Relevant bibliographies by topics / Aberrant Repair

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Aberrant Repair'

Author: Grafiati
Published: 25 January 2025

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Journal articles on the topic "Aberrant Repair"

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Rawal, Chetan C., Nadejda L. Butova, Anik Mitra, and Irene Chiolo. "An Expanding Toolkit for Heterochromatin Repair Studies." Genes 13, no. 3 (March 17, 2022): 529. http://dx.doi.org/10.3390/genes13030529.

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Pericentromeric heterochromatin is mostly composed of repetitive DNA sequences prone to aberrant recombination. Cells have developed highly specialized mechanisms to enable ‘safe’ homologous recombination (HR) repair while preventing aberrant recombination in this domain. Understanding heterochromatin repair responses is essential to understanding the critical mechanisms responsible for genome integrity and tumor suppression. Here, we review the tools, approaches, and methods currently available to investigate double-strand break (DSB) repair in pericentromeric regions, and also suggest how technologies recently developed for euchromatin repair studies can be adapted to characterize responses in heterochromatin. With this ever-growing toolkit, we are witnessing exciting progress in our understanding of how the ‘dark matter’ of the genome is repaired, greatly improving our understanding of genome stability mechanisms.
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Leong, Merrin Man Long, Arthur Kwok Leung Cheung, Wei Dai, Sai Wah Tsao, Chi Man Tsang, Christopher W. Dawson, Josephine Mun Yee Ko, and Maria Li Lung. "EBV infection is associated with histone bivalent switch modifications in squamous epithelial cells." Proceedings of the National Academy of Sciences 116, no. 28 (June 24, 2019): 14144–53. http://dx.doi.org/10.1073/pnas.1821752116.

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Epstein−Barr virus (EBV) induces histone modifications to regulate signaling pathways involved in EBV-driven tumorigenesis. To date, the regulatory mechanisms involved are poorly understood. In this study, we show that EBV infection of epithelial cells is associated with aberrant histone modification; specifically, aberrant histone bivalent switches by reducing the transcriptional activation histone mark (H3K4me3) and enhancing the suppressive mark (H3K27me3) at the promoter regions of a panel of DNA damage repair members in immortalized nasopharyngeal epithelial (NPE) cells. Sixteen DNA damage repair family members in base excision repair (BER), homologous recombination, nonhomologous end-joining, and mismatch repair (MMR) pathways showed aberrant histone bivalent switches. Among this panel of DNA repair members,MLH1, involved in MMR, was significantly down-regulated in EBV-infected NPE cells through aberrant histone bivalent switches in a promoter hypermethylation-independent manner. Functionally, expression ofMLH1correlated closely with cisplatin sensitivity both in vitro and in vivo. Moreover, seven BER members with aberrant histone bivalent switches in the EBV-positive NPE cell lines were significantly enriched in pathway analysis in a promoter hypermethylation-independent manner. This observation is further validated by their down-regulation in EBV-infected NPE cells. The in vitro comet and apurinic/apyrimidinic site assays further confirmed that EBV-infected NPE cells showed reduced DNA damage repair responsiveness. These findings suggest the importance of EBV-associated aberrant histone bivalent switch in host cells in subsequent suppression of DNA damage repair genes in a methylation-independent manner.
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Yamamoto, Masaki, Hironobu Okada, Junko Nakashima, and Takashi Anayama. "Thoracic endovascular aortic repair of an aberrant arterial aneurysm with pulmonary sequestration." Interactive CardioVascular and Thoracic Surgery 30, no. 1 (October 3, 2019): 156–58. http://dx.doi.org/10.1093/icvts/ivz233.

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Abstract We describe a treatment strategy for an aberrant arterial aneurysm associated with pulmonary sequestration. A 58-year-old man with impending aberrant arterial aneurysm rupture underwent a 2-stage surgery that included an emergency thoracic endovascular aortic repair (TEVAR) of the descending aorta to occlude the origin of the aberrant artery, followed by lobectomy. TEVAR can lead to faster occlusion of the aneurysm and can avoid operative risk of aneurysm rupture during lobectomy. The aberrant artery was broad where it branched off the aorta and had a short neck, rendering primary ligation or stump-forming unsuitable. Pathological findings revealed the fragility of the aberrant artery; thus, its root was prone to breakdown of the stump after simple aneurysmectomy. Furthermore, TEVAR may reduce graft infection during lobectomy in the second surgery. The 2-stage surgery may be useful for aberrant aneurysms complicated by pulmonary sequestration.
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Eroshenko, D. A., E. A. Diatlova, V. M. Golyshev, A. V. Endutkin, and D. O. Zharkov. "Aberrant repair of 8-oxoguanine in short DNA bulges." Доклады Российской академии наук. Науки о жизни 515, no. 2 (April 15, 2024): 14–18. http://dx.doi.org/10.31857/s2686738924020031.

