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Journal articles on the topic 'Blood DNA'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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1

Filho, Ednaldo da Silva, and Taianara Tocantins Gomes Almeida. "Optimized Protocols for Extraction of DNA in Plant and Blood Tissues." International Journal of Scientific Research 2, no. 11 (June 1, 2012): 57–58. http://dx.doi.org/10.15373/22778179/nov2013/17.

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2

Fang, Chyang T. "Blood Screening for HBV DNA." Journal of Clinical Virology 36 (May 2006): S30—S32. http://dx.doi.org/10.1016/s1386-6532(06)80006-5.

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3

Ferec, C., C. Verlingue, and JP Saleum. "HBV DNA in blood donors." Transfusion 28, no. 1 (January 1988): 84–85. http://dx.doi.org/10.1046/j.1537-2995.1988.28188127965.x.

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4

Brauner, Paul. "DNA Typing and Blood Transfusion." Journal of Forensic Sciences 41, no. 5 (September 1, 1996): 14020J. http://dx.doi.org/10.1520/jfs14020j.

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5

Kendall, Teresa L., Darryl J. Byerley, and Roger Dean. "Isolation of DNA from blood." Analytical Biochemistry 195, no. 1 (May 1991): 74–76. http://dx.doi.org/10.1016/0003-2697(91)90297-7.

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6

Reid, Marion E. "From DNA to blood groups." Immunohematology 24, no. 4 (2020): 166–69. http://dx.doi.org/10.21307/immunohematology-2019-293.

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7

Signer, Esther, Clive C. Kuenzle, Peter E. Thomann, and Ulrich Hübscher. "DNA fingerprinting: improved DNA extraction from small blood samples." Nucleic Acids Research 16, no. 15 (1988): 7738. http://dx.doi.org/10.1093/nar/16.15.7738.

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8

Jung, Steffen. "DNA-catching BM macrophages set hematopoiesis." Blood 134, no. 16 (August 16, 2019): 1274–75. http://dx.doi.org/10.1182/blood.2019002589.

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9

Mohamed, T., D. Endoh, and S. Oikawa. " DNA damage of blood lymphocytes and neutrophils in cattle with lymphosarcoma." Veterinární Medicína 56, No. 10 (November 11, 2011): 504–9. http://dx.doi.org/10.17221/3295-vetmed.

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  The objective of the present study was to analyze the apoptotic process in peripheral blood mononuclear cells (PBMC) and polymorphonuclear neutrophil leukocytes (PMN) in cows clinically affected with lymphosarcoma. Thirteen cows were studied. Of them, eight, that were referred because of inappetance, loss of body condition, diarrhoea, constipation, protrusion of third eyelid, and exophthalmia, were seropositive for bovine leukemia virus (BLV) based on a serum enzyme-linked immunosorbent assay. Other animals were apparently healthy and were used as controls. DNA damage of PBMC and PMN was assessed using the Comet assay. The results obtained showed a statistically significant difference in DNA damage between the PBMC and PMN isolated from cows infected with BLV compared to PBMC and PMN isolated from healthy cows. This is the first article to document decreased apoptosis of blood PBMC and PMN in cattle in response to BLV infection using the Comet assay.

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10

Liang, Fengshan, Adam S. Miller, Carolilne Tang, Patrick Sung, and Gary M. Kupfer. "UAF1 DNA Binding Activity Is Critical for RAD51-Mediated Homologous DNA Pairing." Blood 134, Supplement_1 (November 13, 2019): 2497. http://dx.doi.org/10.1182/blood-2019-130435.

