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https://www.readbyqxmd.com/read/28346378/dna-repair-pathway-alterations-in-bladder-cancer
#1
REVIEW
Kent W Mouw
Most bladder tumors have complex genomes characterized by a high mutation burden as well as frequent copy number alterations and chromosomal rearrangements. Alterations in DNA repair pathways-including the double-strand break (DSB) and nucleotide excision repair (NER) pathways-are present in bladder tumors and may contribute to genomic instability and drive the tumor phenotype. DNA damaging such as cisplatin, mitomycin C, and radiation are commonly used in the treatment of muscle-invasive or metastatic bladder cancer, and several recent studies have linked specific DNA repair pathway defects with sensitivity to DNA damaging-based therapy...
March 27, 2017: Cancers
https://www.readbyqxmd.com/read/28342452/contribution-of-genetic-factors-to-platinum-based-chemotherapy-sensitivity-and-prognosis-of-non-small-cell-lung-cancer
#2
REVIEW
Cristina Pérez-Ramírez, Marisa Cañadas-Garre, Miguel Ángel Molina, Ana I Robles, María José Faus-Dáder, Miguel Ángel Calleja-Hernández
Although platinum-based chemotherapy remains the standard treatment for advanced NSCLC patients, clinical outcomes are poor and most patients develop high-grade toxicities. Genetic factors, such as single nucleotide polymorphisms (SNPs) involved in platinum pharmacodynamics, metabolism and mechanism of action, may account for inter-individual differences shown in effectiveness and toxicity. Polymorphisms in genes involved in DNA repair and others such as PI3K/PTEN/AKT and TGF-β pathways have been demonstrated to be associated with response, survival and toxicity in advanced NSCLC patients treated with platinum-based chemotherapy...
January 2017: Mutation Research
https://www.readbyqxmd.com/read/28329680/major-roles-for-pyrimidine-dimers-nucleotide-excision-repair-and-atr-in-the-alternative-splicing-response-to-uv-irradiation
#3
Manuel J Muñoz, Nicolás Nieto Moreno, Luciana E Giono, Adrián E Cambindo Botto, Gwendal Dujardin, Giulia Bastianello, Stefania Lavore, Antonio Torres-Méndez, Carlos F M Menck, Benjamin J Blencowe, Manuel Irimia, Marco Foiani, Alberto R Kornblihtt
We have previously found that UV irradiation promotes RNA polymerase II (RNAPII) hyperphosphorylation and subsequent changes in alternative splicing (AS). We show now that UV-induced DNA damage is not only necessary but sufficient to trigger the AS response and that photolyase-mediated removal of the most abundant class of pyrimidine dimers (PDs) abrogates the global response to UV. We demonstrate that, in keratinocytes, RNAPII is the target, but not a sensor, of the signaling cascade initiated by PDs. The UV effect is enhanced by inhibition of gap-filling DNA synthesis, the last step in the nucleotide excision repair pathway (NER), and reduced by the absence of XPE, the main NER sensor of PDs...
March 21, 2017: Cell Reports
https://www.readbyqxmd.com/read/28283089/e-coli-mismatch-repair-enhances-at-to-gc-mutagenesis-caused-by-alkylating-agents
#4
Kota Nakano, Yoko Yamada, Eizo Takahashi, Sakae Arimoto, Keinosuke Okamoto, Kazuo Negishi, Tomoe Negishi
Alkylating agents are known to induce the formation of O(6)-alkylguanine (O(6)-alkG) and O(4)-alkylthymine (O(4)-alkT) in DNA. These lesions have been widely investigated as major sources of mutations. We previously showed that mismatch repair (MMR) facilitates the suppression of GC-to-AT mutations caused by O(6)-methylguanine more efficiently than the suppression of GC-to-AT mutations caused by O(6)-ethylguanine. However, the manner by which O(4)-alkyT lesions are repaired remains unclear. In the present study, we investigated the repair pathway involved in the repair of O(4)-alkT...