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The presence of DNA damage can increase the likelihood of DNA replication errors and promote mutations. In particular, pauses of DNA polymerase at the site of damage can lead to polymerase slippage and the formation of 1–2 nucleotide bulges. Repair of such structures using an undamaged DNA template leads to small deletions. One of the most abundant oxidative DNA lesions, 8-oxoguanine (oxoG), has been shown to induce small deletions but the mechanism of this phenomenon is currently unknown. We have studied the aberrant repair of oxoG, located in one- and two-nucleotide bulges, by the Escherichia coli and human base excision repair systems. Our results indicate that the repair in such substrates can serve as a mechanism for fixing small deletions in bacteria but not in humans.
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An, Kang, Shoujun Li, Jun Yan, Xu Wang, and Zhongdong Hua. "Translocation of aberrant left subclavian artery and resection of Kommerell diverticulum during the concomitant repair of intracardiac anomalies." Interactive CardioVascular and Thoracic Surgery 32, no. 1 (November 21, 2020): 118–21. http://dx.doi.org/10.1093/icvts/ivaa226.

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Abstract OBJECTIVES To assess the safety and efficacy of the translocation of the aberrant left subclavian artery (LSCA) and resection of the Kommerell diverticulum during the concomitant repair of intracardiac anomalies for paediatric patients who had a right-sided aortic arch. METHODS A retrospective review of paediatric patients who were diagnosed right-sided aortic arch, aberrant LSCA, Kommerell diverticulum and intracardiac anomalies between 2015 and 2019 was conducted. Patients who underwent translocation of the aberrant LSCA, diverticulum resection and concomitant intracardiac repair were included. RESULTS Eight patients underwent translocation of aberrant LSCA, diverticulum resection, ligamentum division and concomitant repair of the associated intracardiac anomalies. All patients were male. The median age was 1.3 years (range 0.4–5.5 years) and the median weight was 10.0 kg (range 6.1–21.0 kg). The most commonly combined intracardiac anomaly was a ventricular septal defect. Seven patients (87.5%) had preoperative respiratory or gastrointestinal symptoms. There was no early mortality and no postoperative complications. During the median follow-up of 23 months (range 4–43 months), no patient had residual respiratory or gastrointestinal symptoms. A postoperative computed tomography scan was performed in 3 patients, all of which showed patent LSCA–left carotid artery anastomosis. CONCLUSIONS Translocation of the aberrant LSCA and resection of the Kommerell diverticulum can be safely performed during the concomitant repair of intracardiac anomalies for paediatric patients. This approach could eliminate residual respiratory and gastrointestinal symptoms, and prevent reintervention in the future.
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Campbell, TM, WT Wong, R. Fässler, and EJ Mackie. "Aberrant bone repair in Tenascin-C null mice." Bone 27, no. 4 (October 2000): 26. http://dx.doi.org/10.1016/s8756-3282(00)80085-x.

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Verzini, Fabio, Giacomo Isernia, Gioele Simonte, Paola De Rango, Piergiorgio Cao, Patrizio Castelli, Ciro Ferrer, et al. "Results of aberrant right subclavian artery aneurysm repair." Journal of Vascular Surgery 62, no. 2 (August 2015): 343–50. http://dx.doi.org/10.1016/j.jvs.2015.03.038.

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Mann, Christopher J., Eusebio Perdiguero, Yacine Kharraz, Susana Aguilar, Patrizia Pessina, Antonio L. Serrano, and Pura Muñoz-Cánoves. "Aberrant repair and fibrosis development in skeletal muscle." Skeletal Muscle 1, no. 1 (2011): 21. http://dx.doi.org/10.1186/2044-5040-1-21.

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Henshaw, Timothy F., Michael Feig, and Robert P. Hausinger. "Aberrant activity of the DNA repair enzyme AlkB." Journal of Inorganic Biochemistry 98, no. 5 (May 2004): 856–61. http://dx.doi.org/10.1016/j.jinorgbio.2003.10.021.

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Orion, K. C. "Results of aberrant right subclavian artery aneurysm repair." Yearbook of Vascular Surgery 2016 (2016): 164–66. https://doi.org/10.1016/j.yvas.2016.06.060.

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Dissertations / Theses on the topic "Aberrant Repair"

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Manapkyzy, Diana. "In vitro characterization of aberrant and futile DNA repair initiated by human Thymine-DNA glycosylase." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL131.

