X
Search Filters
Format Format
Format Format
X
Sort by Item Count (A-Z)
Filter by Count
Journal Article (2268) 2268
Publication (368) 368
Book Review (33) 33
Book Chapter (13) 13
Conference Proceeding (4) 4
Government Document (3) 3
Magazine Article (3) 3
Data Set (1) 1
Dissertation (1) 1
Newspaper Article (1) 1
more...
Subjects Subjects
Subjects Subjects
X
Sort by Item Count (A-Z)
Filter by Count
humans (1648) 1648
index medicus (1505) 1505
female (1162) 1162
brca1 (1062) 1062
breast cancer (1017) 1017
oncology (973) 973
cancer (853) 853
mutation (806) 806
brca1 protein - genetics (750) 750
dna repair (670) 670
genetic aspects (613) 613
breast neoplasms - genetics (593) 593
animals (567) 567
dna damage (559) 559
brca1 protein (538) 538
homologous recombination (522) 522
cell biology (452) 452
research (440) 440
brca1 protein - metabolism (437) 437
ovarian cancer (432) 432
tumors (422) 422
genes, brca1 (387) 387
mice (382) 382
deoxyribonucleic acid--dna (369) 369
middle aged (367) 367
biochemistry & molecular biology (348) 348
genetics & heredity (346) 346
adult (339) 339
proteins (335) 335
skin and connective tissue diseases (330) 330
dna (318) 318
brca2 protein - genetics (317) 317
repair (315) 315
article (313) 313
genes (301) 301
breast-cancer (300) 300
ovarian neoplasms - genetics (299) 299
cell line, tumor (297) 297
poly polymerase (297) 297
chemotherapy (296) 296
gene expression (287) 287
ovarian-cancer (269) 269
aged (265) 265
breast neoplasms - pathology (255) 255
gene mutations (252) 252
analysis (250) 250
brca2 (250) 250
health aspects (250) 250
genetic predisposition to disease (244) 244
endocrine system diseases (239) 239
risk factors (230) 230
brca2 protein (223) 223
expression (223) 223
genes, brca2 (221) 221
mutations (219) 219
multidisciplinary sciences (215) 215
care and treatment (211) 211
breast neoplasms - metabolism (210) 210
double-strand breaks (208) 208
genetics (203) 203
cell cycle (201) 201
research article (193) 193
genomic instability (190) 190
medicine (185) 185
cells (184) 184
prognosis (182) 182
apoptosis (179) 179
dna-damage response (178) 178
male (178) 178
breast (174) 174
dna-damage (173) 173
genomes (169) 169
phosphorylation (164) 164
protein (163) 163
gene expression regulation, neoplastic (159) 159
dna methylation (153) 153
breast neoplasms - drug therapy (152) 152
genomics (151) 151
dna breaks, double-stranded (150) 150
gene (150) 150
medicine & public health (150) 150
genetic research (146) 146
dna-binding proteins - genetics (145) 145
physiological aspects (144) 144
brca1 protein - deficiency (143) 143
biology (141) 141
antineoplastic agents - therapeutic use (140) 140
survival (140) 140
dna repair - genetics (139) 139
germ-line mutation (139) 139
ovarian neoplasms - drug therapy (136) 136
p53 (133) 133
development and progression (131) 131
dna-repair (130) 130
risk (130) 130
science (130) 130
dna-binding proteins - metabolism (129) 129
poly polymerase inhibitors (125) 125
patients (123) 123
cancer research (121) 121
more...
Language Language
Publication Date Publication Date
Click on a bar to filter by decade
Slide to change publication date range


Nature medicine, ISSN 1078-8956, 2017, Volume 23, Issue 4, pp. 517 - 525
Journal Article
Nature Structural and Molecular Biology, ISSN 1545-9993, 2010, Volume 17, Issue 6, pp. 688 - 695
Germ-line mutations in breast cancer 1, early onset (BRCA1) result in predisposition to breast and ovarian cancer. BRCA1-mutated tumors show genomic... 
