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https://www.readbyqxmd.com/read/28535128/low-and-high-let-ionizing-radiation-induces-delayed-homologous-recombination-that-persists-for-two-weeks-before-resolving
#1
Christopher P Allen, Hirokazu Hirakawa, Nakako Izumi Nakajima, Sophia Moore, Jingyi Nie, Neelam Sharma, Mayumi Sugiura, Yuko Hoki, Ryoko Araki, Masumi Abe, Ryuichi Okayasu, Akira Fujimori, Jac A Nickoloff
Genome instability is a hallmark of cancer cells and dysregulation or defects in DNA repair pathways cause genome instability and are linked to inherited cancer predisposition syndromes. Ionizing radiation can cause immediate effects such as mutation or cell death, observed within hours or a few days after irradiation. Ionizing radiation also induces delayed effects many cell generations after irradiation. Delayed effects include hypermutation, hyper-homologous recombination, chromosome instability and reduced clonogenic survival (delayed death)...
May 23, 2017: Radiation Research
https://www.readbyqxmd.com/read/28532423/the-various-aspects-of-genetic-and-epigenetic-toxicology-testing-methods-and-clinical-applications
#2
REVIEW
Ning Ren, Manar Atyah, Wan-Yong Chen, Chen-Hao Zhou
Genotoxicity refers to the ability of harmful substances to damage genetic information in cells. Being exposed to chemical and biological agents can result in genomic instabilities and/or epigenetic alterations, which translate into a variety of diseases, cancer included. This concise review discusses, from both a genetic and epigenetic point of view, the current detection methods of different agents' genotoxicity, along with their basic and clinical relation to human cancer, chemotherapy, germ cells and stem cells...
May 22, 2017: Journal of Translational Medicine
https://www.readbyqxmd.com/read/28531315/the-interaction-between-cytosine-methylation-and-processes-of-dna-replication-and-repair-shape-the-mutational-landscape-of-cancer-genomes
#3
Rebecca C Poulos, Jake Olivier, Jason W H Wong
Methylated cytosines (5mCs) are frequently mutated in the genome. However, no studies have yet comprehensively analysed mutation-methylation associations across cancer types. Here we analyse 916 cancer genomes, together with tissue type-specific methylation and replication timing data. We describe a strong mutation-methylation association across colorectal cancer subtypes, most interestingly in samples with microsatellite instability (MSI) or Polymerase epsilon (POLE) exonuclease domain mutations. By analysing genomic regions with differential mismatch repair (MMR) efficiency, we suggest a possible role for MMR in the correction of 5mC deamination events, potentially accounting for the high rate of 5mC mutation accumulation in MSI tumours...
May 22, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28528812/convergence-of-genomic-instability-and-schlap1-weathering-the-storm-of-intraductal-carcinoma-of-the-prostate
#4
EDITORIAL
Daniel E Spratt
No abstract text is available yet for this article.
May 18, 2017: European Urology
https://www.readbyqxmd.com/read/28521575/high-frequency-of-de-novo-daz-microdeletion-in-sperm-nuclei-of-subfertile-men-possible-involvement-of-genome-instability-in-idiopathic-male-infertility
#5
Hossein Mozdarani, Pegah Ghoraeian, Sohail Mozdarani, Parvin Fallahi, Anahita Mohseni-Meybodi
The occurrence and diagnosis of Y-chromosome microdeletions, specifically deletions of the DAZ (Deleted in Azoospermia) genes are an important issue in male infertility. Screening Y chromosome microdeletion is mainly done using polymerase chain reaction (PCR) on blood leukocytes. However, there is some evidence indicating that presence of DAZ in somatic cells might not be indicative of its presence in the germ cell lineage. Therefore, a total of 130 men with poor semen quality were examined for presence of DAZ microdeletion in their leukocytes...
May 19, 2017: Human Fertility: Journal of the British Fertility Society
https://www.readbyqxmd.com/read/28521333/drugging-the-cancers-addicted-to-dna-repair
#6
Jac A Nickoloff, Dennie Jones, Suk-Hee Lee, Elizabeth A Williamson, Robert Hromas
Defects in DNA repair can result in oncogenic genomic instability. Cancers occurring from DNA repair defects were once thought to be limited to rare inherited mutations (such as BRCA1 or 2). It now appears that a clinically significant fraction of cancers have acquired DNA repair defects. DNA repair pathways operate in related networks, and cancers arising from loss of one DNA repair component typically become addicted to other repair pathways to survive and proliferate. Drug inhibition of the rescue repair pathway prevents the repair-deficient cancer cell from replicating, causing apoptosis (termed synthetic lethality)...