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La Thymine-ADN glycosylase humaine (TDG) est connue pour initier l'élimination de la T mis-appariée avec la G dans un contexte CpG dans la voie de réparation par excision de base (BER), prévenant l'effet mutagène de la désamination spontanée de la 5-méthylcytosine (5mC) dans l'ADN. Des études ont montré que TDG joue un rôle clé dans la régulation de la transcription en interagissant avec divers récepteurs nucléaires et facteurs de transcription, soulignant ainsi sa fonction dans la régulation d'expression des gènes, en particulier pendant le développement. De plus, TDG est impliquée dans la régulation épigénétique de transcription en empêchant la méthylation de novo des promoteurs riches en CpG en participant dans la déméthylation active de l'ADN avec les enzymes TETs. TDG humaine est également capable d'initier une voie de BER aberrante en excisant la thymine appariée à une adénine endommagée dans le contexte de la séquence TpG/CpX, où X est une adénine modifiée. L'acide aristolochique, un composé trouvé dans des plantes médicinales chinoises, est activé par des nitroréductases cellulaires, ce qui entraîne la formation des adduits de 7-(désoxyadénosine-N6yl) aristolactame (dA-ALI et dA-ALII) dans l'ADN cellulaire. Des études récentes sur le cancer induit par d'acides aristolochiques ont identifié des transversions de T→A multiples dans le contexte de séquence CpTpG/CpApG, qui ressemble fortement au contexte préféré pour l'excision aberrante de T par TDG dans le duplex endommagé T•X. Étant donné que les adduits dA-AL ne sont pas réparés sur le brin d'ADN non transcrit et peuvent donc persister dans les cellules, nous avons émis l'hypothèse d'une possible implication de TDG dans la mutagénèse induit par l'acide aristolochique.Pour étudier cela nous avons reconstitué la réparation in vitro en utilisant des oligonucléotides contenant dA-AL marqués de manière radioactive. De manière inattendue, après une incubation prolongée à 37 °C, l'enzyme TDG de longueur complète (TDGFL) a montré une activité glycosylase envers les bases C et T normales appariées avec G et A, respectivement, plutôt que T appariée aux adduits dA-AL. TDG cible préférentiellement les pyrimidines non endommagées dans un duplex d'ADN régulier dans les contextes TpG/CpA et CpG/CpG, ce que nous avons appelé « réparation futile ». La cinétique de réparation en conditions de turnover unique montre que le taux maximal d'excision de base (kobs) de T dans le duplex T•A (0.0014 min-1) catalysé par TDGFL est 300 fois plus lent que pour T•G (0,470 min-1). Notamment, TDGFL native, mais non le domaine catalytique tronqué TDG (TDGCAT), a montré une stabilité accrue à 37°C en présence de concentrations équimolaires de duplex d'ADN non spécifiques, suggérant que les domaines désordonnés N- et C-terminaux de la protéine TDG interagissent avec l'ADN, stabilisant ainsi la conformation de la protéine. De plus, nous avons montré que 5mC n'est pas excisée par TDGFL, tandis que 5-hydroxyméthylcytosine (5hmC), au contraire, est excisée aussi bien que la cytosine normale dans le contexte CpG. Ces résultats suggèrent un rôle possible de TDG dans la génération de cassures monocaténaires (SSB) dans les enhancers (amplificateurs) des cellules neuronales postmitotiques, un processus qui pourrait contribuer aux maladies neurodégénératives, car les cassures ont été principalement observées à proximité des sites de déméthylation de l'ADN et des îlots CpG. En conclusion, nos résultats démontrent que dans des conditions expérimentales, TDGFL catalyse la réparation futile des résidus de pyrimidine dans les duplex d'ADN réguliers dépendante du contexte de séquence, ce qui, dans des conditions in vivo, pourrait conduire à la formation persistante de SSB dans les régions non méthylées de l'ADN chromosomique. La découverte de la réparation lente des résidus 5hmC dans l'ADN par la voie TDG/BER est l'un des principaux points d'intérêt pour les études et perspectives futures
The human thymine-DNA glycosylase (TDG) is known for excising T mispaired with G in CpG context and initiating the base excision repair (BER) pathway, thus preventing the mutagenic effect of spontaneous deamination of 5-methylcytosine (5mC). Initially TDG was considered as an inefficient repair enzyme, due to the low catalytic activity on G•T mismatch, with no significant biological function. However, further studies have shown that TDG plays a key role in the regulation of transcription by interacting with various nuclear receptors and transcription factors, emphasizing its function in gene expression, particularly during development. Furthermore, TDG has been implicated in epigenetic regulation of gene expression by preventing CpG-rich promoters from de novo DNA methylation by excising 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC) residues. Human TDG protein is also able to initiate aberrant BER pathway by excising regular T opposite to damaged adenine residue in the TpG/CpX sequence context, where X is a modified adenine.Previously, it was shown that Aristolochic acid, compound found in certain plants used in traditional Chinese medicine, is activated by cellular nitroreductases, resulting in the formation of reactive intermediates that bind covalently to DNA to produce 7-(deoxyadenosin-N6yl)aristolactam (dA-ALI and dA-ALII) adducts. Recent studies on cancer induced by consumption of aristolochic acids have identified mutation hotspots corresponding to T→A transversion in CpTpG/CpApG sequence context, which in turn resembles very much to the preferred sequence context of TDG-catalysed aberrant excision of T in T•X base pair. Given that aristolactam dA-AL adducts are not repaired on the non-transcribed DNA strand and thus can persist in cells, we hypothesized a possible involvement of TDG in the aberrant excision of T opposite to dA-AL adduct, potentially leading to error-prone BER and mutation fixation. To study the involvement of TDG in the initiation of aberrant BER, we carried out reconstitution of repair in vitro using radioactively labeled oligonucleotide DNA substrates. Unexpectedly, under the experimental conditions used, prolonged incubation at 37°C, the full-length TDG (TDGFL) enzyme exhibited glycosylase activity toward normal C and T paired with G and A, respectively, rather than T paired with the dA-AL adducts. TDG targets non-damaged pyrimidines in regular DNA duplex preferentially in TpG/CpA and CpG/CpG contexts, here we referred this unusual activity as “futile repair”. Time course of the cleavage product generation under single-turnover conditions shows that the maximal rate of base excision (kobs) of T from T•A duplex catalyzed by TDGFL (0.0014) is 300-fold lower than that for T•G (0.470 min-1). Notably, native TDGFL, but not the truncated catalytic domain TDG (TDGCAT), exhibited enhanced stability at 37°C in the presence of equimolar concentrations of non-specific DNA duplexes, suggesting that the disordered N- and C-terminal domains of TDG interact with DNA, stabilizing the protein's conformation. Additionally, we showed that 5mC is not excised by TDGFL, while 5hmC, on the contrary, is excised as well as regular cytosine in CpG context. Taken together, these findings imply a possible role of TDG in the generation of single-strand breaks (SSB) in enhancer regions of postmitotic neuronal cells, a process that might contribute to neurodegenerative diseases, as breaks were predominantly observed near sites of DNA demethylation and CpG islands. In conclusion, our findings demonstrate that under experimental conditions used TDGFL catalyses sequence context-dependent futile removal of pyrimidine residues in regular DNA duplex, which under in vivo conditions could lead to persistent SSB formation in non-methylated regions of chromosomal DNA. The discovery of slow repair of 5hmC residues in DNA by TDG/BER pathway is one of the main points of interest for future studies and perspectives
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Akram, Khondoker Mehedi. "Idiopathic pulmonary fibrosis : exploration of aberrant epithelial wound repair and stem cell-mediated regenerative approaches." Thesis, Keele University, 2013. http://eprints.keele.ac.uk/3804/.