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Background: In the Fanconi anemia (FA) DNA repair pathway, DNA damage induces the mono-ubiquitination of the FANCI-FANCD2 (ID2) heterodimer by the FA core complex through its inherent E3 ligase activity. The timely deubiquitination of ID2 by USP1-UAF1 deubiquitinase complex is also critically important for the FA DNA repair. UAF1 has a DNA binding activity, which is required for FANCD2 deubiquitination. UAF1 also enhances RAD51-mediated homologous DNA pairing in a manner that is dependent on complex formation with RAD51AP1. UAF1 deficient cells are impaired for DNA repair by homologous recombination (HR).The biochemical and cellular functions of UAF1 DNA binding activity in HR remain elusive. Methods:UAF1 wild type and DNA binding mutant proteins were purified and used to define its biochemical properties in HR. In vitroD-loop formation and synaptic complex assembly assay were performed to discover the DNA binding of UAF1 in RAD51 recombinase enhancement. U2OS-DR-GFP cell lines with impaired UAF1 or RAD51AP1DNA binding were generated to examine HR efficiency and DNA damage resistance. Results:UAF1 preferentially binds an HR-intermediate-like DNA substrate (D-loop, Fig.1). The DNA binding deficient mutant of UAF1 is unable to stimulate RAD51AP1 promotion of RAD51-mediated D-loop (Fig. 2) and the ability to recruit homologous DNA to form the presynaptic complex formation in HR (Fig. 3). In cells, the UAF1 DNA-binding mutant is compromised for the ability to repair DNA damage and to implement HR (Fig. 4). Such activity correlates with the ability to confer resistance to DNA cross linking agents such as mitomycin C (Fig. 4). The DNA binding of UAF1 and RAD51AP1 have a coordinated role in HR-directed DNA damage repair (Fig. 5). Conclusions: UAF1 DNA binding activity is indispensable for its function in enhancing RAD51-mediated homologous DNA pairing within the context of the UAF1-RAD51AP1 complex. UAF1 DNA binding deficiency causes DNA damage sensitivity and impairs HR efficiency in cells. Translational Applicability:Our findings reveal a critical role of UAF1 DNA binding in DNA repair and genome maintenance. The identification of UAF1's role in repair will enable targeted efforts to improve molecular approaches for FA therapy. Disclosures No relevant conflicts of interest to declare.

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11

Wu, Jie, Cuiying Liu, Shao Qian, and Hongchun Hou. "The Expression of Tim-3 in Peripheral Blood of Ovarian Cancer." DNA and Cell Biology 32, no. 11 (November 2013): 648–53. http://dx.doi.org/10.1089/dna.2013.2116.

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12

Terry, Mary Beth, Lissette Delgado-Cruzata, Neomi Vin-Raviv, Hui Chen Wu, and Regina M. Santella. "DNA methylation in white blood cells." Epigenetics 6, no. 7 (July 2011): 828–37. http://dx.doi.org/10.4161/epi.6.7.16500.

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13

SEKIZAWA, Akihiko, Hiroshi SAITO, and Takumi YANAIHARA. "Fetal DNA Diagnosis from Maternal Blood." Japanese Journal of Thrombosis and Hemostasis 10, no. 2/3 (1999): 174–76. http://dx.doi.org/10.2491/jjsth.10.174.

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14

TallBear, Kimberly. "DNA, Blood, and Racializing the Tribe." Wicazo Sa Review 18, no. 1 (2003): 81–107. http://dx.doi.org/10.1353/wic.2003.0008.

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15

Burckhardt, J. "Amplification of DNA from whole blood." Genome Research 3, no. 4 (February 1, 1994): 239–43. http://dx.doi.org/10.1101/gr.3.4.239.

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16

Taş, S. "Purification of DNA from clotted blood." Clinical Chemistry 36, no. 10 (October 1, 1990): 1851. http://dx.doi.org/10.1093/clinchem/36.10.1851a.

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17

Stanojevic, Maja. "CMV DNA in blood and CSF." Journal of Clinical Virology 12, no. 2 (April 1999): 107. http://dx.doi.org/10.1016/s1386-6532(99)90426-2.

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18

Sahota, A., A. I. Brooks, J. A. Tischfield, and I. B. King. "Preparing DNA from Blood for Genotyping." Cold Spring Harbor Protocols 2007, no. 8 (August 1, 2007): pdb.prot4830. http://dx.doi.org/10.1101/pdb.prot4830.

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19

IKAWA, K., K. YAMAFUJI, T. UKITA, S. KUWABARA, T. IGARASHI, and H. TAKABAYASHI. "Fetal DNA Diagnosis from Maternal Blood." Annals of the New York Academy of Sciences 945, no. 1 (January 25, 2006): 153–55. http://dx.doi.org/10.1111/j.1749-6632.2001.tb03878.x.

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20

Fedorov, N. A., I. S. Yaneva, O. I. Skotnikova, and V. N. Pan'kov. "DNA assay in human blood plasma." Bulletin of Experimental Biology and Medicine 102, no. 3 (September 1986): 1190–92. http://dx.doi.org/10.1007/bf00842228.

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21

Ganshirt-Ahlert, D., N. Basak, K. Aidynli, and W. Holzgreve. "Fetal DNA in uterine vein blood." International Journal of Gynecology & Obstetrics 41, no. 2 (May 1993): 217–18. http://dx.doi.org/10.1016/0020-7292(93)90749-m.

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22

WATT, E. M., and V. M. WATT. "DNA fingerprints from minimal blood volumes." Molecular Ecology 1, no. 2 (August 1992): 131–32. http://dx.doi.org/10.1111/j.1365-294x.1992.tb00165.x.