November 1, 2017: Journal of the National Cancer Institute
https://www.readbyqxmd.com/read/28516305/arsenic-toxicity-and-epimutagenecity-the-new-lineage
#7
REVIEW
Somnath Paul, Pritha Bhattacharjee, Ashok K Giri, Pritha Bhattacharjee
Global methylation pattern regulates the normal functioning of a cell. Research have shown arsenic alter these methylation landscapes within the genome leading to aberrant gene expression and inducts various pathophysiological outcomes. Long interspersed nuclear elements (LINE-1) normally remains inert due to heavy methylation of it's promoters, time and various environmental insults, they lose these methylation signatures and begin retro-transposition that has been associated with genomic instability and cancerous outcomes...
May 17, 2017: Biometals: An International Journal on the Role of Metal Ions in Biology, Biochemistry, and Medicine
https://www.readbyqxmd.com/read/28515422/up-regulation-and-nuclear-translocation-of-y-box-binding-protein-1-yb-1-is-linked-to-poor-prognosis-in-erg-negative-prostate-cancer
#8
Asmus Heumann, Özge Kaya, Christoph Burdelski, Claudia Hube-Magg, Martina Kluth, Dagmar S Lang, Ronald Simon, Burkhard Beyer, Imke Thederan, Guido Sauter, Jakob R Izbicki, Andreas M Luebke, Andrea Hinsch, Frank Jacobsen, Corinna Wittmer, Franziska Büscheck, Doris Höflmayer, Sarah Minner, Maria Christina Tsourlakis, Thorsten Schlomm, Waldemar Wilczak
Y-box binding protein 1 (YB-1) is an RNA and DNA binding factor with potential prognostic cancer. To evaluate the clinical impact of YB-1, a tissue microarray with 11,152 prostate cancers was analysed by immunohistochemistry. Cytoplasmic and nuclear staining was separately analysed. Cytoplasmic YB-1 was absent or weak in normal epithelium but seen in 86,3% of carcinomas. Cytoplasmic staining was weak, moderate, and strong in 29.6%, 43.7% and 13.0% of tumours and was accompanied by nuclear YB-1 staining in 32...
May 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28515316/dna-damage-induced-degradation-of-exo1-limits-dna-end-resection-to-ensure-accurate-dna-repair
#9
Nozomi Tomimatsu, Bipasha Mukherjee, Janelle Louise Harris, Francesca Ludovica Boffo, Molly Hardebeck, Patrick Ryan Potts, Kum Kum Khanna, Sandeep Burma
End resection of DNA double-strand breaks (DSBs) to generate 3'-single-stranded DNA facilitates DSB repair via error-free homologous recombination (HR) while stymieing repair by the error-prone non-homologous end joining (NHEJ) pathway. Activation of DNA end resection involves phosphorylation of the 5' to 3' exonuclease EXO1 by the phosphoinositide 3-kinase-like kinases ATM and ATR, and by the cyclin-dependent kinases 1 and 2. After activation, EXO1 must also be restrained in order to prevent over-resection which is known to hamper optimal HR and trigger global genomic instability...
May 17, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28515154/progerin-sequestration-of-pcna-promotes-replication-fork-collapse-and-mislocalization-of-xpa-in-laminopathy-related-progeroid-syndromes
#10
Benjamin A Hilton, Ji Liu, Brian M Cartwright, Yiyong Liu, Maya Breitman, Youjie Wang, Rowdy Jones, Hui Tang, Antonio Rusinol, Phillip R Musich, Yue Zou
Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disorder that is caused by a point mutation in the LMNA gene resulting in production of a truncated farnesylated-prelamin A protein (progerin). We previously reported that XPA mislocalized to the progerin-induced DNA double-strand break (DSB) sites, blocking DSB repair, which led to DSB accumulation, DNA damage responses, and early replication arrest in HGPS. In this study, the XPA mislocalization to DSBs occurred at stalled or collapsed replication forks, concurrent with a significant loss of PCNA at the forks, whereas PCNA efficiently bound to progerin...
May 17, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28514651/modeling-genomic-instability-and-selection-pressure-in-a-mouse-model-of-melanoma
#11
Lawrence N Kwong, Lihua Zou, Sharmeen Chagani, Chandra Sekhar Pedamallu, Mingguang Liu, Shan Jiang, Alexei Protopopov, Jianhua Zhang, Gad Getz, Lynda Chin
Tumor evolution is an iterative process of selection for pro-oncogenic aberrations. This process can be accelerated by genomic instability, but how it interacts with different selection bottlenecks to shape the evolving genomic landscape remains understudied. Here, we assessed tumor initiation and therapy resistance bottlenecks in mouse models of melanoma, with or without genomic instability. At the initiation bottleneck, whole-exome sequencing revealed that drug-naive tumors were genomically silent, and this was surprisingly unaffected when genomic instability was introduced via telomerase inactivation...