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Idiopathic pulmonary fibrosis (IPF) is a fatal form of fibrotic lung disease. The pathogenesis of IPF is unclear. An aberrant alveolar epithelial wound repair is likely to be involved in the disease process. Alveolar bronchiolisation, a process where bronchiolar Clara cells migrate into the affected alveoli, is a manifestation of abnormal alveolar wound repair. The role of Clara cells during alveolar injury repair in IPF is controversial. This study was undertaken to investigate the role of Clara cells in alveolar epithelial wound repair and pulmonary fibrosis. Currently, there is no curative treatment for IPF; therefore, stem-cell mediated regenerative therapy has been suggested. In this study, the paracrine role hMSC and hESC on pulmonary epithelial wound repair has also been evaluated. A direct-contact co-culture in vitro model was utilised to evaluate the role of Clara cells on alveolar epithelial cell wound repair. Immunohistochemistry was conducted on IPF lung tissue samples to replicate the in vitro findings ex vivo. The paracrine role of hMSC and hESC on pulmonary epithelial cells was evaluated by utilising the in vitro wound repair system. This study demonstrates that Clara cells induce apoptosis in AEC through a TRAILdependent mechanism, resulting in significant inhibition of wound repair. Furthermore in the IPF lungs, TRAIL-expressing Clara cells were detected within the fibrotic alveoli, together with widespread AEC apoptosis. This study also demonstrates that hMSC enhance AEC and SAEC wound repair via a paracrine mechanism through stimulation of cell migration; whereas, secretory factors of differentiated hESC promote AEC wound repair through stimulation of both cell proliferation and migration. Through this study I propose a novel hypothesis which implies that the extensive profibrotic remodelling associated with IPF could be driven by TRAIL-expressing Clara cells inducing AEC apoptosis through a TRAIL-dependent mechanism. My study also supports the notion of clinical application of hMSC and hESC or their secretory products as regenerative therapeutic modality for IPF.
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Vaalamo, Maarit. "Matrix metalloproteinases and their inhibitors in normal and aberrant wound repair : expression patterns of collagenases-1 and -3, stromelysins-1 and -2, matrilysin, metalloelastase and TIMPs-1, -2, -3 and -4 in healing cutaneous wounds and in chrome ulcers of the skin and the intestine." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/vaalamo/.

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Woldhuis, Roy Rolf. "The role of accelerated ageing in aberrant lung tissue repair and remodelling in COPD." Thesis, 2021. http://hdl.handle.net/10453/154792.