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23

Bayart, F., S. Crovella, D. Montagnon, and C. Rabarivola. "Field blood conservation for DNA extraction." International Journal of Anthropology 10, no. 4 (October 1995): 199–201. http://dx.doi.org/10.1007/bf02447877.

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24

Lozano-Gonzalez, Karla, Elba Padilla-Rodríguez, Tomas Texis, Marco N. Gutiérrez, Mauricio Rodríguez-Dorantes, Betzaida Cuevas-Córdoba, Eliseo Ramírez-García, Dolores Mino-León, Sergio Sánchez-García, and Vanessa Gonzalez-Covarrubias. "Allele Frequency of ACE2 Intron Variants and Its Association with Blood Pressure." DNA and Cell Biology 39, no. 11 (November 1, 2020): 2095–101. http://dx.doi.org/10.1089/dna.2020.5804.

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25

Sunaga, Masanobu, Tsukasa Oda, Eiko Yamane, Rei Ishihara, Yuki Murakami, Saki Watanabe, Yuta Asao, et al. "DNA Polymerases Pol θ/Pol η Involved in Error-Prone DNA Repair Are Highly Expressed in Multiple Myeloma and Upregulated By DNA Damage." Blood 134, Supplement_1 (November 13, 2019): 4364. http://dx.doi.org/10.1182/blood-2019-125163.

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Background: DNA polymerases (DNA pols) are essential enzymes for DNA replication. In mammalian cells, DNA pols are divided into four families: A (Pol θ, Pol γ, and Pol ν), B (Pol α, Pol δ, Pol ε, and Pol ζ), X (Pol β, Pol λ, Pol μ, and TDT), and Y (Pol η, Pol ι, Pol κ, and REV1). These DNA pols are required for both genome duplication and protecting cells from DNA damage induced by endogenous and exogenous agents, such as ROS, UV, and chemotherapeutic drugs. For example, Pol β, Pol λ, and Pol ι participate in base excision repair. Contrastingly, Pol ζ, REV1, Pol η, Pol ι, and Pol κ can replicate over various DNA lesions to prevent DNA replication stalling, known as translesion synthesis. Although some DNA pols are highly expressed in cancer cells, indicating chemotherapeutic resistance and poor outcome, their exact roles and expression mechanisms have not been fully elucidated. Multiple myeloma (MM) is a hematological malignancy of terminally differentiated plasma cells, with multistep progression from pre-cancer stage namely. In this study we attempted to elucidate the involvement of DNA pols in multistep oncogenesis of MM. Methods: A total of 63 MM and 29 MGUS patients, 15 controls, and 9 MM cell lines were included in the study. RNA was extracted from purified CD138+ plasma cells. DNA pol expressions were determined by RQ-PCR. Their expression levels were normalized against ACTB levels and calculated with 2-ΔΔCt value. Doxycycline-inducible p53 system (Tet-on p53) and nutlin-3 were used for analyzing the role of p53 in DNA pol expressions in MM cell lines. Melphalan, doxorubicin, and bortezomib were used to examine DNA pol expressions in damaged cells in vitro. JQ1 and CPI203 were used to evaluate the role of bromodomain in DNA pol expressions. Results: Pol α and Pol ε expressions were significantly higher in MM than in control (p=0.007 and p=0.004, respectively), but Pol ε and Pol ζ levels were not significantly different (p=0.631, p=0.0826, respectively). Pol η, REV1, Pol ι, and Pol κ expressions were significantly higher in MM than control (p<0.001, p=0.002, p<0.001, and p<0.001, respectively). Pol θ and Pol γ were expressed at a higher level in MM than in control (p<0.001 and p<0.001, respectively). Pol β and Pol λ expressions were higher in MM than in control (p=0.0088 and p=0.013, respectively). Although the expressions of many DNA pols were higher in MM plasma cells, we focused on Pol η and Pol θ, because Pol λ, Pol μ, Pol ν, and Pol ι were expressed at very low levels, and Pol ε, Pol ζ, Pol γ, Pol κ, and REV1 were expressed in PBMNCs of healthy volunteers at high level. Pol η and Pol θ expressions did not differ due to known risk factors, such as cytogenetic abnormalities and ISS. Pol η expressions were positively correlated with p53 and myc expressions (r=0.718, p<0.001, r=0.528, p<0.001 respectively). p53 overexpression by Tet-on vector or nutlin-3 treatment enhanced Pol η expression, indicating that Pol η expression is regulated by p53. Melphalan or doxorubicin increased Pol η expression, but bortezomib or lenalidomide did not, suggesting that Pol η is upregulated by DNA damage via p53 pathway. Overall survival of the patients with high Pol η expression tended to be worse than with low Pol η expression (24 months survival: 69.6% vs. 57.9%, p=0.29). Pol θ expression was weakly correlated with p53. Melphalan induced Pol θ expression but doxorubicin did not. JQ1 significantly reduced Pol θ expression suggesting that Pol θ was regulated by bromodomain. Conclusion: We found that Pol θ and Pol η are highly expressed in MM, and upregulated by DNA damage. These DNA pols are involved in drug resistance and genomic instability leading to poor prognosis. Thus, DNA pols can be used as novel therapeutic targets and prognostic markers. Disclosures Handa: Ono: Research Funding.