March 2017: Mutation Research
https://www.readbyqxmd.com/read/28278049/mismatch-repair-proteins-recruited-to-ultraviolet-light-damaged-sites-lead-to-degradation-of-licensing-factor-cdt1-in-the-g1-phase
#5
Miyuki Tanaka, Michiyo Takahara, Kohei Nukina, Akiyo Hayashi, Wataru Sakai, Kaoru Sugasawa, Yasushi Shiomi, Hideo Nishitani
Cdt1 is rapidly degraded by CRL4(Cdt2) E3 ubiquitin ligase after UV (UV) irradiation. Previous reports revealed that the nucleotide excision repair (NER) pathway is responsible for the rapid Cdt1-proteolysis. Here, we show that mismatch repair (MMR) proteins are also involved in the degradation of Cdt1 after UV irradiation in the G1 phase. First, compared with the rapid (within ∼15 min) degradation of Cdt1 in normal fibroblasts, Cdt1 remained stable for ∼30 min in NER-deficient XP-A cells, but was degraded within ∼60 min...
February 22, 2017: Cell Cycle
https://www.readbyqxmd.com/read/28256105/cis-nerolidol-induces-endoplasmic-reticulum-stress-and-cell-death-in-human-hepatocellular-carcinoma-cells-through-extensive-cyp2c19-and-cyp1a2-oxidation
#6
Bruna Isabela Biazi, Thalita Alves Zanetti, Adrivanio Baranoski, Amanda Cristina Corveloni, Mário Sérgio Mantovani
Of late, many studies are attempting to find new molecules with anti-cancer properties, especially those with the capability to inhibit cell growth. The aim of this work was to evaluate nerolidol, a plant-based compound, as its cytotoxicity, genotoxicity, antiproliferative and apoptotic induction, cell cycle, mitochondrial membrane potential, and RT-qPCR of transcripts related to those pathways in the human hepatocellular carcinoma cell line (HepG2/C3A). Only cis-nerolidol (C-NER) demonstrated cytotoxicity (100 to 250 μM) activity and was selected to conduct the following experiments...
March 2, 2017: Basic & Clinical Pharmacology & Toxicology
https://www.readbyqxmd.com/read/28237621/inorganic-arsenic-inhibits-the-nucleotide-excision-repair-pathway-and-reduces-the-expression-of-xpc
#7
Nathaniel Holcomb, Mamta Goswami, Sung Gu Han, Tim Scott, John D'Orazio, David K Orren, C Gary Gairola, Isabel Mellon
Chronic exposure to arsenic, most often through contaminated drinking water, has been linked to several types of cancer in humans, including skin and lung cancer. However, the mechanisms underlying its role in causing cancer are not well understood. There is evidence that exposure to arsenic can enhance the carcinogenicity of UV light in inducing skin cancers and may enhance the carcinogenicity of tobacco smoke in inducing lung cancers. The nucleotide excision repair (NER) pathway removes different types of DNA damage including those produced by UV light and components of tobacco smoke...
February 16, 2017: DNA Repair
https://www.readbyqxmd.com/read/28209516/movement-of-the-%C3%AE-hairpin-in-the-third-zinc-binding-module-of-uvra-is-required-for-dna-damage-recognition
#8
Thanyalak Kraithong, Ketsaraphorn Channgam, Ornchuma Itsathitphaisarn, Montip Tiensuwan, David Jeruzalmi, Danaya Pakotiprapha
Nucleotide excision repair (NER) is distinguished from other DNA repair pathways by its ability to process various DNA lesions. In bacterial NER, UvrA is the key protein that detects damage and initiates the downstream NER cascade. Although it is known that UvrA preferentially binds to damaged DNA, the mechanism for damage recognition is unclear. A β-hairpin in the third Zn-binding module (Zn3hp) of UvrA has been suggested to undergo a conformational change upon DNA binding, and proposed to be important for damage sensing...