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University of Technology Sydney. Faculty of Science.
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, while the prevalence is still increasing. Since the exact COPD pathogenesis is still unknown and no effective therapeutics are available to stop the progression of the disease, novel insights into the pathogenesis of COPD are urgently needed. Accelerated ageing has been postulated to play a role in COPD with characteristic of ageing demonstrated in lungs from COPD patients compared to age-matched smokers without COPD. Recently, extracellular matrix (ECM) dysregulation has been described as an additional ageing hallmark of the lungs. ECM dysregulation can cause aberrant lung tissue repair and remodelling. Lung fibroblasts and airway smooth muscle cells (ASMCs) are the major producers and regulators of the ECM and therefore play an important role in lung tissue repair and remodelling. The aim of this thesis was to elucidate the role of accelerated ageing in aberrant tissue repair and remodelling in COPD. We analysed ageing markers and ECM changes in lung fibroblasts and ASMCs from COPD patients compared to ex-smoker controls without COPD matched for age, gender, and smoking history. In addition, we assessed the functional effects of induction of cellular senescence, which is a major ageing hallmark. We found characteristics of accelerated ageing in COPD-derived fibroblasts compared to lung fibroblasts from matched controls, including higher levels of cellular senescence. The increase in cellular senescence in COPD-derived fibroblasts was associated with lower levels of the ECM protein decorin and higher levels of pro-inflammatory protein secretion. Induction of cellular senescence in lung fibroblasts also resulted in ECM changes, secretion of pro-inflammatory proteins and impaired tissue repair functions of the fibroblasts. Furthermore, ASMCs had higher levels of cellular senescence compared to lung fibroblasts from the same patients, but in ASMCs no differences were found between COPD and control. Finally, we showed that E-cigarette extract induces cellular senescence in lung fibroblasts, and the induction in cellular senescence resulted in impaired tissue repair functions. Therefore, we concluded that E-cigarettes, commonly used as smoking alternative or as smoke cessation aid, are not a safe alternative for tobacco smoking. These studies indicate that accelerated ageing plays a role in aberrant tissue repair and remodelling in COPD and thereby contributes to the pathogenesis of COPD. Future studies should unravel the exact mechanisms that lead to accelerated ageing in COPD to discover therapeutics targets to develop therapies that target accelerated ageing in COPD patients.
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Barley, Randall Douglas Corwyn. "Collagen I an aberrantly expressed molecule in chondrocytes or a key player in tissue stabilization and repair both in vivo and in vitro? /." Phd thesis, 2010. http://hdl.handle.net/10048/1015.

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Thesis (Ph.D.)--University of Alberta, 2010.
A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Experimental Surgery, Department of Surgery. Title from pdf file main screen (viewed on February 17, 2010). Includes bibliographical references.
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Book chapters on the topic "Aberrant Repair"

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Lambert, Muriel W., David D. Parrish, and W. Clark Lambert. "Molecular Mechanisms Responsible for Repair of Adducts Induced in Human Cellular DNA by Puva." In Basic Mechanisms of Physiologic and Aberrant Lymphoproliferation in the Skin, 497–533. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-1861-7_41.

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Darby, Ian A., and Alexis Desmoulière. "Scar Formation: Cellular Mechanisms." In Textbook on Scar Management, 19–26. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_3.

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AbstractFibroblasts are key players in the maintenance of skin homeostasis and in orchestrating physiological tissue repair. Fibroblasts secrete and are embedded in a sophisticated extracellular matrix, and a complex and interactive dialogue exists between fibroblasts and their microenvironment. In addition to the secretion of the extracellular matrix, fibroblasts and myofibroblasts secrete extracellular matrix remodeling enzymes, matrix metalloproteinases and their inhibitors, and tissue inhibitors of metalloproteinases and are thus able to remodel the extracellular matrix. Myofibroblasts and their microenvironment form a network that evolves during tissue repair. This network has reciprocal actions affecting cell differentiation, cell proliferation, cell quiescence, or apoptosis and has actions on growth factor bioavailability by binding, sequestration, and activation. Mechanical forces also play a role in regulating the myofibroblast phenotype as cells are subjected to mechanical stress and mechanical signaling is activated. Innervation is also involved in both skin repair processes and differentiation of myofibroblasts. In pathological situations, for example, in excessive scarring, the dialogue between myofibroblasts and their microenvironment can be altered or disrupted, leading to defects in tissue repair or to pathological scarring, such as that seen in hypertrophic scars. Better understanding of the intimate dialogue between myofibroblasts and their local microenvironment is needed and will be important in aiding the identification of new therapeutic targets and discovery of new drugs to treat or prevent aberrant tissue repair and scarring.
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Hans, Sachinder Singh. "Thoracic Endovascular Repair for Ruptured Aberrant Right Subclavian Artery Aneurysm Without Subclavian Artery Revascularization." In Challenging Arterial Reconstructions, 341–45. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44135-7_77.

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Sminia, Peter, Olivier Guipaud, Kristina Viktorsson, Vidhula Ahire, Sarah Baatout, Tom Boterberg, Jana Cizkova, et al. "Clinical Radiobiology for Radiation Oncology." In Radiobiology Textbook, 237–309. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-18810-7_5.

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AbstractThis chapter is focused on radiobiological aspects at the molecular, cellular, and tissue level which are relevant for the clinical use of ionizing radiation (IR) in cancer therapy. For radiation oncology, it is critical to find a balance, i.e., the therapeutic window, between the probability of tumor control and the probability of side effects caused by radiation injury to the healthy tissues and organs. An overview is given about modern precision radiotherapy (RT) techniques, which allow optimal sparing of healthy tissues. Biological factors determining the width of the therapeutic window are explained. The role of the six typical radiobiological phenomena determining the response of both malignant and normal tissues in the clinic, the 6R’s, which are Reoxygenation, Redistribution, Repopulation, Repair, Radiosensitivity, and Reactivation of the immune system, is discussed. Information is provided on tumor characteristics, for example, tumor type, growth kinetics, hypoxia, aberrant molecular signaling pathways, cancer stem cells and their impact on the response to RT. The role of the tumor microenvironment and microbiota is described and the effects of radiation on the immune system including the abscopal effect phenomenon are outlined. A summary is given on tumor diagnosis, response prediction via biomarkers, genetics, and radiomics, and ways to selectively enhance the RT response in tumors. Furthermore, we describe acute and late normal tissue reactions following exposure to radiation: cellular aspects, tissue kinetics, latency periods, permanent or transient injury, and histopathology. Details are also given on the differential effect on tumor and late responding healthy tissues following fractionated and low dose rate irradiation as well as the effect of whole-body exposure.
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Elsharkawy, Ahmed. "Safeguards and pitfalls in the management of Retrograde Dissection Complicating Thoracic Endovascular Aortic Repair." In Advances in Vascular Surgery [Working Title]. IntechOpen, 2024. http://dx.doi.org/10.5772/intechopen.1005782.

