scholarly journals Chronic inflammation-related DNA damage response: a driving force of gastric cardia carcinogenesis

Oncotarget ◽  
2014 ◽  
Vol 6 (5) ◽  
pp. 2856-2864 ◽  
Author(s):  
Runhua Lin ◽  
Dejun Xiao ◽  
Yi Guo ◽  
Dongping Tian ◽  
Hailong Yun ◽  
...  
Keyword(s):  
Dna Damage ◽  
Chronic Inflammation ◽  
Dna Damage Response ◽  
Driving Force ◽  
Gastric Cardia ◽  
Damage Response

scholarly journals Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway

Neoplasia ◽  
2007 ◽  
Vol 9 (10) ◽  
pp. 840-IN12 ◽  
Author(s):  
David Blanco ◽  
Silvestre Vicent ◽  
Mario F. Fraga ◽  
Ignacio Fernandez-Garcia ◽  
Javier Freire ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Damage ◽  
Chronic Inflammation ◽  
Molecular Analysis ◽  
Dna Damage Response ◽  
Epigenetic Regulation ◽  
Cancer Model ◽  
Damage Response ◽  
Lung Cancer Model ◽  
Dna Damage Response Pathway

DNA-damage response associated with occupational exposure, age and chronic inflammation in workers in the automotive industry

2012 ◽  
Vol 748 (1-2) ◽  
pp. 21-28 ◽  
Author(s):  
Natalya V. Savina ◽  
Marharyta P. Smal ◽  
Tatyana D. Kuzhir ◽  
Alla A. Ershova-Pavlova ◽  
Roza I. Goncharova
Keyword(s):  
Dna Damage ◽  
Occupational Exposure ◽  
Chronic Inflammation ◽  
Dna Damage Response ◽  
Automotive Industry ◽  
Exposure Age ◽  
Damage Response

Genetic instability

2016 ◽  
pp. 72-81
Author(s):  
Jennifer Wilding ◽  
Walter Bodmer
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Genetic Instability ◽  
Molecular Basis ◽  
Driving Force ◽  
Germline Mutations ◽  
Absolute Requirement ◽  
Damage Response ◽  
Repair Pathways ◽  
Chromosome Level

Most cancers are thought to exhibit some form of genetic instability, which can either be at the nucleotide or chromosome level. It is tempting to speculate that because genetic instability accelerates the rate of accumulation of mutations, it would act as a necessary driving force for the development and progression of cancer, and there has been much debate as to whether there is an absolute requirement for genetic instability during tumorigenesis. Although the mechanism of the acquired genetic instability is clear in many germline cancer-predisposing syndromes, the molecular basis for genetic instability in sporadic cancers remains unclear. This chapter will give a very brief summary of the main features of the major DNA damage response and repair pathways, the germline mutations in genes within these pathways which predispose to cancers, and an overview of some of the possible mechanisms through which sporadic cancers may become genetically unstable.

scholarly journals Accelerated carcinogenesis following liver regeneration is associated with chronic inflammation-induced double-strand DNA breaks

2010 ◽  
Vol 107 (5) ◽  
pp. 2207-2212 ◽  
Author(s):  
Hila Barash ◽  
Eitan R. Gross ◽  
Yifat Edrei ◽  
Ezra Ella ◽  
Ariel Israel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Liver Regeneration ◽  
Chronic Inflammation ◽  
Dna Damage Response ◽  
Molecular Mechanisms ◽  
Survival Rates ◽  
Dna Breaks ◽  
Double Strand Dna Breaks ◽  
Damage Response

Hepatocellular carcinoma (HCC) is the third leading cause of cancer mortality worldwide and is considered to be the outcome of chronic liver inflammation. Currently, the main treatment for HCC is surgical resection. However, survival rates are suboptimal partially because of tumor recurrence in the remaining liver. Our aim was to understand the molecular mechanisms linking liver regeneration under chronic inflammation to hepatic tumorigenesis. Mdr2-KO mice, a model of inflammation-associated cancer, underwent partial hepatectomy (PHx), which led to enhanced hepatocarcinogenesis. Moreover, liver regeneration in these mice was severely attenuated. We demonstrate the activation of the DNA damage-response machinery and increased genomic instability during early liver inflammatory stages resulting in hepatocyte apoptosis, cell-cycle arrest, and senescence and suggest their involvement in tumor growth acceleration subsequent to PHx. We propose that under the regenerative proliferative stress induced by liver resection, the genomic unstable hepatocytes generated during chronic inflammation escape senescence and apoptosis and reenter the cell cycle, triggering the enhanced tumorigenesis. Thus, we clarify the immediate and long-term contributions of the DNA damage response to HCC development and recurrence.

scholarly journals The Multifunctional Protein p62 and Its Mechanistic Roles in Cancers

2019 ◽  
Vol 19 (6) ◽  
pp. 468-478 ◽  
Author(s):  
Shunbin Ning ◽  
Ling Wang
Keyword(s):  
Immune Response ◽  
Dna Damage ◽  
Chronic Inflammation ◽  
Dna Damage Response ◽  
Translational Regulation ◽  
Multifunctional Protein ◽  
Selective Autophagy ◽  
Cellular Processes ◽  
Promising Strategy ◽  
Damage Response

The multifunctional signaling hub p62 is well recognized as a ubiquitin sensor and a selective autophagy receptor. As a ubiquitin sensor, p62 promotes NFκB activation by facilitating TRAF6 ubiquitination and aggregation. As a selective autophagy receptor, p62 sorts ubiquitinated substrates including p62 itself for lysosome-mediated degradation. p62 plays crucial roles in myriad cellular processes including DNA damage response, aging/senescence, infection and immunity, chronic inflammation, and cancerogenesis, dependent on or independent of autophagy. Targeting p62-mediated autophagy may represent a promising strategy for clinical interventions of different cancers. In this review, we summarize the transcriptional and post-translational regulation of p62, and its mechanistic roles in cancers, with the emphasis on its roles in regulation of DNA damage response and its connection to the cGAS-STING-mediated antitumor immune response, which is promising for cancer vaccine design.

2118-P: Regulation of Ataxia-Telangiectasia and Rad3-Related (ATR)–Dependent DNA Damage Response by Nitric Oxide in ß-Cells

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 2118-P
Author(s):  
CHAY TENG YEO ◽  
BRYNDON OLESON ◽  
JOHN A. CORBETT ◽  
JAMIE K. SCHNUCK
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Ataxia Telangiectasia ◽  
Damage Response
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