March 2017: DNA Repair
https://www.readbyqxmd.com/read/28192636/paracrine-regulation-of-melanocyte-genomic-stability-a-focus-on-nucleotide-excision-repair
#9
REVIEW
Stuart Gordon Jarrett, Katharine Marie Carter, John August D'Orazio
UV radiation is a major environmental risk factor for the development of melanoma by causing DNA damage and mutations. Resistance to UV damage is largely determined by the capacity of melanocytes to respond to UV injury by repairing mutagenic photolesions. The nucleotide excision repair (NER) pathway is the major mechanism by which cells correct UV photodamage. This multi-step process involves the basic steps of damage recognition, isolation, localized strand unwinding, assembly of a repair complex, excision of the damage-containing strand 3' and 5' to the photolesion, synthesis of a sequence-appropriate replacement strand and finally ligation to restore continuity of genomic DNA...
February 13, 2017: Pigment Cell & Melanoma Research
https://www.readbyqxmd.com/read/28120709/dna-damaging-anticancer-drugs-a-perspective-for-dna-repair-oriented-therapy
#10
Janusz Blasiak
DNA-damaging drugs in cancer present two main problems: therapeutic resistance and side effects and both can associate with DNA repair, which can be targeted in cancer therapy. Bleomycin (BLM) induces complex DNA damages, including strand breaks, base loss and 3'-phosphoglycolate (3'PG) residues repaired by several pathways, but 3'PGs must be processed to the 3'-OH ends, usually by tyrosyl-DNA phosphodiesterase 1 (Tdp1). Therefore, targeting Tdp1 can improve anticancer therapy with BLM. Mitomycin C (MMC) produces a variety of adducts with DNA, including inter-strand cross-links (ICLs) and Xeroderma pigmentosum (XP) proteins, including XPG, XPE and XPF can be crucial for the initial stage of ICL repair, so they can be targeted by inhibitors to increase toxicity of MMC in cancer cells...
January 24, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28110804/differential-role-of-base-excision-repair-proteins-in-mediating-cisplatin-cytotoxicity
#11
Akshada Sawant, Ashley M Floyd, Mohan Dangeti, Wen Lei, Robert W Sobol, Steve M Patrick
Interstrand crosslinks (ICLs) are covalent lesions formed by cisplatin. The mechanism for the processing and removal of ICLs by DNA repair proteins involves nucleotide excision repair (NER), homologous recombination (HR) and fanconi anemia (FA) pathways. In this report, we monitored the processing of a flanking uracil adjacent to a cisplatin ICL by the proteins involved in the base excision repair (BER) pathway. Using a combination of extracts, purified proteins, inhibitors, functional assays and cell culture studies, we determined the specific BER proteins required for processing a DNA substrate with a uracil adjacent to a cisplatin ICL...
March 2017: DNA Repair
https://www.readbyqxmd.com/read/28109975/dna-damage-response-in-patients-with-pediatric-acute-lymphoid-leukemia-during-induction-therapy
#12
Júlia Plentz Portich, Rafael Pereira Dos Santos, Nathalia Kersting, Karolina Brochado Jorge, Pietro Rebelo Casagrande, Gabriela Dos Santos Costa, Jéssica Maria Gonçalves Dias Cionek, Danielly Brufatto Olguins, Marialva Sinigaglia, Franciele Faccio Busatto, Jenifer Saffi, Sharbel Weidner Maluf, Jiseh Fagundes Loss, Algemir Lunardi Brunetto, Rafael Roesler, Caroline Brunetto de Farias
Predicting the individual response to chemotherapy is a crucial challenge in cancer treatment. DNA damage caused by antitumor therapies evokes different repair mechanisms responses, such as Nucleotide Excision Repair (NER), whose components are being studied as prognosis biomarkers and target therapies. However, few reports have addressed DNA damages in pediatric Acute Lymphoid Leukemia (ALL). Hence, we conducted an observational follow-up study with pediatric patients to assess DNA damage (by Comet Assay) and gene expression from NER pathway during chemotherapy induction...