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The aim of this chapter is to give hint on some special situations related to aortic dissection. Although they are not frequently encountered, these situations need a clear management strategy in mind of every aortic surgeon. The first one is retrograde proximal dissection complicating endovascular stenting of descending aortic pathologies: when to expect and how to manage. The second one is the different anatomical variations of aortic arch branches that may coexist with aortic dissection, such as aberrant subclavian artery and isolated vertebral artery. These variations, when present, add to the complexity of dissection repair and affect the management plan, either open surgical or endovascular.
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Kharaishvili, Gvantsa, Mariam Kacheishvili, and Giorgi Akhvlediani. "BRCA Gene Mutations and Prostate Cancer." In BRCA1 and BRCA2 Mutations - Diagnostic and Therapeutic Implications [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108792.

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Prostate cancer remains the second most common cancer in men, with diverse courses from indolent cases to aggressive diseases. Among the key factors implicated in its pathogenesis are genomic alterations such as the TMPRSS2-ERG and related fusion oncogenes, loss of tumor suppressor PTEN, p53 or NKX3.1, inflammation, enhanced DNA damage, and chromosomal instability. Men with prostate cancer who carry BRCA1/2 mutations are at more risk of worse disease and poor prognosis. Cancer cells with mutant BRCA1 or BRCA2 repair genes with defects in homologous recombination are vulnerable to PARP inhibitors that target the genetic phenomenon known as synthetic lethality to exploit faulty DNA repair mechanisms. With relevance to prostate cancer, other features of cancer cells may also sensitize to PARP inhibitors, including aberrant transcription due to the androgen-driven fusion oncogene TMPRSS2-ERG or PTEN loss. Several models of synthetic lethality and potential biomarkers suggested up to date are also discussed. The chapter also highlights the importance of genetic screening of men with BRCA and shows diagnostic utility of plasma-derived circulating tumor DNA.
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Mondal, Susmita, Sutapa Saha, Saptarshi Chatterjee, and Biplab Bhowmik. "Chemoresistance of Cervical Cancer Stem Cells: Challenges and Prospects." In Life as Basic Science: An Overview and Prospects for the Future [Volume: 1], 197–207. International Academic Publishing House (IAPH), 2024. http://dx.doi.org/10.52756/lbsopf.2024.e01.016.

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Cervical cancer (CC) is one of the leading causes of death among women, with thousands of women diagnosed each year, particularly in developing countries where access to healthcare resources may be limited. Persistent infection with high-risk human papillomavirus (HPV) induces CC. While advancements in treatment modalities, such as chemotherapy, have improved outcomes for many patients, a significant challenge remains in the form of chemoresistance, particularly in the context of cervical cancer stem cells (cCSCs). cCSCs are a small subpopulation of cells within CC with self-renewal and aberrant differentiation capacity. Upregulation of biomarkers expression such as CD44, CD133, Sox2, ALDH1 and etc. is often associated with robustness of cCSCs. cCSCs possess higher invasion, metastasis and drug resistance ability thereby leading to poor prognosis and relapse. Therapeutic strategies to manage advanced CC typically involve surgery, radiotherapy and chemotherapy mostly using platinum-based drugs. However, acquired chemoresistance of cCSCs is the biggest challenge to therapeutic outcomes. There are several mechanisms involved in chemotherapy resistance in cCSCs, such as enhanced DNA damage repair mechanisms, which include nucleotide excision repair and homologous recombination, and promoting survival pathways like PI3K/AKT, Wnt, Notch. Elevated drug transporters like ABCG2 are one of the key feature for the resistance phenotype of cCSCs. Furthermore, epigenetic modulation and mutual interaction of cCSCs with tumour microenvironment play crucial role to avoid chemotherapeutic damage. This chapter aims to explore the mechanisms underlying chemoresistance in cCSCs and discuss potential therapeutic strategies to overcome this challenge.
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Singh, Shivani, Saurav Panicker, and Satish Ramalingam. "Chromosome 6." In Cancer Genes, 159–222. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815080292123010009.

