scholarly journals Chloroplast DNA Copy Number Changes during Plant Development in Organelle DNA Polymerase Mutants

2016 ◽  
Vol 7 ◽  
Author(s):  
Stewart A. Morley ◽  
Brent L. Nielsen
Keyword(s):  
Chloroplast Dna ◽  
Dna Polymerase ◽  
Plant Development ◽  
Copy Number ◽  
Dna Copy Number ◽  
Organelle Dna ◽  
Copy Number Changes ◽  
Polymerase Mutants

scholarly journals Genomic Adaption and Mutational Patterns in a HaCaT Subline Resistant to Alkylating Agents and Ionizing Radiation

2021 ◽  
Vol 22 (3) ◽  
pp. 1146
Author(s):  
Reinhard Ullmann ◽  
Benjamin Valentin Becker ◽  
Simone Rothmiller ◽  
Annette Schmidt ◽  
Horst Thiermann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Copy Number ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Chromosomal Translocations ◽  
Dna Copy Number ◽  
Mutational Signatures ◽  
Copy Number Changes ◽  
And Oxidative Stress

Sulfur mustard (SM) is a chemical warfare agent that can damage DNA via alkylation and oxidative stress. Because of its genotoxicity, SM is cancerogenic and the progenitor of many chemotherapeutics. Previously, we developed an SM-resistant cell line via chronic exposure of the popular keratinocyte cell line HaCaT to increasing doses of SM over a period of 40 months. In this study, we compared the genomic landscape of the SM-resistant cell line HaCaT/SM to its sensitive parental line HaCaT in order to gain insights into genetic changes associated with continuous alkylation and oxidative stress. We established chromosome numbers by cytogenetics, analyzed DNA copy number changes by means of array Comparative Genomic Hybridization (array CGH), employed the genome-wide chromosome conformation capture technique Hi-C to detect chromosomal translocations, and derived mutational signatures by whole-genome sequencing. We observed that chronic SM exposure eliminated the initially prevailing hypotetraploid cell population in favor of a hyperdiploid one, which contrasts with previous observations that link polyploidization to increased tolerance and adaptability toward genotoxic stress. Furthermore, we observed an accumulation of chromosomal translocations, frequently flanked by DNA copy number changes, which indicates a high rate of DNA double-strand breaks and their misrepair. HaCaT/SM-specific single-nucleotide variants showed enrichment of C > A and T > A transversions and a lower rate of deaminated cytosines in the CpG dinucleotide context. Given the frequent use of HaCaT in toxicology, this study provides a valuable data source with respect to the original genotype of HaCaT and the mutational signatures associated with chronic alkylation and oxidative stress.

scholarly journals GEAR: genomic enrichment analysis of regional DNA copy number changes

2007 ◽  
Vol 24 (3) ◽  
pp. 420-421 ◽  
Author(s):  
T.-M. Kim ◽  
Y.-C. Jung ◽  
M.-G. Rhyu ◽  
M. H. Jung ◽  
Y.-J. Chung
Keyword(s):  
Copy Number ◽  
Enrichment Analysis ◽  
Dna Copy Number ◽  
Copy Number Changes

scholarly journals DNA copy number changes in young gastric cancer patients with special reference to chromosome 19

2003 ◽  
Vol 88 (12) ◽  
pp. 1914-1919 ◽  
Author(s):  
A Varis ◽  
B van Rees ◽  
M Weterman ◽  
A Ristimäki ◽  
J Offerhaus ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Special Reference ◽  
Cancer Patients ◽  
Copy Number ◽  
Chromosome 19 ◽  
Dna Copy Number ◽  
Copy Number Changes ◽  
Gastric Cancer Patients

DNA copy number changes correlate with clinical behavior in melanocytic neoplasms: proposal of an algorithmic approach

2020 ◽  
Vol 33 (7) ◽  
pp. 1307-1317
Author(s):  
Ahmed K. Alomari ◽  
Jayson R. Miedema ◽  
Michael D. Carter ◽  
Paul W. Harms ◽  
Lori Lowe ◽  
...  
Keyword(s):  
Copy Number ◽  
Dna Copy Number ◽  
Algorithmic Approach ◽  
Clinical Behavior ◽  
Copy Number Changes

High-resolution array CGH of metanephric adenomas: lack of DNA copy number changes