January 11, 2017: Leukemia Research
https://www.readbyqxmd.com/read/28109890/sunlight-damage-to-cellular-dna-focus-on-oxidatively-generated-lesions
#13
REVIEW
André Passaglia Schuch, Natália Cestari Moreno, Natielen Jacques Schuch, Carlos Frederico Martins Menck, Camila Carrião Machado Garcia
The routine and often unavoidable exposure to solar ultraviolet (UV) radiation makes it one of the most significant environmental DNA-damaging agents to which humans are exposed. Sunlight, specifically UVB and UVA, triggers various types of DNA damage. Although sunlight, mainly UVB, is necessary for the production of vitamin D, which is necessary for human health, DNA damage may have several deleterious consequences, such as cell death, mutagenesis, photoaging and cancer. UVA and UVB photons can be directly absorbed not only by DNA, which results in lesions, but also by the chromophores that are present in skin cells...
January 18, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28094871/divergence-of-camp-signaling-pathways-mediating-augmented-nucleotide-excision-repair-and-pigment-induction-in-melanocytes
#14
Erin M Wolf Horrell, Stuart G Jarrett, Katharine M Carter, John A D'Orazio
Loss-of-function melanocortin 1 receptor (MC1R) polymorphisms are common in UV-sensitive fair-skinned individuals and are associated with blunted cAMP second messenger signaling and higher lifetime risk of melanoma because of diminished ability of melanocytes to cope with UV damage. cAMP signaling positions melanocytes to resist UV injury by up-regulating synthesis of UV-blocking eumelanin pigment and by enhancing the repair of UV-induced DNA damage. cAMP enhances melanocyte nucleotide excision repair (NER), the genome maintenance pathway responsible for the removal of mutagenic UV photolesions, through cAMP-activated protein kinase (protein kinase A)-mediated phosphorylation of the ataxia telangiectasia mutated and Rad3 related (ATR) protein on the S435 residue...
January 17, 2017: Experimental Dermatology
https://www.readbyqxmd.com/read/28088761/amplification-of-unscheduled-dna-synthesis-signal-enables-fluorescence-based-single-cell-quantification-of-transcription-coupled-nucleotide-excision-repair
#15
Franziska Wienholz, Wim Vermeulen, Jurgen A Marteijn
Nucleotide excision repair (NER) comprises two damage recognition pathways: global genome NER (GG-NER) and transcription-coupled NER (TC-NER), which remove a wide variety of helix-distorting lesions including UV-induced damage. During NER, a short stretch of single-stranded DNA containing damage is excised and the resulting gap is filled by DNA synthesis in a process called unscheduled DNA synthesis (UDS). UDS is measured by quantifying the incorporation of nucleotide analogues into repair patches to provide a measure of NER activity...
January 13, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28074905/mir-488-inhibits-proliferation-and-cisplatin-sensibility-in-non-small-cell-lung-cancer-nsclc-cells-by-activating-the-eif3a-mediated-ner-signaling-pathway
#16
Chao Fang, Yi-Xin Chen, Na-Yiyuan Wu, Ji-Ye Yin, Xiang-Ping Li, Hsuan-Shun Huang, Wei Zhang, Hong-Hao Zhou, Zhao-Qian Liu
Our previous studied indicated that eukaryotic translation initiation factor 3a (eIF3a) increases the sensitive of platinum-based chemotherapy in lung cancer. MiRNAs play an important role in lung carcinogenesis and drug response. In this study, we aimed to identify potential endogenous miRNAs that inhibit eIF3a expression and determine their influence of this inhibition on cisplatin resistance. Using bioinformatics analysis prediction and confirmation with dual-luciferase reporter assays, we found that miRNA-488 inhibited eIF3a expression by directly binding to the 3'UTR of eIF3a...
