Int J Mol Sci
Department of Anatomy and Cell Biology, University of Saskatchewan, Saskatoon, SK S7N 5E5, Canada.
Published: June 2018
In aging cells, genomic instability is now recognized as a hallmark event. Throughout life, cells encounter multiple endogenous and exogenous DNA damaging events that are mostly repaired, but inevitably DNA mutations, chromosome rearrangements, and epigenetic deregulation begins to mount. Now that people are living longer, more and more late life time is spent suffering from age-related disease, in which genomic instability plays a critical role. However, several major questions remain heavily debated, such as the following: When does aging start? How long can we live? In order to minimize the impact of genomic instability on longevity, it is important to understand when aging starts, and to ensure repair mechanisms remain optimal from the very start to the very end. In this review, the interplay between the stress and nutrient response networks, and the regulation of homeostasis and genomic stability, is discussed. Mechanisms that link these two networks are predicted to be key lifespan determinants. The Anaphase Promoting Complex (APC), a large evolutionarily conserved ubiquitin ligase, can potentially serve this need. Recent work demonstrates that the APC maintains genomic stability, mounts a stress response, and increases longevity in yeast. Furthermore, inhibition of APC activity by glucose and nutrient response factors indicates a tight link between the APC and the stress/nutrient response networks.
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http://dx.doi.org/10.3390/ijms19071888 | DOI Listing |
Sci Rep
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Department of Oncology, The First Affiliated Hospital of Yangtze University, Jingzhou, Hubei, China.
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Sorbonne Université, CNRS, Laboratory of Computational and Quantitative Biology, LCQB, Paris, France.
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View Article and Find Full Text PDFZhonghua Bing Li Xue Za Zhi
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Department of Pathology, the First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
Zhonghua Bing Li Xue Za Zhi
February 2025
Department of Pathology, the Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, China.
To investigate whether the immunohistochemical results of two markers PMS2 and MSH6 (2-MMR) could replace the four markers MLH1, PMS2, MSH2 and MSH6 (4-MMR) to detect mismatch repair deficient (dMMR) cancers. A retrospective analysis was conducted with summary of immunohistochemical data from 7 867 cases of gastric cancer, colorectal cancer, endometrial cancer, and other diseases in the Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China, from March 2018 to March 2023. The consistency of 2-MMR and 4-MMR results was examined.
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Université de Caen Normandie, INSERM U1086 ANTICIPE, Caen, France; UNICANCER, Comprehensive Cancer Center François Baclesse, Caen, France; Université de Caen Normandie, US PLATON- ORGAPRED core facility, Caen, France; Université de Caen Normandie, US PLATON, UNICANCER, Comprehensive Cancer Center François Baclesse- Biological Resource Center 'OvaRessources', Caen, France. Electronic address:
PARP inhibitors (PARPi) have been shown to improve progression-free survival, particularly in homologous recombination deficient (HRD) ovarian cancers. Identifying patients eligible to PARPi is currently based on next-generation sequencing (NGS), but the persistence of genomic scars in tumors after restoration of HR or epigenetic changes can be a limitation. Functional assays could thus be used to improve this profiling and faithfully identify HRD tumors.
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