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Chromosome 6 is among the 23 pairs of chromosomes in humans and it spans about 170 million base pairs. Several cancer genes have been identified to have a role in cancer development. Cancer is also a genetic disease caused due to changes in the genes that control cell function, such as cell division and cell growth. Most of these cancer genes either act as tumor suppressors or possess an oncogenic potential. Oncogenes like ROS1, MYB, HMGA1, etc., induce tumorigenesis by playing a role in DNA repair, replication, transcriptional regulation, and mRNA splicing. When these genes are highly expressed, they result in the transformation of normal cells to malignant cells; on the other side, tumor suppressor genes like IGF2R, AIM1, IRF4, etc., reduce tumorigenicity and invasive potential. Thus, reduced expression of these genes due to loss of heterozygosity, deletion or any epigenetic modifications can induce tumor formation. Also, some genes can either suppress or induce tumor formation given the cellular location and condition, such as CCN2, TNF, etc. Along with these, different types of structural abnormalities can be observed on chromosome 6, such as chromosomal translocation, deletion, duplication, and inversion. These abnormalities on both p and q arms have been known to contribute to the growth and spread of cancer by impacting the expression of cancer genes. Aberrant expression of the genes can also be influenced by fusions, missense mutations, non-missense mutations, silent mutations, frame-shift deletions, and insertion at the molecular level. Some genes can maintain stem-cell-like properties by regulating the expression of cell surface markers like Oct4, Nanog, Sox4, etc. This chapter explains important cancer genes, genetic mutations, and gene variations that can influence the risk of having cancer and induces cancer formation.
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Borts, Rhona H., and David T. Kirkpatrick. "The Role of the Genome in the Initiation of Meiotic Recombination." In The Implicit Genome, 208–24. Oxford University PressNew York, NY, 2006. http://dx.doi.org/10.1093/oso/9780195172706.003.0013.

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Abstract Initiation of recombination is an essential and highly regulated process. Recombination during meiosis is important for enabling exchange of information between the paternal and maternal contributions to a genome. In addition, in most organisms, the absence of meiotic crossovers causes homologous chromosomes to segregate aberrantly. Recombination is not randomly distributed along or between chromosomes. Rather, the genomes of many species contain regions that have an elevated level of recombination (“hotspots”) or a decreased level (“coldspots”). Factors that determine the level of recombination at a specific site are the primary sequence, the configuration of the chromatin, and the nature and function of the DNA sequence. Also, prior recombination initiations repress additional events in their vicinity. The probability of recombination within a region of the genome is very context dependent. It can be modulated by factors that include the nutritional state of the cell, the base composition of the region, and the level of primary sequence variation present between the maternally and paternally inherited chromosomes, as well as the action of DNA repair proteins on sequence mismatches occurring in regions of recombination between maternal and paternal chromosomes. Thus, initiation of meiotic recombination is tightly controlled. Due to the importance of the DNA sequences themselves and their interaction with meiotic proteins, there are regions where the probability of meiotic recombination can be considered to be encoded implicitly in the DNA sequences as a result of interactions with the meiotic protein complement.
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Conference papers on the topic "Aberrant Repair"

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Kalifa, Mohamed, Andrew Starr, and Muhammad Khan. "Analyzing Frictional Noise for Wear Monitoring under Dry and Lubrication Condition: Experimental Modelling with Pin-on-Disc Tribometer." In The 12th International Conference on Fracture Fatigue and Wear, 19–31. Switzerland: Trans Tech Publications Ltd, 2025. https://doi.org/10.4028/p-4mmtt5.

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In industrial settings, the use of frictional noise to improve wear monitoring is highly promising. It enables the identification of changes in friction and wear conditions, the assessment of different phases of wear, and the examination of the impact of wear on machine performance. By analysing acoustic signatures, it is conceivable to continuously monitor the wear characteristics and surface conditions. This helps in predicting wear and detecting aberrant wear regimes in real-time. The data demonstrate that in dry conditions, the aluminum disc has higher coefficients of friction relative to cast iron and mild steel, likely due to the absence of graphite flakes in aluminum. Under lubricated conditions, a layer of lube significantly decreases the coefficient of friction, with no apparent deviations across the materials, demonstrating that complete lubrication avoids direct metal contact. In lubrication-starved applications, oily depictions nevertheless help minimize friction, though less efficiently than complete lubrication. In dry conditions, frictional sound levels for mild steel are higher due to direct surface hits, while lubrication reduces noise by eliminating metal-on-metal contact. As a result, monitoring noise levels is a helpful indicator of lubrication difficulties, aiding in maintenance and repairs.
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Wang, Yikan, Ali Bashashati, Michael S. Anglesio, Dawn Cochrane, Diljot Grewal, Hugo Horlings, Anthony Karnezis, et al. "Abstract LB-324: Genomic consequences of aberrant DNA repair stratify ovarian cancer histotypes." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-lb-324.

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Heijink, Irene H., Antoon van Oosterhout, Andras Kapus, and Dirkje S. Postma. "The Role Of Caveolin-1 In Aberrant Epithelial Repair In Response To House Dust Mite." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1437.

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Gokey, J. J., G. T. DiGiovanni, A. S. Mccall, S. S. Gutor, T. Sherrill, U. K. Singha, N. Geis, C. Taylor, T. S. Blackwell, and J. Kropski. "Sustained Activation of Yap/Taz After Injury Leads to Aberrant Alveolar Differentiation and Failure of Alveolar Repair." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4722.

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Karpathak, Supriya, Rajiv Garg, Mohammad Kaleem Ahmad, Anand Srivastava, Neelam Misra, and Anurag Kumar Srivastav. "Association of DNA repair gene O6-Methylguanine-DNA Methyltransferase (MGMT) expression with aberrant promoter methylation in Lung Cancer Progression." In ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa2208.