May 16, 2017: Cell Reports
https://www.readbyqxmd.com/read/28514051/the-ppar%C3%AE-setd8-axis-constitutes-an-epigenetic-p53-independent-checkpoint-on-p21-mediated-cellular-senescence
#12
Chieh-Tien Shih, Yi-Feng Chang, Yi-Tung Chen, Chung-Pei Ma, Hui-Wen Chen, Chang-Ching Yang, Juu-Chin Lu, Yau-Sheng Tsai, Hua-Chien Chen, Bertrand Chin-Ming Tan
Cellular senescence is a permanent proliferative arrest triggered by genome instability or aberrant growth stresses, acting as a protective or even tumor-suppressive mechanism. While several key aspects of gene regulation have been known to program this cessation of cell growth, the involvement of the epigenetic regulation has just emerged but remains largely unresolved. Using a systems approach that is based on targeted gene profiling, we uncovered known and novel chromatin modifiers with putative link to the senescent state of the cells...
May 17, 2017: Aging Cell
https://www.readbyqxmd.com/read/28511883/a-prostate-cancer-nimbosus-genomic-instability-and-schlap1-dysregulation-underpin-aggression-of-intraductal-and-cribriform-subpathologies
#13
Melvin L K Chua, Winnie Lo, Melania Pintilie, Jure Murgic, Emilie Lalonde, Vinayak Bhandari, Osman Mahamud, Anuradha Gopalan, Charlotte F Kweldam, Geert J L H van Leenders, Esther I Verhoef, Agnes Marije Hoogland, Julie Livingstone, Alejandro Berlin, Alan Dal Pra, Alice Meng, Junyan Zhang, Michèle Orain, Valérie Picard, Hélène Hovington, Alain Bergeron, Louis Lacombe, Yves Fradet, Bernard Têtu, Victor E Reuter, Neil Fleshner, Michael Fraser, Paul C Boutros, Theodorus H van der Kwast, Robert G Bristow
BACKGROUND: Intraductal carcinoma (IDC) and cribriform architecture (CA) represent unfavorable subpathologies in localized prostate cancer. We recently showed that IDC shares a clonal ancestry with the adjacent glandular adenocarcinoma. OBJECTIVE: We investigated for the co-occurrence of "aggression" factors, genomic instability and hypoxia, and performed gene expression profiling of these tumors. DESIGN, SETTING, AND PARTICIPANTS: A total of 1325 men were treated for localized prostate cancer from four academic institutions (University Health Network, CHU de Québec-Université Laval, Memorial Sloan Kettering Cancer Center [MSKCC], and Erasmus Medical Center)...
May 13, 2017: European Urology
https://www.readbyqxmd.com/read/28507204/detection-of-an-alk-fusion-in-colorectal-carcinoma-by-hybrid-capture-based-assay-of-circulating-tumor-dna
#14
Andrea Z Lai, Alexa B Schrock, Rachel L Erlich, Jeffrey S Ross, Vincent A Miller, Evgeny Yakirevich, Siraj M Ali, Fadi Braiteh
ALK rearrangements have been observed in 0.05%-2.5% of patients with colorectal cancers (CRCs) and are predicted to be oncogenic drivers largely mutually exclusive of KRAS, NRAS, or BRAF alterations. Here we present the case of a patient with metastatic CRC who was treatment naïve at the time of molecular testing. Initial ALK immunohistochemistry (IHC) staining was negative, but parallel genomic profiling of both circulating tumor DNA (ctDNA) and tissue using similar hybrid capture-based assays each identified an identical STRN-ALK fusion...
May 15, 2017: Oncologist
https://www.readbyqxmd.com/read/28505005/gastric-cancer-with-primitive-enterocyte-phenotype-an-aggressive-subgroup-of-intestinal-type-adenocarcinoma
#15
Sho Yamazawa, Tetsuo Ushiku, Aya Shinozaki-Ushiku, Akimasa Hayashi, Akiko Iwasaki, Hiroyuki Abe, Amane Tagashira, Hiroharu Yamashita, Yasuyuki Seto, Hiroyuki Aburatani, Masashi Fukayama
A primitive cell-like gene expression signature is associated with aggressive phenotypes of various cancers. We assessed the expression of phenotypic markers characterizing primitive cells and its correlation with clinicopathologic and molecular characteristics in gastric cancer. Immunohistochemical analysis of a panel of primitive phenotypic markers, including embryonic stem cell markers (OCT4, NANOG, SALL4, CLDN6, and LIN28) and known oncofetal proteins (AFP and GPC3), was performed using tissue microarray on 386 gastric cancers...
