Removal of benzo(a)pyrene diol epoxide (BPDE)-DNA adducts as a measure of DNA repair capacity in lymphoblastoid cell lines from sisters discordant for breast cancer

2002 ◽  
Vol 40 (2) ◽  
pp. 93-100 ◽  
Author(s):  
Grazyna Motykiewicz ◽  
Beatrice Faraglia ◽  
Lian Wen Wang ◽  
Mary Beth Terry ◽  
Ruby T. Senie ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Repair ◽  
Cell Lines ◽  
Dna Adducts ◽  
Lymphoblastoid Cell Lines ◽  
Repair Capacity ◽  
Dna Repair Capacity ◽  
Diol Epoxide

scholarly journals DNA Repair Capacity of Lymphoblastoid Cell Lines From Sisters Discordant for Breast Cancer

2005 ◽  
Vol 97 (2) ◽  
pp. 127-132 ◽  
Author(s):  
D. O. Kennedy ◽  
M. Agrawal ◽  
J. Shen ◽  
M. B. Terry ◽  
F. F. Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Repair ◽  
Cell Lines ◽  
Lymphoblastoid Cell Lines ◽  
Repair Capacity ◽  
Dna Repair Capacity

Abstract 1206:HER2/neu positivereceptor status is associated with a low DNA repair capacity in women with breast cancer

2011 ◽  
Author(s):  
Jaime L. Matta ◽  
Luisa Morales ◽  
Heidi Acosta ◽  
Wanda Vargas ◽  
Michelle Colon ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Repair ◽  
Repair Capacity ◽  
Dna Repair Capacity

DNA repair capacity and acute radiotherapy adverse effects in Italian breast cancer patients

2010 ◽  
Vol 684 (1-2) ◽  
pp. 43-48 ◽  
Author(s):  
Silvia Sterpone ◽  
Tommaso Cornetta ◽  
Luca Padua ◽  
Valeria Mastellone ◽  
Daniela Giammarino ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Repair ◽  
Adverse Effects ◽  
Cancer Patients ◽  
Breast Cancer Patients ◽  
Repair Capacity ◽  
Dna Repair Capacity

scholarly journals DNA repair-based classification of melanoma cell lines reveals an effect of mutations in BRAF and NRAS driver genes on DNA repair capacity

2020 ◽  
Author(s):  
Sylvie Sauvaigo ◽  
Manel Benkhiat ◽  
Florian Braisaz ◽  
Julien Girard ◽  
Sarah Libert ◽  
...  
Keyword(s):  
Dna Repair ◽  
Signaling Pathways ◽  
Cell Lines ◽  
Melanoma Cell ◽  
Excision Repair ◽  
Mapk Pathway ◽  
Repair Capacity ◽  
Signaling Mechanism ◽  
Dna Repair Capacity ◽  
Melanoma Cell Lines

AbstractMelanoma, the most serious form of skin cancer, frequently involves the dysregulation of key signaling pathways. Treatment strategies presently target the MAPK/ERK pathway, which is overactive in melanomas due in part to BRAF and NRAS mutations, and involve inhibitors against mutated BRAF (vemurafenib or dabrafenib) or MEK kinases (cobimetinib or trametinib), or a combination of the two. Using an established biochip technology, we assessed base excision repair (BER) and nucleotide excision repair (NER) activities in a collection of BRAF mutated (A-375, Colo 829, HT-144, Malme-3M, SK-mel5, SK-mel24 and SK-mel28) and NRAS mutated (M18, MZ2 and SK-mel2) melanoma cell lines, as well as wild-type controls (A7, CHL-1). We evaluated both basal activities (i.e., without treatment) and repair capacities after treatment with vemurafenib or cobimetinib alone, or in combination. Our results indicate that globally the DNA repair capacity of the cell lines was determined by the mutation status of the BRAF and NRAS genes, indicating that the MAPK pathway participates in the regulation of both BER and NER. Treatment of BRAF mutated melanoma cells with vemurafenib alone or the vemurafenib/cobimetinib combination, but not cobimetinib alone, led to reduced DNA repair capacity in about 60% of the BRAF mutated samples, indicating that signaling pathway inhibition can alter DNA repair activity. Upregulation of some DNA repair activities was also observed in several of the treated samples, suggesting activation of compensatory signaling pathways upon treatment. The data collectively indicate that mutations in the BRAF and NRAS genes exert distinct regulatory effects on the excision/synthesis steps of the BER and NER pathways and that targeted pharmacological inactivation of the signaling mechanism can translate into specific consequences in DNA repair capacity. The heterogeneity of the responses reported herein could help define subtypes of melanoma that are associated with resistance to targeted therapies.

scholarly journals Cell lines of the same anatomic site and histologic type show large variability in radiosensitivity and relative biological effectiveness to protons and carbon ions

2020 ◽  
Author(s):  
David B. Flint ◽  
Scott J. Bright ◽  
Conor H. McFadden ◽  
Teruaki Konishi ◽  
Daisuke Ohsawa ◽  
...  
Keyword(s):  
Dna Repair ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cancer Cell Lines ◽  
Histologic Type ◽  
Anatomic Site ◽  
Repair Capacity ◽  
Dna Repair Capacity ◽  
Biological Effectiveness

AbstractPurposeTo show that radiation response across cancer cell lines of the same anatomic site and histologic type varies remarkably for protons and carbon (C) ions.Materials and MethodsWe measured and obtained from the literature clonogenic survival of human cancer cell lines of the lung (n=18), brain (n=10) and pancreas (n=10) exposed to photons, protons, and C-ions to assess their variability in response. We also treated cancer cell lines with DNA repair inhibitors prior to irradiation to assess how DNA repair capacity affects their variability in response. We quantified the variability in response by calculating the relative range (range/mean) and the coefficient of variation (COV) of the dose at 10% survival fraction (D10%) and relative biological effectiveness (RBE10%).ResultsThe relative range of D10% for lung cancer cell lines varied from 55-92% for photons, protons, and C-ions, with the relative range in RBE varying from 16-45% for protons and C-ions. For brain and pancreatic cancer cell lines, the relative range of D10% varied from 95-112%, and 39-75%, respectively, with the relative range in RBE varying from 27-33% and 25-50%, respectively. However, the COVs in D10% were approximately equal across radiation qualities, varying from 0.24±0.07–0.35±0.10, 0.35±0.09–0.69±0.62 and 0.13±0.03– 0.21±0.04 for lung, brain and pancreatic cancer cell lines, respectively. Greater relative ranges in D10% were observed in the cell lines with inhibited DNA repair, varying from 108%-157% for photons, protons, and C-ions, with relative ranges in RBE varying from 29-67%. The COVs in the D10% were also greater for the cell lines treated with inhibitors of DNA repair, varying from 0.34±0.09–0.41±0.06.ConclusionCell lines of the same anatomic site and histologic type have a remarkable variability in response, not only to photons but also to protons and C-ions. We attributed this variability to differences in DNA repair capacity.CategoryBiological Physics and Response Prediction

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