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Peabody, J. E., S. E. Phillips, V. Y. Lin, A. T. Adewale, S. Bodduluri, J. M. Lever, M. Weupe, et al. "Mucus Matters: Ferrets Demonstrate Restrictive Lung Physiology, Sustained Fibrosis, Mucociliary Decrement in Airways, and Aberrant Repair Following Bleomycin-Induced Pulmonary Fibrosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2579.

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Balayev, A., T. Adams, A. Justet, J. C. Schupp, J. E. Mcdonough, and N. Kaminski. "Aberrant Basaloid Cells and Closely Connected Intermediate State Cells Are Involved in the Injury Repair Process of the Fibrotic Lungs in the Aftermath of Severe COVID-19." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5667.

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Brett, S. J. "The Practical Application of Small Scale Sampling and Impression Creep Testing to Grade 91 Components." In AM-EPRI 2013, edited by D. Gandy and J. Shingledecker. ASM International, 2013. http://dx.doi.org/10.31399/asm.cp.am-epri-2013p1173.

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Abstract The Creep Strength Enhanced Ferritic steel grade 91 is widely used for both retrofit applications and primary construction on high temperature power plant. Although to date most structural integrity issues with this material have been associated with welds, as the operating hours of these plants accumulate, there will be a growing need for remanent creep life assessment of the base material. Arguably this is already the case for aberrant grade 91 material entering service in an incorrectly heat treated condition. In these circumstances the strength may fall below the normally accepted lower bound of the creep strength range and some indication of actual strength may be required. One strategy to address potential base material failure is to use small scale sampling of individual components, followed by small scale creep testing, to investigate the current creep strength present. The data can be compared with the equivalent data produced for well characterised material known to be at the lower bound of the creep strength range. This paper describes a methodology for using the impression creep data obtained to provide both creep strength ranking and an estimate of absolute creep strength for individual grade 91 components. This will enable appropriate judgements to be made by plant operators on repair/run decisions. For those components remaining in service, it allows for the weakest items to be given priority for early re-inspection at future outages. The ultimate goal is to identify base material creep damage development at as early a stage as possible and well in advance of failure in service.
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Amadeu, Simone Oliveira, Luís Fernando Barbisan, Nelci Antunes De Moura, and Ariane Rocha Bartolomeu. "EFEITOS BENÉFICOS DA INGESTÃO DE SPIRULINA PLATENSIS DURANTE A ETAPA DE INICIAÇÃO DA CARCINOGÊNESE DE CÓLON EM RATOS." In II Congresso Brasileiro de Biologia Molecular On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/2327.

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Introdução: O câncer colorretal (CCR) é uma neoplasia que acomete pessoas com vida sedentária e alimentação rica em gordura, carne vermelha e pobre em fibras estão relacionadas incidência e mortalidade para esse câncer. A Spirulina platensis (Sp) possui capacidade antioxidante e anti-inflamatória podendo ser um alimento com potencial preventivo contra o CCR. Objetivo: Este trabalho tem como objetivo avaliar o efeito preventivo da Sp (1 e 2% na dieta) nas etapas da iniciação e da promoção da carcinogênese de cólon induzida pela 1,2-dimetihidrazina (DMH) em ratos Sprague-Dawley. Metodologia: iniciação contendo cinco grupos de animais contendo 15 ratos → 4 injeções subcutâneas de DMH (40mg/Kg) e solução de EDTA (veículo da DMH) na 3 e 4ª semana do experimento e eutanásias na 10ª semana, a alimentação e promoção contendo cinco grupos de animais contendo 12 ratos → 4 injeções subcutâneas de DMH (40mg/Kg) e solução de EDTA (veículo da DMH) na 1 e 2ª semana do experimento e eutanásias na 17ª semana. A alimentação constou nas seguintes divisões tanto para o processo de iniciação como na promoção sendo o grupo 1: ração basal + DMH; grupo 2: ração basal + Spirulina platensis 1% + DMH; grupo 3: ração basal + Spirulina platensis 2% + DMH; grupo 4: ração basal + Spirulina platensis 2% + EDTA; grupo 5: ração basal + EDTA. Resultados: Tanto no protocolo de iniciação quanto de promoção, a ingestão da Sp reduziu o desenvolvimento de focos de criptas aberrantes (FCA). No estudo da iniciação, a ingestão de Sp 2% modulou a expressão de 17 genes, sendo 16 hipoexpressos (Chek2, Dffb, Msh2, Nthl1, Wee, Mgmt, Wnt2b, Igf1r, Ogg1, Xrcc6, Atm, Sod1, Cyp2e1, Notch1, Notch2, Jag1, e um hiperexpresso (Casp4) envolvidos principalmente em vias de reparo de DNA, 24 horas após a última administração da DMH. Ao final do estudo da promoção, a ingestão de Sp2% alterou a expressão de dois genes na mucosa colônica, sendo um hipoexpresso (Aifm1) e um hiperexpresso (Casr). Conclusão: Podemos concluir que a ingestão de Sp é capaz de modular a expressão de genes associados em diferentes fases da carcinogênese de cólon induzida pela DMH.
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