May 12, 2017: American Journal of Surgical Pathology
https://www.readbyqxmd.com/read/28504713/elevated-pttg-and-pbf-predicts-poor-patient-outcome-and-modulates-dna-damage-response-genes-in-thyroid-cancer
#16
M L Read, J C Fong, B Modasia, A Fletcher, W Imruetaicharoenchoke, R J Thompson, H Nieto, J J Reynolds, A Bacon, U Mallick, A Hackshaw, J C Watkinson, K Boelaert, A S Turnell, V E Smith, C J McCabe
The proto-oncogene PTTG and its binding partner PBF have been widely studied in multiple cancer types, particularly thyroid and colorectal, but their combined role in tumourigenesis is uncharacterised. Here, we show for the first time that together PTTG and PBF significantly modulate DNA damage response (DDR) genes, including p53 target genes, required to maintain genomic integrity in thyroid cells. Critically, DDR genes were extensively repressed in primary thyrocytes from a bitransgenic murine model (Bi-Tg) of thyroid-specific PBF and PTTG overexpression...
May 15, 2017: Oncogene
https://www.readbyqxmd.com/read/28502582/upregulation-of-rad51-expression-is-associated-with-progression-of-thyroid-carcinoma
#17
R Sarwar, A K Sheikh, I Mahjabeen, K Bashir, S Saeed, M A Kayani
AIMS: RAD51 participates in homologous recombination repair (HRR) of double-stranded DNA breaks (DSBs) which may cause genomic instability and cancer. The aim of this study was to investigate RAD51 gene expression at transcriptional and translational levels to measure mRNA and protein level and to correlate its relationship with proliferation marker, Ki67 in thyroid cancer patients. This study also explored correlation of these genes with different clinicopathological parameters of the study cohort by Spearman's rank correlation coefficient...
May 11, 2017: Experimental and Molecular Pathology
https://www.readbyqxmd.com/read/28501701/radb-acts-in-homologous-recombination-in-the-archaeon-haloferax-volcanii-consistent-with-a-role-as-recombination-mediator
#18
Kayleigh Wardell, Sam Haldenby, Nathan Jones, Susan Liddell, Greg H P Ngo, Thorsten Allers
Homologous recombination plays a central role in the repair of double-strand DNA breaks, the restart of stalled replication forks and the generation of genetic diversity. Regulation of recombination is essential since defects can lead to genome instability and chromosomal rearrangements. Strand exchange is a key step of recombination - it is catalysed by RecA in bacteria, Rad51/Dmc1 in eukaryotes and RadA in archaea. RadB, a paralogue of RadA, is present in many archaeal species. RadB has previously been proposed to function as a recombination mediator, assisting in RadA-mediated strand exchange...
April 26, 2017: DNA Repair
https://www.readbyqxmd.com/read/28491820/endoplasmic-reticulum-stress-unfolded-protein-response-and-cancer-cell-fate
#19
REVIEW
Marco Corazzari, Mara Gagliardi, Gian Maria Fimia, Mauro Piacentini
Perturbation of endoplasmic reticulum (ER) homeostasis results in a stress condition termed "ER stress" determining the activation of a finely regulated program defined as unfolded protein response (UPR) and whose primary aim is to restore this organelle's physiological activity. Several physiological and pathological stimuli deregulate normal ER activity causing UPR activation, such as hypoxia, glucose shortage, genome instability, and cytotoxic compounds administration. Some of these stimuli are frequently observed during uncontrolled proliferation of transformed cells, resulting in tumor core formation and stage progression...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/28487279/single-cell-sequencing-deciphers-a-convergent-evolution-of-copy-number-alterations-from-primary-to-circulating-tumour-cells
#20
Yan Gao, Xiaohui Ni, Hua Guo, Zhe Su, Yi Ba, Zhongsheng Tong, Zhi Guo, Xin Yao, Xixi Chen, Jian Yin, Zhao Yan, Lin Guo, Ying Liu, Fan Bai, Xiaoliang Sunney Xie, Ning Zhang
Copy number alteration (CNA) is a major contributor to genome instability, a hallmark of cancer. Here we studied genomic alterations in single primary tumour cells and circulating tumour cells (CTCs) from the same patient. Single-nucleotide variations (SNVs) in single cells from both samples occurred sporadically, whereas CNAs among primary tumour cells emerged accumulatively rather than abruptly, converging toward that of CTCs. Focal CNAs affecting MYC gene and PTEN gene were observed only in a minor portion of primary tumour cells but were present in all CTCs, suggesting a strong selection toward metastasis...
May 9, 2017: Genome Research
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