Refine
Has Fulltext
- yes (37)
Is part of the Bibliography
- yes (37)
Year of publication
Document Type
- Journal article (37)
Language
- English (37)
Keywords
- DNA methylation (9)
- epigenetics (3)
- Medizin (2)
- STR profile (2)
- bisulfite pyrosequencing (2)
- copy number variation (2)
- exome sequencing (2)
- extracellular matrix (2)
- fetal programming (2)
- fibrosis (2)
- genomic imprinting (2)
- gestational diabetes mellitus (2)
- hearing loss (2)
- hepatic stellate cell (2)
- liver (2)
- methylation (2)
- myofibroblast (2)
- sperm DNA methylation (2)
- (classical and atypical) Werner syndrome (1)
- 3D modeling (1)
- 5-methylcytosine (1)
- ADHD (1)
- ART outcome (1)
- Autism (1)
- Autism spectrum disorders (1)
- BRCA1 (1)
- CAGSSS (1)
- CDC14A (1)
- CLRN2 (1)
- Checkpoints (1)
- Copy number variation (1)
- Cortex (1)
- DFNB32 (1)
- DFNB68 (1)
- DNA Methylation (1)
- DNA damage (1)
- DNA double-strand break (1)
- DNA methylation dynamics (1)
- Damage (1)
- Down syndrome (1)
- Environment (1)
- Epigenetics (1)
- FISH (1)
- Familial Beckwith-Wiedemann syndrome (1)
- Fetal brain development (1)
- Frontal cortex (1)
- GTL2 (1)
- Gecko (1)
- Gene-expression (1)
- Genes (1)
- Genome (1)
- Genotype-phenotype association (1)
- Human prefrontal cortex (1)
- IARS2 (1)
- ICSI (1)
- IMSI (1)
- Instability (1)
- Malignant neoplasms (1)
- Methylome (1)
- Neanderthal (1)
- Pakistan (1)
- Parent-of-origin (1)
- Patterns (1)
- Repair (1)
- S1PR2 (1)
- SKY analysis (1)
- SLC2A3 (1)
- SNP array (1)
- SNP-microarray (1)
- Schizophrenia (1)
- Stability (1)
- Suicidal behavior (1)
- Susceptibility (1)
- Terminal 4q deletion syndrome (1)
- Th17 (1)
- Transcription (1)
- Transcription regulation (1)
- Tregs (1)
- Usher syndrome (1)
- Y chromosome degeneration (1)
- ZW sex chromosomes (1)
- adenoma (1)
- adipose (1)
- adipose tissue dysfunction (1)
- adrenal insufficiency (1)
- age-related differentially methylated regions (ageDMRs) (1)
- alu elements (1)
- antidepressants (1)
- anxiety disorders (1)
- autosomal recessive hearing loss (1)
- autosomal recessive non-synstromic hearing loss (1)
- banding analyses (1)
- blood (1)
- cancer treatment (1)
- cataracts (1)
- childhood cancer (1)
- combined retinal dystrophy (1)
- complex chromosome rearrangements (1)
- complex disorders (1)
- consanguinity (1)
- deafness (1)
- deep bisulfite sequencing (1)
- developmental origins hypothesis (1)
- duplication-deficiency (1)
- epigenetic heterogeneity (1)
- epimutation (1)
- fetal brain development (1)
- fetal cord blood (1)
- fetal overnutrition (1)
- fibroblasts (1)
- frameshift (1)
- frontal cortex (1)
- geckos (1)
- gene (1)
- gene expression (1)
- genetic diagnosis (1)
- genetic heterogeneity (1)
- genetics (1)
- genome-wide association study (GWAS) (1)
- genome-wide linkage analysis (1)
- genotyping arrays (1)
- growth hormone deficiency (1)
- haploinsufficiency (1)
- hearing impairment (1)
- hereditary hearing loss (1)
- heterochromatin (1)
- histological subtype (1)
- human evolution (1)
- hypoxia-inducible factor 3A (1)
- illumina (1)
- in vitro model (1)
- induced pluripotent stem cells (1)
- infinium HumanOmni1-Quad (1)
- inflammatory diseases (1)
- insulin treatment (1)
- karyotype evolution (1)
- mammalian male germline (1)
- meiosis (1)
- meiotic chromosomes (1)
- metabolic disease (1)
- methylation array (1)
- mitotic chromosomes (1)
- mixed hearing loss (1)
- mixed mutation mechanisms (1)
- monozygotic twins (1)