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26

Jauhani, Muhammad Afiful, and Sheilla Rachmania. "DNA Quality and Quantity on Blood Spot Post Soil and Ultraviolet-C Exposure." Journal of Agromedicine and Medical Sciences 6, no. 3 (October 12, 2020): 181. http://dx.doi.org/10.19184/ams.v6i3.19937.

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Bercak darah dapat ditemukan di tempat kejadian perkara (TKP) pada banyak kasus tindak kekerasan. Asam deoksiribonukleat (DNA) pada darah dapat digunakan sebagai data primer untuk proses identifikasi akan tetapi bercak darah di TKP berisiko rusak akibat pajanan tanah dan ultraviolet. Tujuan utama dari penelitian ini adalah untuk mempelajari efek kombinasi dari pajanan sinar ultraviolet-C dan tanah terhadap kualitas dan kuantitas DNA pada bercak darah. Sebanyak 20 gelas berisi 200 gram tanah ditetesi 900µl darah dan diberikan pajanan sinar ultraviolet-C dalam tiga kelompok berdasarkan durasi pajanan yakni satu hari, tiga hari, dan lima hari. Satu kelompok digunakan sebagai kontrol. Ekstraksi DNA dilakukan menggunakan DNAZol dilanjutkan dengan pengukuran spektrofotometri untuk mengetahui kualitas dan kuantitas DNA. Peningkatan konsentrasi DNA dapat diamati yaitu 681,1 pada hari pertama menjadi 1274,7 pada hari ketiga dan mulai menurun menjadi 1090,6 pada hari kelima, sedangkan kemurnian DNA terus menurun secara konstan seiring dengan meningkatnya durasi pajanan. Penelitian ini menunjukkan bahwa pajanan sinar ultraviolet-C dan tanah menyebabkan degradasi molekul DNA menjadi fragmen-fragmen molekul yang lebih kecil sehingga terjadi peningkatan kuantitas DNA yang disertai penurunan kualitas DNA. Penurunan kualitas DNA dapat mempersulit proses identifikasi sehingga isolasi DNA sampel pada tanah terbuka yang terpajan matahari harus dilakukan sesegera mungkin. Kata Kunci: DNA, darah, tanah, ultraviolet C, patologi forensik

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27

Yeh, Ching-Sheng, Fu-Yen Chung, Chih-Ju Chen, Wen-Juun Tsai, Hong-Wen Liu, Gow-Jaw Wang, and Shiu-Ru Lin. "PPARγ-2andBMPR2Genes Were Differentially Expressed in Peripheral Blood of SLE Patients with Osteonecrosis." DNA and Cell Biology 27, no. 11 (November 2008): 623–28. http://dx.doi.org/10.1089/dna.2008.0772.

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28

Sang, Ming, Xuanbin Wang, Hanyao Zhang, Xiaodong Sun, Xudong Ding, Puqing Wang, Rong Jiao, Huaxian Cheng, Sijun Yang, and Guibin Zhang. "Gene Expression Profile of Peripheral Blood Mononuclear Cells in Response to Intracerebral Hemorrhage." DNA and Cell Biology 36, no. 8 (August 2017): 647–54. http://dx.doi.org/10.1089/dna.2017.3650.

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29

Kaur, Gurvinder, Lea Ann Thompson, Rachel L. Babcock, Karl Mueller, and Jannette M. Dufour. "Sertoli Cells Engineered to Express Insulin to Lower Blood Glucose in Diabetic Mice." DNA and Cell Biology 37, no. 8 (August 2018): 680–90. http://dx.doi.org/10.1089/dna.2017.3937.

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30

Enko, Dietmar, Gabriele Halwachs-Baumann, and Gernot Kriegshäuser. "Plasma free DNA." Biochemia medica 29, no. 1 (December 24, 2018): 153–56. http://dx.doi.org/10.11613/bm.2019.010904.