January 11, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28074003/dna-polymerase-beta-germline-variant-confers-cellular-response-to-cisplatin-therapy
#17
Antonia A Nemec, Laura Abriola, Jane S Merkel, Elisa de Stanchina, Michelle DeVeaux, Daniel Zelterman, Peter M Glazer, Joann B Sweasy
Resistance to cancer chemotherapies leads to deadly consequences, yet current research focuses only on the roles of somatically acquired mutations in this resistance. The mutational status of the germline is also likely to play a role in the way cells respond to chemotherapy. The carrier status for the POLB rs3136797 germline mutation encoding P242R DNA polymerase beta (Pol β) is associated with poor prognosis for lung cancer, specifically in response to treatment with cisplatin. Here, it is revealed that the P242R mutation is sufficient to promote resistance to cisplatin in human cells and in mouse xenografts...
March 2017: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/28049704/the-nucleotide-excision-repair-pathway-limits-l1-retrotransposition
#18
Geraldine Servant, Vincent A Streva, Rebecca S Derbes, Madushani I Wijetunge, Marc Neeland, Travis B White, Victoria P Belancio, Astrid M Roy-Engel, Prescott L Deininger
Long interspersed elements 1 (L1) are active mobile elements that constitute almost 17% of the human genome. They amplify through a "copy-and-paste" mechanism termed retrotransposition, and de novo insertions related to these elements have been reported to cause 0.2% of genetic diseases. Our previous data demonstrated that the endonuclease complex ERCC1-XPF, which cleaves a 3' DNA flap structure, limits L1 retrotransposition. Although the ERCC1-XPF endonuclease participates in several different DNA repair pathways, such as single-strand annealing, or in telomere maintenance, its recruitment to DNA lesions is best characterized in the nucleotide excision repair (NER) pathway...
January 2017: Genetics
https://www.readbyqxmd.com/read/28027876/ercc2-xpd-lys751gln-alter-dna-repair-efficiency-of-platinum-induced-dna-damage-through-p53-pathway
#19
Guopei Zhang, Yangyang Guan, Yuejiao Zhao, Tahar van der Straaten, Sha Xiao, Ping Xue, Guolian Zhu, Qiufang Liu, Yuan Cai, Cuihong Jin, Jinghua Yang, Shengwen Wu, Xiaobo Lu
Platinum-based treatment causes Pt-DNA adducts which lead to cell death. The platinum-induced DNA damage is recognized and repaired by the nucleotide excision repair (NER) system of which ERCC2/XPD is a critical enzyme. Single nucleotide polymorphisms in ERCC2/XPD have been found to be associated with platinum resistance. The aim of the present study was to investigate whether ERCC2/XPD Lys751Gln (rs13181) polymorphism is causally related to DNA repair capacity of platinum-induced DNA damage. First, cDNA clones expressing different genotypes of the polymorphism was transfected to an ERCC2/XPD defective CHO cell line (UV5)...
February 1, 2017: Chemico-biological Interactions
https://www.readbyqxmd.com/read/28011151/the-cyclopurine-deoxynucleosides-dna-repair-biological-effects-mechanistic-insights-and-unanswered-questions
#20
REVIEW
Philip J Brooks
Patients with the genetic disease xeroderma pigmentosum (XP) who lack the capacity to carry out nucleotides excision repair (NER) have a dramatically elevated risk of skin cancer on sun exposed areas of the body. NER is the DNA repair mechanism responsible for the removal of DNA lesions resulting from ultraviolet light. In addition, a subset of XP patients develop a progressive neurodegenerative disease, referred to as XP neurologic disease, which is thought to be the result of accumulation of endogenous DNA lesions that are repaired by NER but not other repair pathways...
December 21, 2016: Free Radical Biology & Medicine
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