STEM-CELLS | GENE BRCA1 | DNA-DAMAGE RESPONSE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CONDITIONAL MOUSE MODEL | DOUBLE-STRAND BREAKS | OVARIAN-CANCER | CELL BIOLOGY | GENOMIC INSTABILITY | MAMMARY-TUMORS | BIOPHYSICS | TUMOR-SUPPRESSOR | CELL-CYCLE | Embryonic Stem Cells - metabolism | Cell Proliferation | Embryonic Stem Cells - cytology | Humans | Breast Neoplasms - metabolism | Intracellular Signaling Peptides and Proteins - deficiency | Gene Deletion | Genes, BRCA2 | Female | Genes, BRCA1 | Tumor Cells, Cultured | BRCA1 Protein - deficiency | Intracellular Signaling Peptides and Proteins - genetics | DNA-Binding Proteins | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | Chromosomal Proteins, Non-Histone | Breast Neoplasms - drug therapy | Mice, Knockout | BRCA1 Protein - genetics | Drug Resistance, Neoplasm - genetics | Animals | Apoptosis Regulatory Proteins | Breast Neoplasms - genetics | Cell Cycle | Breast Neoplasms - pathology | DNA Repair | BRCA2 Protein - deficiency | Mice | Mutagenesis, Insertional | DNA Damage | Mutation | Tumor Suppressor p53-Binding Protein 1 | Drug Resistance, Neoplasm - physiology | BRCA2 Protein - genetics | BRCA mutations | DNA damage | Physiological aspects | Breast cancer | Genetic aspects | Research | Health aspects | DNA repair | Risk factors | Molecular biology | Ovarian cancer
Journal Article
Molecular Cell, ISSN 1097-2765, 08/2009, Volume 35, Issue 4, pp. 534 - 541
The molecular pathways leading from genomic instability to cellular senescence and/or cell death remain incompletely characterized. Using mouse embryonic... 
CELLCYCLE | DNA | HUMDISEASE | APOPTOSIS | ACTIVATION | TUMOR SUPPRESSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | ONCOGENE-INDUCED SENESCENCE | CELLULAR SENESCENCE | TUMORIGENESIS | CANCER | MICE LACKING | P53 | CELL BIOLOGY | Gamma Rays | Cellular Senescence - drug effects | Apoptosis - genetics | Intracellular Signaling Peptides and Proteins - metabolism | DNA-Binding Proteins - metabolism | Aging - genetics | Cell Transformation, Neoplastic - genetics | Tumor Suppressor Proteins - genetics | Cellular Senescence - radiation effects | Cell Cycle Proteins - genetics | Genomic Instability - drug effects | BRCA1 Protein - deficiency | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Hydrogen Peroxide - toxicity | Cellular Senescence - genetics | Genomic Instability - radiation effects | Tumor Suppressor Proteins - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Chromosomal Proteins, Non-Histone | Protein-Serine-Threonine Kinases - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Fibroblasts - pathology | Cell Transformation, Neoplastic - metabolism | Doxorubicin - toxicity | Mice, Knockout | BRCA1 Protein - genetics | Animals | Histones - genetics | Checkpoint Kinase 2 | Mice | Histones - metabolism | Tumor Suppressor p53-Binding Protein 1 | Aging - metabolism | Gene mutations | Cell death | Kidney diseases | Tumor proteins | Health aspects | Tumors | Protein binding | Index Medicus
Journal Article
Molecular Cell, ISSN 1097-2765, 02/2016, Volume 61, Issue 3, pp. 449 - 460
G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers. Stalled replication forks can be stabilized and... 
HUMAN GENOME | REPLICATION | MAMMALIAN TELOMERES | SMALL-MOLECULE | HUMAN-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | HOMOLOGOUS RECOMBINATION | CANCER | TUMORS | LIGAND RHPS4 | CELL BIOLOGY | Purines | Lung cancer | DNA damage | Genomics | Radiation | Chromosomes | DNA repair | Telomeres | Cells
Journal Article
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 2280 - 14
Defects in DNA repair can cause various genetic diseases with severe pathological phenotypes. Fanconi anemia ( FA) is a rare disease characterized by bone... 
UBIQUITINATION | DAMAGE RESPONSE | CHROMATIN | CROSS-LINK REPAIR | HUMAN-CELLS | MULTIDISCIPLINARY SCIENCES | SENSITIVITY | HOMOLOGOUS RECOMBINATION | BRCA1 | ENRICHMENT ANALYSIS | ASSOCIATION | Genetic Therapy | Ubiquitin-Specific Proteases - genetics | Fanconi Anemia Complementation Group D2 Protein - genetics | Fanconi Anemia - metabolism | Humans | DNA Repair - physiology | DNA Repair - genetics | Fanconi Anemia Complementation Group C Protein - genetics | Fanconi Anemia Complementation Group A Protein - genetics | Fanconi Anemia Complementation Group D2 Protein - deficiency | Fanconi Anemia Complementation Group A Protein - metabolism | Fanconi Anemia Complementation Group Proteins - metabolism | Ubiquitination | Fanconi Anemia Complementation Group G Protein - genetics | Ubiquitin-Specific Proteases - deficiency | Fanconi Anemia Complementation Group G Protein - deficiency | BRCA1 Protein - metabolism | Fanconi Anemia - genetics | Ubiquitin-Specific Proteases - metabolism | Chromosomal Instability | Rad51 Recombinase - metabolism | Cell Line | Fanconi Anemia Complementation Group Proteins - deficiency | Fanconi Anemia Complementation Group Proteins - genetics | Fanconi Anemia Complementation Group G Protein - metabolism | Gene Knockout Techniques | Fanconi Anemia Complementation Group C Protein - metabolism | Fanconi Anemia Complementation Group D2 Protein - metabolism | Fanconi Anemia Complementation Group A Protein - deficiency | CRISPR-Cas Systems | Fanconi Anemia Complementation Group C Protein - deficiency | Fanconi Anemia - therapy | DNA Damage | Histones - metabolism | Mutation
Journal Article
Nature, ISSN 0028-0836, 2015, Volume 521, Issue 7553, pp. 541 - U308
Journal Article
Journal Article
Oncogene, ISSN 0950-9232, 12/2018, Volume 37, Issue 49, pp. 6341 - 6356
Journal Article
Nature, ISSN 0028-0836, 08/2018, Volume 560, Issue 7716, pp. 122 - 127
53BP1 governs a specialized, context-specific branch of the classical non-homologous end joining DNA double-strand break repair pathway. Mice lacking 53bp1... 
