scholarly journals Recent Advances in Plant DNA Repair

Author(s):  
Nathalia Maira Cabral de Medeiros ◽  
Amanda Larissa Marques de Medeiros ◽  
Helaine Cristiane Silva ◽  
Katia Castanho Scortecci
Keyword(s):  
F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 1779 ◽  
Author(s):  
Raghavendra A. Shamanna ◽  
Deborah L. Croteau ◽  
Jong-Hyuk Lee ◽  
Vilhelm A. Bohr

Aging, the universal phenomenon, affects human health and is the primary risk factor for major disease pathologies. Progeroid diseases, which mimic aging at an accelerated rate, have provided cues in understanding the hallmarks of aging. Mutations in DNA repair genes as well as in telomerase subunits are known to cause progeroid syndromes. Werner syndrome (WS), which is characterized by accelerated aging, is an autosomal-recessive genetic disorder. Hallmarks that define the aging process include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulation of nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. WS recapitulates these hallmarks of aging and shows increased incidence and early onset of specific cancers. Genome integrity and stability ensure the normal functioning of the cell and are mainly guarded by the DNA repair machinery and telomeres. WRN, being a RecQ helicase, protects genome stability by regulating DNA repair pathways and telomeres. Recent advances in WS research have elucidated WRN’s role in DNA repair pathway choice regulation, telomere maintenance, resolution of complex DNA structures, epigenetic regulation, and stem cell maintenance.


1993 ◽  
Vol 294 (2) ◽  
pp. 187-198
Author(s):  
Peter Strike
Keyword(s):  

Author(s):  
Qiudeng Que ◽  
Zhongying Chen ◽  
Tim Kelliher ◽  
David Skibbe ◽  
Shujie Dong ◽  
...  

2016 ◽  
Vol 22 (23) ◽  
pp. 3527-3546 ◽  
Author(s):  
Francesco Gentile ◽  
Jack A. Tuszynski ◽  
Khaled H. Barakat

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 1173 ◽  
Author(s):  
Sander Frank ◽  
Peter Nelson ◽  
Valeri Vasioukhin

Prostate cancer (PCa) is a disease of mutated and misregulated genes. However, primary prostate tumors have relatively few mutations, and only three genes (ERG, PTEN, and SPOP) are recurrently mutated in more than 10% of primary tumors. On the other hand, metastatic castration-resistant tumors have more mutations, but, with the exception of the androgen receptor gene (AR), no single gene is altered in more than half of tumors. Structural genomic rearrangements are common, including ERG fusions, copy gains involving the MYC locus, and copy losses containing PTEN. Overall, instead of being associated with a single dominant driver event, prostate tumors display various combinations of modifications in oncogenes and tumor suppressors. This review takes a broad look at the recent advances in PCa research, including understanding the genetic alterations that drive the disease and how specific mutations can sensitize tumors to potential therapies. We begin with an overview of the genomic landscape of primary and metastatic PCa, enabled by recent large-scale sequencing efforts. Advances in three-dimensional cell culture techniques and mouse models for PCa are also discussed, and particular emphasis is placed on the benefits of patient-derived xenograft models. We also review research into understanding how ETS fusions (in particular, TMPRSS2-ERG) and SPOP mutations contribute to tumor initiation. Next, we examine the recent findings on the prevalence of germline DNA repair mutations in about 12% of patients with metastatic disease and their potential benefit from the use of poly(ADP-ribose) polymerase (PARP) inhibitors and immune modulation. Lastly, we discuss the recent increased prevalence of AR-negative tumors (neuroendocrine and double-negative) and the current state of immunotherapy in PCa. AR remains the primary clinical target for PCa therapies; however, it does not act alone, and better understanding of supporting mutations may help guide the development of novel therapeutic strategies.


2017 ◽  
Vol 22 (4) ◽  
pp. 611-618 ◽  
Author(s):  
Katsutoshi Oda ◽  
Michihiro Tanikawa ◽  
Kenbun Sone ◽  
Mayuyo Mori-Uchino ◽  
Yutaka Osuga ◽  
...  

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