scholarly journals Abstract 3217: Newly identified role of tumor treating fields in DNA damage repair and replication stress pathways

2018 ◽  
Author(s):  
Narasimha Kumar Karanam ◽  
Lianghao Ding ◽  
Brock Sishc ◽  
Debabrata Saha ◽  
Michael D. Story
Keyword(s):  
Dna Damage ◽  
Dna Damage Repair ◽  
Replication Stress ◽  
Tumor Treating Fields ◽  
Damage Repair

scholarly journals Targeting DNA Replication Stress and DNA Double-Strand Break Repair for Optimizing SCLC Treatment

Cancers ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1289 ◽  
Author(s):  
Xing Bian ◽  
Wenchu Lin
Keyword(s):  
Lung Cancer ◽  
Dna Damage ◽  
Dna Replication ◽  
Dna Damage Repair ◽  
Predictive Biomarkers ◽  
Replication Stress ◽  
Genotoxic Stress ◽  
Repair System ◽  
Damage Repair ◽  
Repair Pathways

Small cell lung cancer (SCLC), accounting for about 15% of all cases of lung cancer worldwide, is the most lethal form of lung cancer. Despite an initially high response rate of SCLC to standard treatment, almost all patients are invariably relapsed within one year. Effective therapeutic strategies are urgently needed to improve clinical outcomes. Replication stress is a hallmark of SCLC due to several intrinsic factors. As a consequence, constitutive activation of the replication stress response (RSR) pathway and DNA damage repair system is involved in counteracting this genotoxic stress. Therefore, therapeutic targeting of such RSR and DNA damage repair pathways will be likely to kill SCLC cells preferentially and may be exploited in improving chemotherapeutic efficiency through interfering with DNA replication to exert their functions. Here, we summarize potentially valuable targets involved in the RSR and DNA damage repair pathways, rationales for targeting them in SCLC treatment and ongoing clinical trials, as well as possible predictive biomarkers for patient selection in the management of SCLC.

scholarly journals Metabolomics Reveals Aging-associated Attenuation of Noninvasive Radiation Biomarkers in Mice: Potential Role of Polyamine Catabolism and Incoherent DNA Damage-repair

2013 ◽  
Vol 12 (5) ◽  
pp. 2269-2281 ◽  
Author(s):  
Soumen K. Manna ◽  
Kristopher W. Krausz ◽  
Jessica A. Bonzo ◽  
Jeffrey R. Idle ◽  
Frank J. Gonzalez
Keyword(s):  
Dna Damage ◽  
Potential Role ◽  
Dna Damage Repair ◽  
Polyamine Catabolism ◽  
Damage Repair

Investigating the Role of SF3B1 Mutations in DNA Damage Repair in Myeloid Malignancies

2017 ◽  
Vol 55 ◽  
pp. S159-S160
Author(s):  
K. Lappin ◽  
F. Liberante ◽  
K. Savage ◽  
K. Mills
Keyword(s):  
Dna Damage ◽  
Dna Damage Repair ◽  
Myeloid Malignancies ◽  
Damage Repair

Abstract 1186: Efficacy of Tumor Treating Fields (TTFields) in mesothelioma is associated with reduced capacity for DNA damage repair

2021 ◽  
Author(s):  
Helena Mumblat ◽  
Antonia Martinez ◽  
Ori Braten ◽  
Mijal Munster ◽  
Eyal Dor-On ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Repair ◽  
Tumor Treating Fields ◽  
Damage Repair

Abstract 2039: The role of HORMAD1 in DNA damage repair in squamous cell carcinomas

2021 ◽  
Author(s):  
Jennifer Gantchev ◽  
Amelia Martinez Villarreal ◽  
Brandon Ramchatesingh ◽  
Ivan V. Litvinov
Keyword(s):  
Dna Damage ◽  
Squamous Cell ◽  
Dna Damage Repair ◽  
Squamous Cell Carcinomas ◽  
Damage Repair

scholarly journals SIRT7-mediated ATM deacetylation is essential for its deactivation and DNA damage repair

2019 ◽  
Vol 5 (3) ◽  
pp. eaav1118 ◽  
Author(s):  
Ming Tang ◽  
Zhiming Li ◽  
Chaohua Zhang ◽  
Xiaopeng Lu ◽  
Bo Tu ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Repair ◽  
Class Iii ◽  
Ataxia Telangiectasia Mutated ◽  
Damage Repair ◽  
Damage Response ◽  
Late Stages

The activation of ataxia-telangiectasia mutated (ATM) upon DNA damage involves a cascade of reactions, including acetylation by TIP60 and autophosphorylation. However, how ATM is progressively deactivated after completing DNA damage repair remains obscure. Here, we report that sirtuin 7 (SIRT7)–mediated deacetylation is essential for dephosphorylation and deactivation of ATM. We show that SIRT7, a class III histone deacetylase, interacts with and deacetylates ATM in vitro and in vivo. In response to DNA damage, SIRT7 is mobilized onto chromatin and deacetylates ATM during the late stages of DNA damage response, when ATM is being gradually deactivated. Deacetylation of ATM by SIRT7 is prerequisite for its dephosphorylation by its phosphatase WIP1. Consequently, depletion of SIRT7 or acetylation-mimic mutation of ATM induces persistent ATM phosphorylation and activation, thus leading to impaired DNA damage repair. Together, our findings reveal a previously unidentified role of SIRT7 in regulating ATM activity and DNA damage repair.

scholarly journals Tumor treating fields (TTFields) delay DNA damage repair following radiation treatment of glioma cells

2017 ◽  
Vol 12 (1) ◽  
Author(s):  
Moshe Giladi ◽  
Mijal Munster ◽  
Rosa S. Schneiderman ◽  
Tali Voloshin ◽  
Yaara Porat ◽  
...  
Keyword(s):  
Dna Damage ◽  
Radiation Treatment ◽  
Dna Damage Repair ◽  
Glioma Cells ◽  
Tumor Treating Fields ◽  
Damage Repair

scholarly journals Long noncoding RNA HCP5 participates in premature ovarian insufficiency by transcriptionally regulating MSH5 and DNA damage repair via YB1

2020 ◽  
Vol 48 (8) ◽  
pp. 4480-4491 ◽  
Author(s):  
Xiaoyan Wang ◽  
Xinyue Zhang ◽  
Yujie Dang ◽  
Duan Li ◽  
Gang Lu ◽  
...  
Keyword(s):  
Dna Damage ◽  
Noncoding Rna ◽  
Dna Damage Repair ◽  
Noncoding Rnas ◽  
Epigenetic Mechanism ◽  
Premature Ovarian Insufficiency ◽  
Genetic Etiology ◽  
Ovarian Insufficiency ◽  
Damage Repair

Abstract The genetic etiology of premature ovarian insufficiency (POI) has been well established to date, however, the role of long noncoding RNAs (lncRNAs) in POI is largely unknown. In this study, we identified a down-expressed lncRNA HCP5 in granulosa cells (GCs) from biochemical POI (bPOI) patients, which impaired DNA damage repair and promoted apoptosis of GCs. Mechanistically, we discovered that HCP5 stabilized the interaction between YB1 and its partner ILF2, which could mediate YB1 transferring into the nucleus of GCs. HCP5 silencing affected the localization of YB1 into nucleus and reduced the binding of YB1 to the promoter of MSH5 gene, thereby diminishing MSH5 expression. Taken together, we identified that the decreased expression of HCP5 in bPOI contributed to dysfunctional GCs by regulating MSH5 transcription and DNA damage repair via the interaction with YB1, providing a novel epigenetic mechanism for POI pathogenesis.

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