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Introduction: Standardized pre-analytical blood sample procedures for the analysis of circulating cell-free DNA (ccfDNA) are still not available. Therefore, the present study aimed at evaluating the impact of storage conditions related to different times (24 and 48 h) and temperatures (room temperature (RT) and 4 - 8 °C) on the plasma ccfDNA concentration of blood samples drawn into Cell-Free DNA collection tubes (Roche Diagnostics GmbH, Mannheim, Germany). Materials and methods: Venous blood from 30 healthy individuals was collected into five 8.5 mL Cell-Free DNA Collection Tubes (Roche Diagnostics GmbH) each. Plasma samples were processed at time point of blood collection (tube 1), and after storage under the following conditions: 24 h at RT (tube 2) or 4-8 °C (tube 3), and 48 h at RT (tube 4) or 4 - 8 °C (tube 5). Circulating cell-free DNA concentrations were determined by EvaGreen chemistry-based droplet digital PCR (ddPCR). Results: No statistically significant differences between median (interquartile range) plasma ccfDNA concentrations (ng/mL) at time point of blood collection (3.17 (2.13 – 3.76)) and after storage for 24 h (RT: 3.02 (2.41 – 3.68); 4-8 °C: 3.21 (2.19 – 3.46)) and 48 h (RT: 3.13 (2.10 – 3.76); 4-8 °C: 3.09 (2.19 – 3.50)) were observed (P values from 0.102 – 0.975). Conclusions: No unwanted release of genomic DNA from white blood cells could be detected in plasma samples after tube storage for 24 and 48 h regardless of storage temperature.

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31

Popp, Henning D., Vanessa Kohl, Johanna Flach, Susanne Brendel, Helga Kleiner, Wolfgang Seifarth, Christel Weiss, Susanne Saussele, Wolf-Karsten Hofmann, and Alice Fabarius. "Accumulation of DNA Damage and Alteration of the DNA Damage Response in Chronic Myeloid Leukemia." Blood 134, Supplement_1 (November 13, 2019): 5364. http://dx.doi.org/10.1182/blood-2019-122698.

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The accumulation of DNA damage and the alteration of the DNA damage response (DDR) are critical features of genetic instability that is presumed to be implicated in BCR/ABL1-mediated blastic transformation of chronic myeloid leukemia (CML). The aim of our study was to analyze underlying mechanisms of genetic instability with regard to DNA damage such as DNA double-strand breaks (DSB), DSB repair and DDR signaling during blastic transformation of CML. Immunofluorescence microscopy of γH2AX was performed for quantification of DSB in peripheral blood mononuclear cells (PBMC) of 8 healthy individuals, 24 chronic phase (CP)-CML patients under current/discontinued tyrosine kinase inhibitor (TKI) treatment (21 patients in deep molecular response (DMR), 3 patients in major molecular response (MMR)), 5 CP-CML patients under current/discontinued TKI treatment with loss of MMR, 3 de novo non-treated CP-CML patients and 2 blast phase (BP)-CML patients. In addition, immunofluorescence microscopy of γH2AX/53BP1 was used for semi-quantification of error-prone DSB repair. Furthermore, immunoblotting of p-ATM, p-ATR, p-CHK1, p-CHK2 and p-TP53 was performed in PBMC of CML patients in comparison to PBMC of healthy individuals. Our analysis revealed an increase in numbers of γH2AX foci in PBMC of CP-CML patients under current/discontinued TKI treatment with loss of MMR (1.8 γH2AX foci per PBMC ± 0.4), in PBMC of de novo non-treated CP-CML patients (2.3 γH2AX foci per PBMC ± 0.7) and in PBMC of BP-CML patients (4.9 γH2AX foci per PBMC ± 0.9) as compared to the number of γH2AX foci in PBMC of healthy individuals (1.0 γH2AX foci per PBMC ± 0.1) and in PBMC of CP-CML patients under current/discontinued TKI treatment in DMR/MMR (1.0 γH2AX foci per PBMC ± 0.1) (Figure 1A and B). Analysis of co-localizing γH2AX/53BP1 foci in PBMC suggested progressive activation of error-prone nonhomologous end-joining repair mechanisms during blastic transformation in CML. Signatures of p-ATM, p-ATR, p-CHK1, p-CHK2 and p-TP53 indicated alterations of the DDR. In summary, our data provide evidence for an accumulation of DNA damage in PBMC of CML patients towards BP-CML patients. We hypothesize that ongoing DSB generation, error-prone DSB repair and DDR alterations might be critical mechanisms of blastic transformation in CML. Figure 1 Analysis of γH2AX foci in freshly isolated peripheral blood mononuclear cells (PBMC) of healthy individuals and chronic myeloid leukemia (CML) patients. (A) Exemplary immunofluorescence microscopic images of γH2AX foci (green, Alexa 488) and cell nuclei (blue, DAPI) in PBMC of a healthy individual (HEALTHY#3), a chronic phase CML patient with a deep molecular response to tyrosine kinase inhibitor (CP-CML DMR#16), a de novo non-treated chronic phase CML patient (CP-CML#1) and a blast phase CML patient (BP-CML#2). (B) γH2AX foci levels in PBMC of healthy individuals and in PBMC of CML patients. Figure 1 Disclosures Saussele: Pfizer: Honoraria; Novartis: Honoraria, Research Funding; Incyte: Honoraria, Research Funding; BMS: Honoraria, Research Funding. Fabarius:Novartis: Research Funding.

