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Genomic instability cancer

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https://www.readbyqxmd.com/read/28537880/biological-effects-and-epidemiological-consequences-of-arsenic-exposure-and-reagents-that-can-ameliorate-arsenic-damage-in-vivo
#1
REVIEW
Chinthalapally V Rao, Sanya Pal, Altaf Mohammed, Mudassir Farooqui, Mark P Doescher, Adam S Asch, Hiroshi Y Yamada
Through contaminated diet, water, and other forms of environmental exposure, arsenic affects human health. There are many U.S. and worldwide "hot spots" where the arsenic level in public water exceeds the maximum exposure limit. The biological effects of chronic arsenic exposure include generation of reactive oxygen species (ROS), leading to oxidative stress and DNA damage, epigenetic DNA modification, induction of genomic instability, and inflammation and immunomodulation, all of which can initiate carcinogenesis...
May 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/28535128/low-and-high-let-ionizing-radiation-induces-delayed-homologous-recombination-that-persists-for-two-weeks-before-resolving
#2
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
#3
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
#4
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/28521333/drugging-the-cancers-addicted-to-dna-repair
#5
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
#6
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
#7
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/28511883/a-prostate-cancer-nimbosus-genomic-instability-and-schlap1-dysregulation-underpin-aggression-of-intraductal-and-cribriform-subpathologies
#8
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
#9
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
#10
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
#11
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
#12
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/28491820/endoplasmic-reticulum-stress-unfolded-protein-response-and-cancer-cell-fate
#13
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
#14
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
https://www.readbyqxmd.com/read/28485537/mechanisms-of-dna-damage-repair-and-mutagenesis
#15
REVIEW
Nimrat Chatterjee, Graham C Walker
Living organisms are continuously exposed to a myriad of DNA damaging agents that can impact health and modulate disease-states. However, robust DNA repair and damage-bypass mechanisms faithfully protect the DNA by either removing or tolerating the damage to ensure an overall survival. Deviations in this fine-tuning are known to destabilize cellular metabolic homeostasis, as exemplified in diverse cancers where disruption or deregulation of DNA repair pathways results in genome instability. Because routinely used biological, physical and chemical agents impact human health, testing their genotoxicity and regulating their use have become important...
May 9, 2017: Environmental and Molecular Mutagenesis
https://www.readbyqxmd.com/read/28482151/trisubstituted-imidazoles-with-a-rigidized-hinge-binding-motif-act-as-single-digit-nm-inhibitors-of-clinically-relevant-egfr-l858r-t790m-and-l858r-t790m-c797s-mutants-an-example-of-target-hopping
#16
Michael Juchum, Marcel Günther, Eva Döring, Adrian Sievers-Engler, Michael Lämmerhofer, Stefan Laufer
The high genomic instability of non-small cell lung cancer tumors leads to the rapid development of resistance against promising EGFR tyrosine kinase inhibitors (TKIs). A recently detected triple mutation compromises the activity of the gold standard third-generation EGFR inhibitors. We have prepared a set of trisubstituted imidazoles with a rigidized 7-azaindole hinge binding motif as a new structural class of EGFR inhibitors by a target hopping approach from p38α MAPK inhibitor templates. On the basis of an iterative approach of docking, compound preparation, biological testing, and SAR interpretation, robust and flexible synthetic routes were established...
May 23, 2017: Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28482095/prl-3-promotes-telomere-deprotection-and-chromosomal-instability
#17
Shenyi Lian, Lin Meng, Yongyong Yang, Ting Ma, Xiaofang Xing, Qin Feng, Qian Song, Caiyun Liu, Zhihua Tian, Like Qu, Chengchao Shou
Phosphatase of regenerating liver (PRL-3) promotes cell invasiveness, but its role in genomic integrity remains unknown. We report here that shelterin component RAP1 mediates association between PRL-3 and TRF2. In addition, TRF2 and RAP1 assist recruitment of PRL-3 to telomeric DNA. Silencing of PRL-3 in colon cancer cells does not affect telomere integrity or chromosomal stability, but induces reactive oxygen species-dependent DNA damage response and senescence. However, overexpression of PRL-3 in colon cancer cells and primary fibroblasts promotes structural abnormalities of telomeres, telomere deprotection, DNA damage response, chromosomal instability and senescence...
May 8, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28481899/lumican-and-versican-protein-expression-are-associated-with-colorectal-adenoma-to-carcinoma-progression
#18
Meike de Wit, Beatriz Carvalho, Pien M Delis-van Diemen, Carolien van Alphen, Jeroen A M Beliën, Gerrit A Meijer, Remond J A Fijneman
BACKGROUND: One prominent event associated with colorectal adenoma-to-carcinoma progression is genomic instability. Approximately 85% of colorectal cancer cases exhibit chromosomal instability characterized by accumulation of chromosome copy number aberrations (CNAs). Adenomas with gain of chromosome 8q, 13q, and/or 20q are at high risk of progression to cancer. Tumor progression is also associated with expansion of the extracellular matrix (ECM) and the activation of non-malignant cells within the tumor stroma...
2017: PloS One
https://www.readbyqxmd.com/read/28480304/viral-vector-based-innovative-approaches-to-directly-abolishing-tumorigenic-pluripotent-stem-cells-for-safer-regenerative-medicine
#19
REVIEW
Kaoru Mitsui, Kanako Ide, Tomoyuki Takahashi, Ken-Ichiro Kosai
Human pluripotent stem cells (hPSCs) are a promising source of regenerative material for clinical applications. However, hPSC transplant therapies pose the risk of teratoma formation and malignant transformation of undifferentiated remnants. These problems underscore the importance of developing technologies that completely prevent tumorigenesis to ensure safe clinical application. Research to date has contributed to establishing safe hPSC lines, improving the efficiency of differentiation induction, and indirectly ensuring the safety of products...
June 16, 2017: Molecular Therapy. Methods & Clinical Development
https://www.readbyqxmd.com/read/28477317/tp53-germline-and-somatic-mutations-in-a-patient-with-fibrolamellar-hepatocellular-carcinoma
#20
Raissa C Andrade, Maria A F D de Lima, Paulo A S de Faria, Fernando R Vargas
Li-Fraumeni syndrome is a rare hereditary cancer predisposition syndrome associated with germline pathogenic variants in TP53 gene. The phenotype may vary from classical to variant forms, known as Li-Fraumeni-like phenotypes. We searched for pathogenic variants in TP53 in a 14 year-old female diagnosed with fibrolamellar hepatocellular carcinoma, a rare subtype of hepatocellular carcinoma. The proband is a heterozygote carrier of the TP53 c.467G>A (p.Arg156His) in exon 5, and her mother is an asymptomatic carrier...
May 5, 2017: Familial Cancer
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