- next generation sequencing (1)
- next-generation sequencing (1)
- non-sense mediated mRNA decay (1)
- obesity (1)
- panic disorder (1)
- paternal age effect (1)
- phalloidin stain (1)
- polymerase chain reaction (1)
- premature aging (1)
- promoter methylation (1)
- protocadherin gamma cluster (1)
- reciprocal translocation (1)
- recombination (1)
- recurrence (1)
- regulatory T cells (1)
- rhodamine–phalloidin stain (1)
- secondary cancer (1)
- segmental progeria (1)
- sensorineural hearing loss (1)
- sensory neuropathy (1)
- sequence alignment (1)
- sex chromosomes (1)
- sex linked pigmentation pattern (1)
- sexual antagonistic genes (1)
- skeletal dysplasia (1)
- somatic mosaicism (1)
- species-specific epigenetic marks (1)
- spectral karyotyping (1)
- sperm (1)
- splicing (1)
- stress fibers (1)
- structural genome variations (1)
- submicroscopic chromosome rearrangement (1)
- suppression (1)
- synaptonemal complex (1)
- systemic sclerosis (1)
- telomere length (1)
- testosterone (1)
- tinnitus (1)
- transcription deficiency (1)
- treatment guidelines (1)
- triplosufficiency (1)
- trisomy 21 (1)
- twin study (1)
- type II esophageal achalasia (1)
- whole exome sequencing (1)
Institute
- Institut für Humangenetik (36)
- Theodor-Boveri-Institut für Biowissenschaften (11)
- Kinderklinik und Poliklinik (2)
- Klinik und Poliklinik für Hals-, Nasen- und Ohrenkrankheiten, plastische und ästhetische Operationen (2)
- Institut für Anatomie und Zellbiologie (1)
- Klinik und Poliklinik für Dermatologie, Venerologie und Allergologie (1)
- Klinik und Poliklinik für Psychiatrie, Psychosomatik und Psychotherapie (1)
- Klinik und Poliklinik für Unfall-, Hand-, Plastische und Wiederherstellungschirurgie (Chirurgische Klinik II) (1)
- Lehrstuhl für Molekulare Psychiatrie (1)
- Medizinische Klinik und Poliklinik II (1)
Sonstige beteiligte Institutionen
Background:
The etiology of secondary cancer in childhood cancer survivors is largely unclear. Exposure of normal somatic cells to radiation and/or chemotherapy can damage DNA and if not all DNA lesions are properly fixed, the mis-repair may lead to pathological consequences. It is plausible to assume that genetic differences, i.e. in the pathways responsible for cell cycle control and DNA repair, play a critical role in the development of secondary cancer.
Methodology/Findings:
To identify factors that may influence the susceptibility for second cancer formation, we recruited 20 individuals who survived a childhood malignancy and then developed a second cancer as well as 20 carefully matched control individuals with childhood malignancy but without a second cancer. By antibody microarrays, we screened primary fibroblasts of matched patients for differences in the amount of representative DNA repair-associated proteins. We found constitutively decreased levels of RAD9A and several other DNA repair proteins in two-cancer patients, compared to one-cancer patients. The RAD9A protein level increased in response to DNA damage, however to a lesser extent in the two-cancer patients. Quantification of mRNA expression by real-time RT PCR revealed lower RAD9A mRNA levels in both untreated and 1 Gy gamma-irradiated cells of two-cancer patients.
Conclusions/Significance:
Collectively, our results support the idea that modulation of RAD9A and other cell cycle arrest and DNA repair proteins contribute to the risk of developing a second malignancy in childhood cancer patients.