2010 ◽  
Vol 56 (2) ◽  
pp. 212-216 ◽  
Author(s):  
Adrianna Szponar ◽  
Maria V Yusenko ◽  
Gyula Kovacs
Keyword(s):  
High Resolution ◽  
Copy Number ◽  
Array Cgh ◽  
Dna Copy Number ◽  
Copy Number Changes

Prognostic impacts of DNA copy number changes in gastrointestinal stromal tumors

2004 ◽  
Vol 200 (4) ◽  
pp. 317
Author(s):  
S. Lukas ◽  
B. Gunawan ◽  
C. Enders ◽  
H.-J. Schulten ◽  
A. Von Heydebreck ◽  
...  
Keyword(s):  
Copy Number ◽  
Gastrointestinal Stromal Tumors ◽  
Dna Copy Number ◽  
Stromal Tumors ◽  
Copy Number Changes

Genomic DNA Copy Number Alterations Present in AML Bone Marrow Samples with Normal Cytogenetics.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 142-142 ◽  
Author(s):  
Matthew J. Walter ◽  
Rhonda E. Ries ◽  
Jon Armstrong ◽  
Brian O’Gara ◽  
James W. Vardiman ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Copy Number ◽  
Genomic Dna ◽  
Array Cgh ◽  
Comparative Genomic ◽  
Copy Number Alterations ◽  
Dna Copy Number ◽  
Prognostic Information ◽  
Normal Cytogenetics ◽  
Copy Number Changes

Abstract Cytogenetics and comparative genomic hybridization (CGH) have been used to identify large genomic amplifications and deletions in all subtypes of acute myeloid leukemia (AML). Up to 15–20% of AML patients have a normal karyotype at diagnosis. While cytogenetic abnormalities confer important prognostic information for patients with AML, there remain differences in the therapeutic response and outcome among patients with the same cytogenetic profile, implying that other, more subtle, genetic abnormalities may exist. We hypothesized that a subset of AML patients with normal cytogenetics may contain genomic DNA copy number changes that are too small to be detected using standard cytogenetic techniques. To address this possibility, we used high-resolution bacterial artificial chromosome (BAC) array CGH technology to examine 31 AML patients with normal cytogenetics. The BAC arrays contain 2,464 BAC clones spotted in triplicate on glass slides, and provide a 1 Mb resolution of the entire human genome. Technical generation of the arrays, hybridization parameters, and analysis were similar to that reported for murine BAC array CGH (Nat Genet. 2001 Dec;29(4):459–64). The 31 AML samples included 4 M0, 8 M1, 10 M2, and 9 M4 patients. Array CGH experiments were performed using 500 nanograms of Cyanine 5 labeled genomic DNA from unmanipulated AML bone marrow, mixed with an equal amount of control DNA (a pool of DNA from 4 cancer-free individuals) labeled with Cyanine 3. Using the human 1 Mb BAC arrays, we identified amplifications and deletions from multiple samples that were confirmed with G-banding cytogenetics [del(7)(q31), del(7)(p11.2), +8, del(11)(q13q23), +21, add(21)(q22), −X, −Y, +Y]. In addition, BAC arrays robustly detected copy number alterations that were identified in as few as 4/21 metaphases. We identified 5/31 (16%) patients with normal cytogenetics that contained altered genomic DNA copy numbers using BAC array CGH. Copy number changes were confirmed for several of these genomic loci using a dye-swap experiment, where the AML DNA was labeled with Cyanine 3, and the control DNA with Cyanine 5. Two of the 5 patients with abnormalities detected using array CGH would be reclassified from “intermediate” to “unfavorable” cytogenetics [del(7)(q31.31q34), add(11)(q23.3qter), and 17(p12pter)]. These results suggest that a subset of AML patients with normal cytogenetics contain genomic copy number alterations that may effect treatment and outcome. Patient # FAB subtype Genomic location Gain or loss Size (Megabase) Dye-Swap confirmed 1 M0 7(q31.31q34) loss 2.0 Not done 1 11(q23.3qter) gain 16.5 Not done 2 M1 11(p14) loss 7.4 Yes 3 M1 11(q13.2q14.1) gain 15.8 Yes 3 19(p) gain 64.0 Yes 4 M2 17(p12pter) gain 8.6 Not Done 5 M2 19(p13.1pter) loss 14.8 Yes 5 12(q13) loss 5.0 Yes

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