang, Peter P Lee, Peiguo Chu, Marwan Fakih
Recent clinical evidence has demonstrated that microsatellite instability (MSI) or defective mismatch repair (MMR) and high tumor mutational load can predict response to the programmed cell death 1 (PD-1) receptor inhibitor pembrolizumab in metastatic colorectal cancer (mCRC). Mutations in polymerase ε (POLE), a DNA polymerase involved in DNA replication and repair, contribute to an ultramutated but microsatellite stable (MSS) phenotype in colorectal tumors that is uniquely distinct from MSI tumors. This report presents the first case in the literature describing a clinical response to pembrolizumab in an 81-year-old man with treatment-refractory mCRC characterized by an MSS phenotype and POLE mutation identified on genomic profiling by next-generation sequencing...
February 2017: Journal of the National Comprehensive Cancer Network: JNCCN
https://www.readbyqxmd.com/read/28187286/endogenous-dna-damage-as-a-source-of-genomic-instability-in-cancer
#11
REVIEW
Anthony Tubbs, André Nussenzweig
Genome instability, defined as higher than normal rates of mutation, is a double-edged sword. As a source of genetic diversity and natural selection, mutations are beneficial for evolution. On the other hand, genomic instability can have catastrophic consequences for age-related diseases such as cancer. Mutations arise either from inactivation of DNA repair pathways or in a repair-competent background due to genotoxic stress from celluar processes such as transcription and replication that overwhelm high-fidelity DNA repair...
February 9, 2017: Cell
https://www.readbyqxmd.com/read/28186092/epstein-barr-virus-particles-induce-centrosome-amplification-and-chromosomal-instability
#12
Anatoliy Shumilov, Ming-Han Tsai, Yvonne T Schlosser, Anne-Sophie Kratz, Katharina Bernhardt, Susanne Fink, Tuba Mizani, Xiaochen Lin, Anna Jauch, Josef Mautner, Annette Kopp-Schneider, Regina Feederle, Ingrid Hoffmann, Henri-Jacques Delecluse
Infections with Epstein-Barr virus (EBV) are associated with cancer development, and EBV lytic replication (the process that generates virus progeny) is a strong risk factor for some cancer types. Here we report that EBV infection of B-lymphocytes (in vitro and in a mouse model) leads to an increased rate of centrosome amplification, associated with chromosomal instability. This effect can be reproduced with virus-like particles devoid of EBV DNA, but not with defective virus-like particles that cannot infect host cells...
February 10, 2017: Nature Communications
https://www.readbyqxmd.com/read/28179585/oncogenomic-disruptions-in-arsenic-induced-carcinogenesis
#13
REVIEW
Adam P Sage, Brenda C Minatel, Kevin W Ng, Greg L Stewart, Trevor J B Dummer, Wan L Lam, Victor D Martinez
Chronic exposure to arsenic affects more than 200 million people worldwide, and has been associated with many adverse health effects, including cancer in several organs. There is accumulating evidence that arsenic biotransformation, a step in the elimination of arsenic from the human body, can induce changes at a genetic and epigenetic level, leading to carcinogenesis. At the genetic level, arsenic interferes with key cellular processes such as DNA damage-repair and chromosomal structure, leading to genomic instability...
January 5, 2017: Oncotarget
https://www.readbyqxmd.com/read/28179486/serum-25-hydroxyvitamin-d-has-a-modest-positive-association-with-leukocyte-telomere-length-in-middle-aged-us-adults
#14
Julia Beilfuss, Carlos A Camargo, Elena Kamycheva
Background: Vitamin D deficiency has been linked to all-cause mortality and cancer. However, the biological plausibility of these associations is not well established. Leukocyte telomere length (LTL) shortening is associated with aging and is a hallmark of genomic instability and carcinogenesis.Objective: We aimed to investigate the association between serum 25-hydroxyvitamin D [25(OH)D] concentrations and LTL in the general US population.Methods: We analyzed data from the US NHANES 2001-2002. The study population comprised 1542 younger adults (aged 20-39 y), 1336 middle-aged adults (aged 40-59 y), and 1382 older adults (aged ≥60 y)...
February 8, 2017: Journal of Nutrition
https://www.readbyqxmd.com/read/28177281/copy-number-and-gene-dependency-analysis-reveals-partial-copy-loss-of-wild-type-sf3b1-as-a-novel-cancer-vulnerability
#15
Brenton R Paolella, William J Gibson, Laura M Urbanski, John A Alberta, Travis I Zack, Pratiti Bandopadhayay, Caitlin A Nichols, Pankaj K Agarwalla, Meredith S Brown, Rebecca Lamothe, Yong Yu, Peter S Choi, Esther A Obeng, Dirk Heckl, Guo Wei, Belinda Wang, Aviad Tsherniak, Francisca Vazquez, Barbara A Weir, David E Root, Glenn S Cowley, Sara J Buhrlage, Charles D Stiles, Benjamin L Ebert, William C Hahn, Robin Reed, Rameen Beroukhim
Genomic instability is a hallmark of human cancer, and results in widespread somatic copy number alterations. We used a genome-scale shRNA viability screen in human cancer cell lines to systematically identify genes that are essential in the context of particular copy-number alterations (copy-number associated gene dependencies). The most enriched class of copy-number associated gene dependencies was CYCLOPS (Copy-number alterations Yielding Cancer Liabilities Owing to Partial losS) genes, and spliceosome components were the most prevalent...