CELLS | REV7 | RESECTION | TRANSLOCATIONS | POL-ZETA | MULTIDISCIPLINARY SCIENCES | BRCA1 DEFICIENCY | CLASS-SWITCH RECOMBINATION | MECHANISMS | POLYMERASE-ZETA | GENE-FUNCTION | Mad2 Proteins - metabolism | Humans | Male | Tumor Suppressor p53-Binding Protein 1 - deficiency | DNA Breaks, Double-Stranded | DNA-Binding Proteins - metabolism | Multiprotein Complexes - metabolism | DNA End-Joining Repair | Female | Mad2 Proteins - deficiency | Tumor Suppressor p53-Binding Protein 1 - metabolism | Cell Line | DNA, Single-Stranded - metabolism | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | DNA - metabolism | DNA, Single-Stranded - chemistry | V(D)J Recombination - genetics | DNA - chemistry | Multiprotein Complexes - chemistry | Animals | Mad2 Proteins - genetics | Mice | Mutation | Immunoglobulin Class Switching - genetics | Genetic research | Genetic recombination | Recombinant proteins | Analysis | DNA structure | Chromatin | Animal models | Single-stranded DNA | DNA damage | Homology | DNA repair | Genomic instability | Proteins | Immunology | Lymphocytes | Cooperation | Bone marrow | Tumorigenesis | Repair | Deoxyribonucleic acid--DNA | Stability | V(D)J recombination | Immunodeficiency | Crosslinking | Double-strand break repair | Substrates | Class switching | Telomeres | Non-homologous end joining | Instability | Tumors
Journal Article
Oncogene, ISSN 0950-9232, 04/2008, Volume 27, Issue 17, pp. 2501 - 2506
The ataxia- telangiectasia- mutated ( ATM) kinase is a key transducer of DNA damage signals within the genome maintenance machinery and a tumour suppressor... 
Genetic instability | DNA damage response | ATM defects | BRCA1/BRCA2 familial cancer | Triple-negative breast cancer | genetic instability | POLY(ADP-RIBOSE) POLYMERASE | triple-negative breast cancer | BRCA2 MUTATIONS | HISTOPATHOLOGICAL FEATURES | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOUBLE-STRAND BREAKS | ANTICANCER BARRIER | ONCOGENE-INDUCED SENESCENCE | TUMORS | CELL BIOLOGY | ONCOLOGY | FAMILIES | PROTEIN EXPRESSION | GENETICS & HEREDITY | ATAXIA-TELANGIECTASIA | Protein-Serine-Threonine Kinases - deficiency | Receptors, Estrogen - metabolism | Tumor Suppressor Proteins - metabolism | Signal Transduction | Humans | Cell Cycle Proteins - metabolism | Receptor, ErbB-2 - metabolism | Tumor Suppressor Protein p53 - metabolism | Ataxia Telangiectasia Mutated Proteins | Receptors, Estrogen - deficiency | DNA-Binding Proteins - deficiency | Breast Neoplasms - metabolism | Receptors, Progesterone - metabolism | DNA-Binding Proteins - metabolism | Receptors, Progesterone - deficiency | BRCA2 Protein - metabolism | Breast Neoplasms - genetics | Tumor Suppressor Proteins - deficiency | BRCA1 Protein - metabolism | DNA Damage - genetics | BRCA2 Protein - deficiency | BRCA1 Protein - deficiency | Receptor, ErbB-2 - deficiency | Protein-Serine-Threonine Kinases - metabolism | Complications and side effects | Control | BRCA mutations | Ataxia telangiectasia | Genetic aspects | Breast cancer | Research | Health aspects | Risk factors | Signal transduction | Cellular biology | DNA damage | Oncology | Kinases | Gene expression | Medical and Health Sciences | Medicin och hälsovetenskap | MEDICIN | MEDICINE
Journal Article