Results 141 to 150 of about 3,725,761 (393)

DNA alteration and repair

Ecotoxicology and Environmental Safety, 1980
DNA alteration and repair is undoubtedly as essential stage in the mechanism of chemical carcinogenesis. Present knowledge has in fact shown, and in a rather convincing manner, that the majority of known chemical carcinogens, in addition to radiations and viruses, are also mutagens in the widest sense of the word and usually induce alteration of the ...
Cesarone Cf, Silvio Parodi, Maurizio Taningher, Leonardo Santi, C. Bolognes   +4 more
openaire   +3 more sources

DNA Damage and Repair Biomarkers of Immunotherapy Response.

Cancer Discovery, 2017
DNA-damaging agents are widely used in clinical oncology and exploit deficiencies in tumor DNA repair. Given the expanding role of immune checkpoint blockade as a therapeutic strategy, the interaction of tumor DNA damage with the immune system has ...
K. Mouw, Michael S. Goldberg, P. Konstantinopoulos, A. D’Andrea   +3 more
semanticscholar   +1 more source

Targeting DNA Repair

, 2017
Genomic instability is a characteristic of most human cancers and plays critical roles in both cancer development and progression. There are various forms of genomic instability arising from many different pathways, such as DNA damage from endogenous and exogenous sources, centrosome amplification, telomere damage, and epigenetic modifications.
openaire   +3 more sources

A large‐scale retrospective study in metastatic breast cancer patients using circulating tumour DNA and machine learning to predict treatment outcome and progression‐free survival

Molecular Oncology, EarlyView.
There is an unmet need in metastatic breast cancer patients to monitor therapy response in real time. In this study, we show how a noninvasive and affordable strategy based on sequencing of plasma samples with longitudinal tracking of tumour fraction paired with a statistical model provides valuable information on treatment response in advance of the ...
Emma J. Beddowes, Mario Ortega Duran, Solon Karapanagiotis, Alistair Martin, Meiling Gao, Riccardo Masina, Ramona Woitek, James Tanner, Fleur Tippin, Justine Kane, Jonathan Lay, Anja Brouwer, Stephen‐John Sammut, Suet‐Feung Chin, Davina Gale, Dana W. Y. Tsui, Sarah‐Jane Dawson, Nitzan Rosenfeld, Maurizio Callari, Oscar M. Rueda, Carlos Caldas   +20 more
wiley   +1 more source

Mutational signatures are jointly shaped by DNA damage and repair

bioRxiv, 2019
Cells possess an armamentarium of DNA repair pathways to counter DNA damage and prevent mutation. Here we use C. elegans whole genome sequencing to systematically quantify the contributions of these factors to mutational signatures.
Nadezda V. Volkova, B. Meier, V. González-Huici, S. Bertolini, Santiago Gonzalez, F. Abascal, I. Martincorena, P. Campbell, A. Gartner, M. Gerstung   +9 more
semanticscholar   +1 more source

Base-excision repair pathway shapes 5-methylcytosine deamination signatures in pan-cancer genomes

Nature Communications
Transition of cytosine to thymine in CpG dinucleotides is the most frequent type of mutation in cancer. This increased mutability is commonly attributed to the spontaneous deamination of 5-methylcytosine (5mC), which is normally repaired by the base ...
André Bortolini Silveira, Alexandre Houy, Olivier Ganier, Begüm Özemek, Sandra Vanhuele, Anne Vincent-Salomon, Nathalie Cassoux, Pascale Mariani, Gaelle Pierron, Serge Leyvraz, Damian Rieke, Alberto Picca, Franck Bielle, Marie-Laure Yaspo, Manuel Rodrigues, Marc-Henri Stern   +15 more
doaj   +1 more source

Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal‐like and malignant urothelial cells

Molecular Oncology, EarlyView.
Loss of the frequently mutated chromatin remodeler ARID1A, a subunit of the SWI/SNF cBAF complex, results in less open chromatin, alternative splicing, and the failure to stop cells from progressing through the cell cycle after DNA damage in bladder (cancer) cells. Created in BioRender. Epigenetic regulators, such as the SWI/SNF complex, with important
Rebecca M. Schlösser, Florian Krumbach, Eyleen Corrales, Geoffroy Andrieux, Christian Preisinger, Franziska Liss, Alexandra Golzmann, Melanie Boerries, Kerstin Becker, Ruth Knüchel, Stefan Garczyk, Bernhard Lüscher   +11 more
wiley   +1 more source

E-cigarette smoke damages DNA and reduces repair activity in mouse lung, heart, and bladder as well as in human lung and bladder cells

Proceedings of the National Academy of Sciences of the United States of America, 2018
Significance E-cigarette smoke (ECS) delivers nicotine through aerosols without burning tobacco. ECS is promoted as noncarcinogenic. We found that ECS induces DNA damage in mouse lung, bladder, and heart and reduces DNA-repair functions and proteins in ...
Hyun-wook Lee, Sung-Hyun Park, Mao‐wen Weng, Hsiang-Tsui Wang, William C. Huang, H. Lepor, Xue-Ru Wu, Lung-Chi Chen, M. Tang   +8 more
semanticscholar   +1 more source

Escape from TGF‐β‐induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

Molecular Oncology, EarlyView.
Chronic TGF‐β exposure drives epithelial HCC cells from a senescent state to a TGF‐β resistant mesenchymal phenotype. This transition is characterized by the loss of Smad3‐mediated signaling, escape from senescence, enhanced invasiveness and metastatic potential, and upregulation of key resistance modulators such as MARK1 and GRM8, ultimately promoting
Minenur Kalyoncu, Dilara Demirci, Sude Eris, Bengisu Dayanc, Ece Cakiroglu, Merve Basol, Merve Uysal, Gulcin Cakan‐Akdogan, Fang Liu, Mehmet Ozturk, Gökhan Karakülah, Serif Senturk   +11 more
wiley   +1 more source

Synthesis and Quantitative Structure–Activity Relationship of Imidazotetrazine Prodrugs with Activity Independent of O6-Methylguanine-DNA-methyltransferase, DNA Mismatch Repair and p53. [PDF]

, 2013
The antitumor prodrug Temozolomide is compromised by its dependence for activity on DNA mismatch repair (MMR) and the repair of the chemosensitive DNA lesion, O6-methylguanine (O6-MeG), by O6-methylguanine-DNA-methyltransferase (EC 2.1.1.63, MGMT). Tumor
Arris C. E., Arrowsmith J., Barvaux V. A., Boberg F., Boyd M. R., Bunz F., Damera K., Darkes M. J. M., De K., Denny B. J., Dimitrios Pletsas, Dinca E. B., Elrashied A. E. Garelnabi, Garelnabi E. A. E., Hirose Y., Honnalli S. S., Judson P. L., Karran P., Karran P., Kotera M., Leteurtre F., Li Li, Liu L., McElhinney R. S., McGarrity J. F., Mladek A. C., Nishizuka S., Pletsas D., Richard T. Wheelhouse, Roger M. Phillips, Sarkaria J. N., Schmidt B. F., Schmiedekamp A., Shealy Y. F., Siddiqui A. A., Smith R. H., Stevens M. F. G., Svilar D., Wang Y., Wheelhouse R. T., Wheelhouse R. T., Zhang J., Zhang J.   +42 more
core   +1 more source