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32

Molenaar-de Backer, M. W. A., A. Russcher, A. C. M. Kroes, M. H. G. M. Koppelman, M. Lanfermeijer, and H. L. Zaaijer. "Detection of parvovirus B19 DNA in blood: Viruses or DNA remnants?" Journal of Clinical Virology 84 (November 2016): 19–23. http://dx.doi.org/10.1016/j.jcv.2016.09.004.

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33

Genovese, Giulio, Anna K. Kähler, Robert E. Handsaker, Johan Lindberg, Samuel A. Rose, Samuel F. Bakhoum, Kimberly Chambert, et al. "Clonal Hematopoiesis and Blood-Cancer Risk Inferred from Blood DNA Sequence." New England Journal of Medicine 371, no. 26 (December 25, 2014): 2477–87. http://dx.doi.org/10.1056/nejmoa1409405.

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34

Dobrzyńska, Małgorzata M., Krzysztof A. Pachocki, and Katarzyna Owczarska. "DNA strand breaks in peripheral blood leucocytes of Polish blood donors." Mutagenesis 33, no. 1 (September 13, 2017): 69–76. http://dx.doi.org/10.1093/mutage/gex024.

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35

Bider-Canfield, Zoë, and Michelle Cotterchio. "Self-Reported ABO Blood Type Compared With DNA-Derived Blood Group." Epidemiology 25, no. 6 (November 2014): 936–37. http://dx.doi.org/10.1097/ede.0000000000000156.

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36

BRANT, MARTA, NICOLE NACHMANSSON, KERSTIN NORRMAN, INGEGÄRD REGNELL, and ANDERS BREDBERG. "Shuttle Vector Plasmid Propagation in Human Peripheral Blood Lymphocytes Facilitated by Liposome-Mediated Transfection." DNA and Cell Biology 10, no. 1 (January 1991): 75–79. http://dx.doi.org/10.1089/dna.1991.10.75.

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37

Fang, Tiancheng, Yurun Zhang, Vivian Y. Chang, Martina Roos, Christina M. Termini, Lia Signaevskaia, Mamle Quarmyne, et al. "Epidermal growth factor receptor–dependent DNA repair promotes murine and human hematopoietic regeneration." Blood 136, no. 4 (July 23, 2020): 441–54. http://dx.doi.org/10.1182/blood.2020005895.

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Abstract Chemotherapy and irradiation cause DNA damage to hematopoietic stem cells (HSCs), leading to HSC depletion and dysfunction and the risk of malignant transformation over time. Extrinsic regulation of HSC DNA repair is not well understood, and therapies to augment HSC DNA repair following myelosuppression remain undeveloped. We report that epidermal growth factor receptor (EGFR) regulates DNA repair in HSCs following irradiation via activation of the DNA-dependent protein kinase–catalytic subunit (DNA-PKcs) and nonhomologous end joining (NHEJ). We show that hematopoietic regeneration in vivo following total body irradiation is dependent upon EGFR-mediated repair of DNA damage via activation of DNA-PKcs. Conditional deletion of EGFR in hematopoietic stem and progenitor cells (HSPCs) significantly decreased DNA-PKcs activity following irradiation, causing increased HSC DNA damage and depressed HSC recovery over time. Systemic administration of epidermal growth factor (EGF) promoted HSC DNA repair and rapid hematologic recovery in chemotherapy-treated mice and had no effect on acute myeloid leukemia growth in vivo. Further, EGF treatment drove the recovery of human HSCs capable of multilineage in vivo repopulation following radiation injury. Whole-genome sequencing analysis revealed no increase in coding region mutations in HSPCs from EGF-treated mice, but increased intergenic copy number variant mutations were detected. These studies demonstrate that EGF promotes HSC DNA repair and hematopoietic regeneration in vivo via augmentation of NHEJ. EGF has therapeutic potential to promote human hematopoietic regeneration, and further studies are warranted to assess long-term hematopoietic effects.

