scholarly journals The impact of CDK9 on radiosensitivity, DNA damage repair and cell cycling of HNSCC cancer cells

2015 ◽  
Vol 48 (1) ◽  
pp. 191-198 ◽  
Author(s):  
KATJA STORCH ◽  
NILS CORDES
Keyword(s):  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Repair ◽  
Damage Repair ◽  
Cell Cycling ◽  
The Impact

scholarly journals Assessing BRCA1 activity in DNA damage repair using human induced pluripotent stem cells as an approach to assist classification of BRCA1 variants of uncertain significance

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0260852
Author(s):  
Meryem Ozgencil ◽  
Julian Barwell ◽  
Marc Tischkowitz ◽  
Louise Izatt ◽  
Ian Kesterton ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Repair ◽  
Ips Cells ◽  
Variants Of Uncertain Significance ◽  
Cellular Models ◽  
Pathogenic Variants ◽  
Damage Repair ◽  
Uncertain Significance ◽  
Induced Pluripotent ◽  
The Impact

Establishing a universally applicable protocol to assess the impact of BRCA1 variants of uncertain significance (VUS) expression is a problem which has yet to be resolved despite major progresses have been made. The numerous difficulties which must be overcome include the choices of cellular models and functional assays. We hypothesised that the use of induced pluripotent stem (iPS) cells might facilitate the standardisation of protocols for classification, and could better model the disease process. We generated eight iPS cell lines from patient samples expressing either BRCA1 pathogenic variants, non-pathogenic variants, or BRCA1 VUSs. The impact of these variants on DNA damage repair was examined using a ɣH2AX foci formation assay, a Homologous Repair (HR) reporter assay, and a chromosome abnormality assay. Finally, all lines were tested for their ability to differentiate into mammary lineages in vitro. While the results obtained from the two BRCA1 pathogenic variants were consistent with published data, some other variants exhibited differences. The most striking of these was the BRCA1 variant Y856H (classified as benign), which was unexpectedly found to present a faulty HR repair pathway, a finding linked to the presence of an additional variant in the ATM gene. Finally, all lines were able to differentiate first into mammospheres, and then into more advanced mammary lineages expressing luminal- or basal-specific markers. This study stresses that BRCA1 genetic analysis alone is insufficient to establish a reliable and functional classification for assessment of clinical risk, and that it cannot be performed without considering the other genetic aberrations which may be present in patients. The study also provides promising opportunities for elucidating the physiopathology and clinical evolution of breast cancer, by using iPS cells.

Abstract 2403: Imaging of UVB and UVC-induced DNA damage repair in cancer cells in Gelfoam histoculture and minimal cancer in mice

2014 ◽  
Author(s):  
Fuminari Uehara ◽  
Shinji Miwa ◽  
Yasunori Tome ◽  
Hiroki Maehara ◽  
Fuminori Kanaya ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Repair ◽  
Damage Repair

scholarly journals APC loss affects DNA damage repair causing doxorubicin resistance in breast cancer cells

Neoplasia ◽  
2019 ◽  
Vol 21 (12) ◽  
pp. 1143-1150 ◽  
Author(s):  
Casey D. Stefanski ◽  
Kaitlyn Keffler ◽  
Stephanie McClintock ◽  
Lauren Milac ◽  
Jenifer R. Prosperi
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Dna Damage Repair ◽  
Doxorubicin Resistance ◽  
Damage Repair

Radiosensitization of metformin in pancreatic cancer cells via abrogating the G2 checkpoint and inhibiting DNA damage repair

2015 ◽  
Vol 369 (1) ◽  
pp. 192-201 ◽  
Author(s):  
Zheng Wang ◽  
Song-Tao Lai ◽  
Ning-Yi Ma ◽  
Yun Deng ◽  
Yong Liu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Repair ◽  
G2 Checkpoint ◽  
Pancreatic Cancer Cells ◽  
Damage Repair

scholarly journals Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells

2011 ◽  
Vol 3 (1) ◽  
Author(s):  
Praveen Rajendran ◽  
Emily Ho ◽  
David E Williams ◽  
Roderick H Dashwood
Keyword(s):  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Repair ◽  
Hdac Inhibition ◽  
Damage Repair ◽  
Dietary Phytochemicals

scholarly journals Persistent DNA Double-Strand Breaks After Repeated Diagnostic CT Scans in Breast Epithelial Cells and Lymphocytes

2021 ◽  
Vol 11 ◽  
Author(s):  
Natalia V. Bogdanova ◽  
Nina Jguburia ◽  
Dhanya Ramachandran ◽  
Nora Nischik ◽  
Katharina Stemwedel ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Repair ◽  
Cell Types ◽  
Strand Break ◽  
Ct Scans ◽  
Breast Epithelial Cell ◽  
Damage Repair ◽  
Breast Epithelial ◽  
The Impact ◽  
Diagnostic Ct

DNA double-strand break (DSB) induction and repair have been widely studied in radiation therapy (RT); however little is known about the impact of very low exposures from repeated computed tomography (CT) scans for the efficiency of repair. In our current study, DSB repair and kinetics were investigated in side-by-side comparison of RT treatment (2 Gy) with repeated diagnostic CT scans (≤20 mGy) in human breast epithelial cell lines and lymphoblastoid cells harboring different mutations in known DNA damage repair proteins. Immunocytochemical analysis of well known DSB markers γH2AX and 53BP1, within 48 h after each treatment, revealed highly correlated numbers of foci and similar appearance/disappearance profiles. The levels of γH2AX and 53BP1 foci after CT scans were up to 30% of those occurring 0.5 h after 2 Gy irradiation. The DNA damage repair after diagnostic CT scans was monitored and quantitatively assessed by both γH2AX and 53BP1 foci in different cell types. Subsequent diagnostic CT scans in 6 and/or 12 weeks intervals resulted in elevated background levels of repair foci, more pronounced in cells that were prone to genomic instability due to mutations in known regulators of DNA damage response (DDR). The levels of persistent foci remained enhanced for up to 6 months. This “memory effect” may reflect a radiation-induced long-term response of cells after low-dose x-ray exposure.

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