February 8, 2017: ELife
https://www.readbyqxmd.com/read/28176634/targeting-the-akt-pi3k-signaling-pathway-as-a-potential-therapeutic-strategy-for-the-treatment-of-pancreatic-cancer
#16
Safieh Ebrahimi, Mina Hosseini, Soodabeh Shahidsales, Mina Maftouh, Gordon A Ferns, Majid Ghayour-Mobarhan, Seyed Mahdi Hassanian, Amir Avan
The phosphoinositide 3 kinase AKT mammalian target of rapamycin (PI3K-AKT-mTOR) signaling pathway is an important signaling pathway in pancreatic cancer (PC). It is frequently activated in PC and is associated with worse outcome. Aberrant activation of this pathway is involved in cell metabolism and survival, cell cycle progression, regulation of apoptosis, protein synthesis, and genomic instability. Several agents have been developed to target Akt/PI3K pathways, including PI3K inhibitors, (e.g. LY294002, Wortmannin), PI3K/mTOR inhibitors (e...
February 6, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28176176/amplification-of-sox4-promotes-pi3k-akt-signaling-in-human-breast-cancer
#17
Gaurav A Mehta, Joel S Parker, Grace O Silva, Katherine A Hoadley, Charles M Perou, Michael L Gatza
PURPOSE: The PI3K/Akt signaling axis contributes to the dysregulation of many dominant features in breast cancer including cell proliferation, survival, metabolism, motility, and genomic instability. While multiple studies have demonstrated that basal-like or triple-negative breast tumors have uniformly high PI3K/Akt activity, genomic alterations that mediate dysregulation of this pathway in this subset of highly aggressive breast tumors remain to be determined. METHODS: In this study, we present an integrated genomic analysis based on the use of a PI3K gene expression signature as a framework to analyze orthogonal genomic data from human breast tumors, including RNA expression, DNA copy number alterations, and protein expression...
February 7, 2017: Breast Cancer Research and Treatment
https://www.readbyqxmd.com/read/28173837/insulin-like-growth-factor-1-receptor-activation-promotes-mammary-gland-tumor-development-by-increasing-glycolysis-and-promoting-biomass-production
#18
Bas Ter Braak, Christine L Siezen, Joo S Lee, Pooja Rao, Charlotte Voorhoeve, Eytan Ruppin, Jan Willem van der Laan, Bob van de Water
BACKGROUND: The insulin-like growth factor 1 (IGF1) signaling axis plays a major role in tumorigenesis. In a previous experiment, we chronically treated mice with several agonists of the IGF1 receptor (IGF1R). We found that chronic treatment with insulin analogues with high affinity towards the IGF1R (IGF1 and X10) decreased the mammary gland tumor latency time in a p53(R270H/+)WAPCre mouse model. Frequent injections with insulin analogues that only mildly activated the IGF1R in vivo (glargine and insulin) did not significantly decrease the tumor latency time in this mouse model...
February 7, 2017: Breast Cancer Research: BCR
https://www.readbyqxmd.com/read/28166452/rescue-from-replication-stress-during-mitosis
#19
Michalis Fragkos, Valeria Naim
Genomic instability is a hallmark of cancer and a common feature of human disorders, characterized by growth defects, neurodegeneration, cancer predisposition, and aging. Recent evidence has shown that DNA replication stress is a major driver of genomic instability and tumorigenesis. Cells can undergo mitosis with under-replicated DNA or unresolved DNA structures, and specific pathways are dedicated to resolving these structures during mitosis, suggesting that mitotic rescue from replication stress (MRRS) is a key process influencing genome stability and cellular homeostasis...
February 6, 2017: Cell Cycle
https://www.readbyqxmd.com/read/28150817/association-of-genomic-instability-with-hba1c-levels-and-medication-in-diabetic-patients
#20
Annemarie Grindel, Helmut Brath, Armen Nersesyan, Siegfried Knasmueller, Karl-Heinz Wagner
Diabetes Mellitus type 2 (DM2) is associated with increased cancer risk. Instability of the genetic material plays a key role in the aetiology of human cancer. This study aimed to analyse genomic instability with the micronucleus cytome assay in exfoliated buccal cells depending on glycated haemoglobin (HbA1c) levels and medication in 146 female DM2 patients. The occurrence of micronuclei was significantly increased in DM2 patients compared to healthy controls. Furthermore, it was doubled in DM2 patients with HbA1c > 7...
February 2, 2017: Scientific Reports
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