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38

Liu, Xiaochang, Jiuxia Pang, Christopher Seiler, Ryan Kempen, Hao Liu, Aref Al-Kali, Y. Natalia Tretyakova, Mark Litzow, and Shujun Liu. "DNA Cytosine-Demethylating Agent 5-Aza-2'-Deoxycytidine Targets Leukemia Cells through Reducing DNA N6-Methyladenine." Blood 134, Supplement_1 (November 13, 2019): 2513. http://dx.doi.org/10.1182/blood-2019-130490.

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Introduction: It is known that overexpression of DNA methyltransferases (e.g., DNMT1) is frequent and changes of DNA cytosine methylation (5mC) are a constant feature of cancers. DNA methylation inhibitors, such as 5-aza-2'-deoxycytidine (Dec), have been in clinics for patients with leukemia. It is classically believed that promoter hypomethylation coupled by reexpression of epigenetically-suppressed tumor suppressors is a core mechanism behind Dec-impaired leukemia cell growth. However, the fact that global DNA methylation profiling barely predicts Dec-response suggests a demethylation-independent mechanism of Dec-induced cell death. N6-methyladenine (m6A) has been identified recently as an abundant DNA modification in eukaryotes (Wu, Nature 2016;532:329). Importantly, m6A is extensively present in the human genome, and m6A abundance is associated with tumorigenesis (Xie, Cell 2018;71:306). Furthermore, the DNA m6A is dynamically modulated by the methyltransferases (i.e., METTL3, N6AMT1) and demethylases (i.e., ALKBH1), and changes in m6A predict gene expression (Wu, Nature 2016;532:329). Given a potential crosstalk between m6A and distinct epigenetic mechanisms (Yao, Nat. Commun 2017;8:1122), we hypothesized that the anticancer actions of Dec may partially result from changes in DNA m6A in leukemia cells. Methods: Protein expression of target genes was assessed by Western blotting. The levels of DNA cytosine methylation (5mC) and N6-methyladenine (m6A) were measured by dotblotting or liquid chromatography-mass spectrometry (LC-MS/MS). The cell viability and apoptosis were determined by the Cell Counting Kit 8 (CCK8) assays as well as the Annexin V/Propidium Iodide staining and flow cytometry. The peripheral blood mononuclear cells (PBMCs) of leukemia patients from Mayo Clinic were prepared by Ficoll-Hypaque gradient centrifugation. Results: To test our hypothesis, leukemia cells, Kasumi-1, MV4-11, K562 and KU812, were exposed to 2 µM Dec, a clinical achievable concentration, for 72 hours. As expected, Dec treatment led to a downregulation of DNMT1 and DNMT3a, a reduction of 5mC levels by dotblotting using anti-5mC antibody, a blockage of cell proliferation and a promotion of cell apoptosis. When genomic DNA was subjected to dotblotting using anti-m6A antibody, the results revealed a marked decrease of DNA m6A levels in all Dec-treated cells. Then genomic DNA from K562 and MV4-11 cells was enzymatically digested to 2'-deoxynucleosides. dA was quantified by HPLC-UV, while the amount of m6A was measured by isotope dilution HPLC-ESI-MS/MS using 15N labeled internal standard. The standard curves were generated using pure standards, from which the m6A/A ratio was calculated. In agreement with dotblotting results, Dec treatment significantly decreased DNA m6A abundance in both cell lines. Mechanistically, exposure to Dec led to a consistent increase of demethylase fat mass and obesity-associated protein (FTO), but not METTL3 nor ALKBH1 and ALKBH5. Further, knockdown of FTO increased DNA m6A, which was further confirmed by treatment with FTO inhibitors rhein and meclofenamic acid (MA). These data indicate that FTO may be responsible for Dec-induced m6A changes in leukemia cells. To investigate the clinical implications of DNA m6A, we obtained PBMCs from AML patients (n = 10), who received Dec therapy (20 mg/m2 daily for 5 days every 4 weeks) in Mayo Clinic. These PBMCs were further cultured for 48 hours, frozen and stored in 100% ethanol before DNA extraction. The results from dotblotting using anti-5mC or anti-m6A showed that a trend of decrease in both m6A and 5mC abundance is observed, and the pattern of changes in m6A and 5mC displays a positive correlation. Finally, exposure of leukemia cells to the combination of Dec (2 µM) with FTO inhibitor MA (50 µM) induced more cell apoptosis and greater inhibition on cell proliferation as compared to single agent in vitro, supporting FTO inhibitors as new therapeutic agents in leukemia. Conclusion: Our studies suggest that the FTO-DNA m6A axis may partially mediate the therapeutic outcomes of Dec in leukemia. Our findings provide a new mechanistic paradigm for the anticancer activities of Dec, and define the m6A methylation status in leukemia cells as a new pharmacodynamic marker for their response to Dec-based therapy, pointing to a novel treatment strategy for incorporating m6A modulators to enhance the therapeutic index of Dec. Disclosures Al-Kali: Astex Pharmaceuticals, Inc.: Research Funding.

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Burdge, Graham C. "DHA supplementation during pregnancy and DNA methylation in cord blood leukocytes." American Journal of Clinical Nutrition 98, no. 6 (December 1, 2013): 1594–95. http://dx.doi.org/10.3945/ajcn.113.072074.

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Maggi, Fabrizio, Lisa Macera, Daniele Focosi, Maria Linda Vatteroni, Ugo Boggi, Guido Antonelli, Marc Eloit, and Mauro Pistello. "Human Gyrovirus DNA in Human Blood, Italy." Emerging Infectious Diseases 18, no. 6 (June 2012): 956–59. http://dx.doi.org/10.3201/eid1806.120179.

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Mulcahy, Hugh E., David T. Croke, and Michael JG Farthing. "Cancer and mutant DNA in blood plasma." Lancet 348, no. 9028 (September 1996): 628. http://dx.doi.org/10.1016/s0140-6736(05)65067-2.

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Rötig, Agnès, Michel Colonna, Stéphane Blanche, Alain Fischer, Françoise Le Deist, Jean Frezal, Jean-Marie Saudubray, and Arnold Munnich. "DELETION OF BLOOD MITOCHONDRIAL DNA IN PANCYTOPENIA." Lancet 332, no. 8610 (September 1988): 567–68. http://dx.doi.org/10.1016/s0140-6736(88)92687-6.

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Simmonte, Matthew, and Mark Bradley. "Polymers for mitochondrial DNA scavenging from blood." New Biotechnology 33 (July 2016): S17. http://dx.doi.org/10.1016/j.nbt.2016.06.785.

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Shuster, Robert C., Andrew J. Rubenstein, and Douglas C. Wallace. "Mitochondrial DNA in anucleate human blood cells." Biochemical and Biophysical Research Communications 155, no. 3 (September 1988): 1360–65. http://dx.doi.org/10.1016/s0006-291x(88)81291-9.

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Crouch, Suzanne J., Kathleen R. Rowell, and Sharon O. Beiser. "Umbilical Cord Blood for Newborn DNA Identification." Journal of Obstetric, Gynecologic & Neonatal Nursing 36, no. 4 (July 2007): 308–12. http://dx.doi.org/10.1111/j.1552-6909.2007.00162.x.

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Jackson, Laird. "Fetal cells and DNA in maternal blood." Prenatal Diagnosis 23, no. 10 (2003): 837–46. http://dx.doi.org/10.1002/pd.705.

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Milne, Elizabeth, Kathryn R. Greenop, Padmaja Ramankutty, Margaret Miller, Nicholas H. de Klerk, Bruce K. Armstrong, Theodora Almond, Nathan J. O'Callaghan, and Michael Fenech. "Blood micronutrients and DNA damage in children." Molecular Nutrition & Food Research 59, no. 10 (August 26, 2015): 2057–65. http://dx.doi.org/10.1002/mnfr.201500110.

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Klote, Mary M., Renata J. M. Engler, Bryan L. Martin, James F. Cummings, Glenn W. Wortmann, and George V. Ludwig. "Vaccinia DNA in Blood After Smallpox Vaccination." JAMA 296, no. 11 (September 20, 2006): 1350. http://dx.doi.org/10.1001/jama.296.11.1350-c.

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Savona, Michael R., and Patrick J. Danaher. "Vaccinia DNA in Blood After Smallpox Vaccination." JAMA 296, no. 11 (September 20, 2006): 1350. http://dx.doi.org/10.1001/jama.296.11.1351.

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Simpson, Joe Leigh, and Farideh Bischoff. "Cell-Free Fetal DNA in Maternal Blood." JAMA 291, no. 9 (March 3, 2004): 1135. http://dx.doi.org/10.1001/jama.291.9.1135.

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